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-gptKey
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-# NCD: data aggregation and classification
-
-## Remarks
-
--
-
-## TODO
-
-### Must
-- Trouver en combien de temps les mesh term sont donnée
-- Explorer les model non-superviser (classification de texte)
-
-- ~~Mesh term vs keyword~~
-- ~~Ou il recherche les term (titre, keywords, meshterms, etc...)~~
-- ~~Etudier les operateur (A or B and C) (A or B) and C A or (B and C)~~
-- Service qui tourne en arriere plan qui récupere les données
-- Reflechire sur la structure de stockage
-
-- Créer un ensemble de validation qui permet de tester la qualité d'un modèle (vrai, proche de vrai, proche de vrai mais faux et complettement faux). Donnée provenantente de pubmed et autre part. Source longue et courte.
-
-- Créer un model de score
-- Créer un script de test
\ No newline at end of file
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-<?xml version="1.0" ?>
-<!DOCTYPE PubmedArticleSet PUBLIC "-//NLM//DTD PubMedArticle, 1st January 2025//EN" "https://dtd.nlm.nih.gov/ncbi/pubmed/out/pubmed_250101.dtd">
-<PubmedArticleSet>
-<PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39674195</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>31</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2542-5196</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The Lancet. Planetary health</Title><ISOAbbreviation>Lancet Planet Health</ISOAbbreviation></Journal><ArticleTitle>The potential for reducing greenhouse gas emissions through disease prevention: a secondary analysis of data from the CREDENCE trial.</ArticleTitle><Pagination><StartPage>e1055</StartPage><EndPage>e1064</EndPage><MedlinePgn>e1055-e1064</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/S2542-5196(24)00281-X</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S2542-5196(24)00281-X</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The health-care sector is responsible for 5·2% of global emissions, however, little data exist regarding the environmental impact of disease management strategies. SGLT2 inhibitors are now widely used to reduce the risk of hospital admission and kidney failure in people with type 2 diabetes and chronic kidney disease. This study aimed to estimate the impact of SGLT2 inhibitors on greenhouse gas emissions using data from the CREDENCE trial.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">For this modelling analysis, we used data from the randomised, double-blind, placebo-controlled, CREDENCE trial, which compared the effect of canagliflozin versus placebo on kidney and cardiovascular outcomes in patients with type 2 diabetes and albuminuric chronic kidney disease. For this secondary analysis, we included all participants randomly assigned to canagliflozin or placebo at baseline in the CREDENCE trial. Data on greenhouse gas emissions resulting from hospital inpatient days, maintenance dialysis therapy, and SGLT2 inhibitor tablet production were derived from published reports and used to model greenhouse gas emissions from total number of hospital inpatient days, total number of days of maintenance dialysis therapy, and from SGLT2 inhibitor treatment over the course of the CREDENCE trial. We compared greenhouse gas emission estimates for participants in the canagliflozin group and placebo group of the CREDENCE trial. We used bootstrapping analyses to calculate uncertainty estimates and permutation tests to generate p values for the difference in number of days on dialysis and inpatient bed days between treatment groups.</AbstractText><AbstractText Label="FINDINGS" NlmCategory="RESULTS">4401 participants who were randomly assigned to the canagliflozin (n=2202) or placebo group (n=2199) were included in the secondary analyses. During a median follow-up of 2·62 years (IQR 0·02 to 4·53), SGLT2 inhibitor production for 2202 participants resulted in greenhouse gas emissions of 63 tonnes of CO<sub>2</sub> equivalent (CO<sub>2</sub>e; 95% CI 62 to 64). The total number of inpatient bed days was 17 002 days in the placebo group versus 13 672 days in the canagliflozin group; the 3330 fewer inpatient days (95% CI 1037 to 5686; p=0·042) with SGLT2 inhibitor treatment equated to a reduction of approximately 126 tonnes of CO<sub>2</sub>e (95% CI 39 to 216). Participants in the placebo group required 24 877 days of maintenance dialysis compared with 16 605 days in the treatment group; 8272 fewer days of dialysis ( -168 to 16 755; p=0·16), equated to a reduction of 161 tonnes of CO<sub>2</sub>e (-3 to 327). Overall, mean greenhouse gas emissions per-participant-year were reduced from 196 kg of CO<sub>2</sub>e per-participant-year to 157 kg of CO<sub>2</sub>e per-participant-year.</AbstractText><AbstractText Label="INTERPRETATION" NlmCategory="CONCLUSIONS">The addition of an SGLT2 inhibitor to routine therapy for people with type 2 diabetes and chronic kidney disease has the potential to reduce greenhouse gas emissions through the prevention of hospital admissions and need for dialysis.</AbstractText><AbstractText Label="FUNDING" NlmCategory="BACKGROUND">None.</AbstractText><CopyrightInformation>Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Talbot</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>The George Institute for Global Health, University of New South Wales, Sydney, NSW, Australia; School of Population Health, University of New South Wales, Sydney, NSW, Australia. Electronic address: btalbot@georgeinstitute.org.au.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fletcher</LastName><ForeName>Robert A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>The George Institute for Global Health, University of New South Wales, Sydney, NSW, Australia; Department of Public Health and Primary Care, British Heart Foundation Cardiovascular Epidemiology Unit and Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Neal</LastName><ForeName>Bruce</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>The George Institute for Global Health, University of New South Wales, Sydney, NSW, Australia; School of Public Health, Imperial College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oshima</LastName><ForeName>Megumi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Nephrology and Laboratory Medicine, Kanazawa University, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adshead</LastName><ForeName>Fiona</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Sustainable Healthcare Coalition, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moore</LastName><ForeName>Keith</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Sustainable Healthcare Coalition, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McGain</LastName><ForeName>Forbes</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>The Healthcare Carbon Lab, Department of Critical Care, University of Melbourne, Melbourne, VIC, Australia; Sydney School of Public Health, University of Sydney, Sydney, NSW, Australia; Western Health, Footscray, Melbourne, VIC, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McAlister</LastName><ForeName>Scott</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>The Healthcare Carbon Lab, Department of Critical Care, University of Melbourne, Melbourne, VIC, Australia; Sydney School of Public Health, University of Sydney, Sydney, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barraclough</LastName><ForeName>Katherine A</ForeName><Initials>KA</Initials><AffiliationInfo><Affiliation>Department of Nephrology, Royal Melbourne Hospital, Parkville, VIC, Australia; Department of Medicine, University of Melbourne, Parkville, VIC, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Knight</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The George Institute for Global Health, University of New South Wales, Sydney, NSW, Australia; Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Neuen</LastName><ForeName>Brendon L</ForeName><Initials>BL</Initials><AffiliationInfo><Affiliation>The George Institute for Global Health, University of New South Wales, Sydney, NSW, Australia; Department of Renal Medicine, Royal North Shore Hospital, Sydney, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arnott</LastName><ForeName>Clare</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>The George Institute for Global Health, University of New South Wales, Sydney, NSW, Australia; Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia; Department of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Lancet Planet Health</MedlineTA><NlmUniqueID>101704339</NlmUniqueID><ISSNLinking>2542-5196</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000074382">Greenhouse Gases</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0SAC974Z85</RegistryNumber><NameOfSubstance UI="D000068896">Canagliflozin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000074382" MajorTopicYN="Y">Greenhouse Gases</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000068896" MajorTopicYN="Y">Canagliflozin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004311" MajorTopicYN="N">Double-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="N">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006760" MajorTopicYN="N">Hospitalization</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>Declaration of interests BT was in receipt of a Scientia Scholarship from University of New South Wales; has stock ownership in Ellen Medical Devices; and has received consultancy fees for Scientific Leadership with George Clinical. RAF acknowledges receipt of studentship awards from the Health Data Research UK-The Alan Turing Institute Wellcome PhD Programme in Health Data Science (grant number 218529/Z/19/Z). FA is chair of the Sustainable Healthcare Coalition. KM has a leadership role in the Sustainable Healthcare Coalition. FM has received an MRFF grant for COVID-19 related infections disease research and received royalties or licences for Medihood (a portable, protective hood for patient care); has patents issued for Medihood (the McMonty) and ReResp (a reusable N95 mask); and is the College of Intensive Care Medicine Sustainability Committee lead. KAB has received consulting fees from AstraZeneca. JK is an honorary professorial fellow at The George Institute for Global Health; has received fees for travel support, advisory boards, scientific presentations, consultancy, and steering committee roles from The Med Tech Actuator, Organ Transport, and Baymatob; and has stock ownership in Johnson & Johnson and Ellen Medical Devices. BLN is supported by an Australian National Health and Medical Research Council Emerging Leader Investigator Grant (number 2026621) and a Ramaciotti Foundation Health Investment Grant (number 2023HIG69); and has received fees for travel support, advisory boards, scientific presentations, and steering committee roles from AstraZeneca, Alexion, Bayer, Boehringer Ingelheim, Cambridge Healthcare Research, Cornerstone Medical Education, Janssen, the Limbic, Medscape, Novo Nordisk, and Travere Therapeutics, with all honoraria paid to The George Institute for Global Health. CA has received honoraria or sat on advisory boards for AstraZeneca and Novo Nordisk; and is supported by a Medical Research Futures Fund Investigator Grant. BN, MO, and SM declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>10</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>0</Hour><Minute>42</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>0</Hour><Minute>41</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>18</Hour><Minute>52</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39674195</ArticleId><ArticleId IdType="doi">10.1016/S2542-5196(24)00281-X</ArticleId><ArticleId IdType="pii">S2542-5196(24)00281-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39674193</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2542-5196</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The Lancet. Planetary health</Title><ISOAbbreviation>Lancet Planet Health</ISOAbbreviation></Journal><ArticleTitle>Health outcomes, environmental impacts, and diet costs of adherence to the EAT-Lancet Diet in China in 1997-2015: a health and nutrition survey.</ArticleTitle><Pagination><StartPage>e1030</StartPage><EndPage>e1042</EndPage><MedlinePgn>e1030-e1042</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/S2542-5196(24)00285-7</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S2542-5196(24)00285-7</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">In 2019, the EAT-Lancet Commission proposed a global reference dietary pattern. Although research on the EAT-Lancet reference diet and its associations with mortality, cardiovascular disease, type 2 diabetes, dietary environmental impacts, and cost of diets is increasing, studies done in low-income and middle-income countries remain scarce. This study aimed to assess the health outcomes, environmental impacts, and dietary costs of adherence to the EAT-Lancet reference diet in China.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">In this health and nutrition survey study, 16 029 participants from the China Health and Nutrition Survey cohort (1997-2015) were included at baseline. All-cause mortality was reported by family members and risk of cardiovascular disease and type 2 diabetes was self-reported. 3-day 24 h recall was used to assess adherence to the EAT-Lancet reference diet (Eat-Lancet Diet Index [ELDI]), diet-related environmental impacts (greenhouse-gas emissions [GHGE]), total water use (TWU), land use, and dietary costs in each survey round. Hazard ratios (HRs) for the ELDI-score were obtained by Cox models with time-varying covariates, adjusted for potential confounders. Multilevel mixed-effects linear regression was used to assess the association of environmental impacts and dietary costs to the ELDI score.</AbstractText><AbstractText Label="FINDINGS" NlmCategory="RESULTS">During a median follow-up of 9·86 years, 803 new cases of incident type 2 diabetes, 563 new cases of cardiovascular disease, and 908 cases of all-cause mortality were recorded. At baseline, the ELDI score ranged from 9·4 points to 110·8 points on a scale of 0 to 140, with a mean of 55·3 points (SD 11·8). With each SD increase in the ELDI score, there was an 8% decreased risk of mortality (95% CI 2·2-14·1), a 16·1% decreased risk of cardiovascular disease (9·2-20·3), and a 25·3% decreased risk of type 2 diabetes (19·5- 28·4). Each SD increase in the index was associated with a decrease of 2·2% (95% CI -2·6 to -1·8) in GHGE, 2·3% (-2·6 to -2·0) in land use, no association with TWU, but an increase in diet costs of 3·3% (2·8 to 3·8).</AbstractText><AbstractText Label="INTERPRETATION" NlmCategory="CONCLUSIONS">High adherence to the ELDI was associated with a lower risk of mortality, cardiovascular disease, and type 2 diabetes. However, the association with diet-related GHGE and land use was modest, and adherence was also linked to higher diet costs. The study advocates for the integration of sustainable indicators into future Chinese dietary guidelines. Additionally, policy measures such as agricultural subsidies on fruit and vegetable and carbon taxes on red meat are recommended to increase affordability, reduce environmental impact, and enhance the overall sustainability of dietary practices in China.</AbstractText><AbstractText Label="FUNDING" NlmCategory="BACKGROUND">The China Scholarship Council and the National Natural Science Foundation of China.</AbstractText><CopyrightInformation>Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cai</LastName><ForeName>Hongyi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, Netherlands; Academy of Global Food Economics and Policy, China Agricultural University, Beijing, China; College of Economics and Management, China Agricultural University, Beijing, China. Electronic address: hongyicai@outlook.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Talsma</LastName><ForeName>Elise F</ForeName><Initials>EF</Initials><AffiliationInfo><Affiliation>Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chang</LastName><ForeName>Zhiyao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, Netherlands; Academy of Global Food Economics and Policy, China Agricultural University, Beijing, China; College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wen</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Shenggen</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Academy of Global Food Economics and Policy, China Agricultural University, Beijing, China; College of Economics and Management, China Agricultural University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Van't Veer</LastName><ForeName>Pieter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Biesbroek</LastName><ForeName>Sander</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Lancet Planet Health</MedlineTA><NlmUniqueID>101704339</NlmUniqueID><ISSNLinking>2542-5196</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002681" MajorTopicYN="N" Type="Geographic">China</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004032" MajorTopicYN="Y">Diet</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009749" MajorTopicYN="Y">Nutrition Surveys</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004777" MajorTopicYN="Y">Environment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Declaration of interests We declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>4</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>10</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>0</Hour><Minute>42</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>0</Hour><Minute>41</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>18</Hour><Minute>52</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39674193</ArticleId><ArticleId IdType="doi">10.1016/S2542-5196(24)00285-7</ArticleId><ArticleId IdType="pii">S2542-5196(24)00285-7</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39656981</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1958-5381</ISSN><JournalIssue CitedMedium="Internet"><Volume>40</Volume><Issue>11</Issue><PubDate><Year>2024</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Medecine sciences : M/S</Title><ISOAbbreviation>Med Sci (Paris)</ISOAbbreviation></Journal><ArticleTitle>[From the discovery of incretin hormones to GIP / GLP-1 / glucagon double and triple agonists].</ArticleTitle><Pagination><StartPage>837</StartPage><EndPage>847</EndPage><MedlinePgn>837-847</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1051/medsci/2024153</ELocationID><Abstract><AbstractText>The concept of treating diabetes with gut hormones was proposed in the early days of endocrinology (1902), but was not put into practice until the early 2000s. The discovery of the incretin effect (potentiation of insulin secretion when glucose is taken orally compared to intravenously) led to the discovery of the two main gut hormones responsible for this effect: GIP and GLP-1. The reduction of the incretin effect is directly involved in the pathogenesis of type 2 diabetes, which has led to the development of a series of innovative therapies such as GLP-1 analogues, GLP-1 receptor agonists, GIP/GLP-1 co-agonists and GIP/GLP-1/glucagon tri-agonists. These therapies, with their potent hypoglycaemic and weight-lowering effects, promote optimal control of excess weight and hyperglycaemia, avoiding the escalation of treatment that was once considered inevitable.</AbstractText><CopyrightInformation>© 2024 médecine/sciences – Inserm.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Phan</LastName><ForeName>Franck</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Service de diabétologie, CHU Pitié-Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bertrand</LastName><ForeName>Romane</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Université Paris-Diderot, Unité de biologie fonctionnelle et adaptative / CNRS UMR 8251, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amouyal</LastName><ForeName>Chloé</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Service de diabétologie, CHU Pitié-Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Andreelli</LastName><ForeName>Fabrizio</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Service de diabétologie, CHU Pitié-Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D016456">Historical Article</PublicationType><PublicationType UI="D004740">English Abstract</PublicationType></PublicationTypeList><VernacularTitle>De la découverte des hormones incrétines aux doubles et triples agonistes GIP / GLP-1 / glucagon.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Med Sci (Paris)</MedlineTA><NlmUniqueID>8710980</NlmUniqueID><ISSNLinking>0767-0974</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>59392-49-3</RegistryNumber><NameOfSubstance UI="D005749">Gastric Inhibitory Polypeptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054795">Incretins</NameOfSubstance></Chemical><Chemical><RegistryNumber>89750-14-1</RegistryNumber><NameOfSubstance UI="D052216">Glucagon-Like Peptide 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-92-5</RegistryNumber><NameOfSubstance UI="D005934">Glucagon</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005749" MajorTopicYN="Y">Gastric Inhibitory Polypeptide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054795" MajorTopicYN="Y">Incretins</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052216" MajorTopicYN="Y">Glucagon-Like Peptide 1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005934" MajorTopicYN="Y">Glucagon</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049673" MajorTopicYN="N">History, 20th Century</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049674" MajorTopicYN="N">History, 21st Century</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="N">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="fre"><AbstractText Label="TITLE" NlmCategory="UNASSIGNED">De la découverte des hormones incrétines aux doubles et triples agonistes GIP / GLP-1 / glucagon.</AbstractText><AbstractText Label="ABSTRACT" NlmCategory="UNASSIGNED">L’idée de traiter les diabètes sucrés par des hormones intestinales a été proposée dès les débuts de l’endocrinologie, en 1902, mais ne sera mise en pratique qu’au début des années 2000. La mise en évidence d’une majoration de la sécrétion d’insuline après l’administration de glucose par voie orale par rapport à son administration intraveineuse, connue sous le nom « d’effet incrétine », a été suivie de la découverte des deux principales hormones intestinales responsables de cet effet : le GIP (glucose-dependent insulinotropic polypeptide) et le GLP-1 (glucagon-like peptide-1). La réduction de l’effet incrétine contribue à la pathogenèse du diabète de type 2, ce qui a conduit à développer des thérapies innovantes successives, comme les analogues du GLP-1, les agonistes du récepteur du GLP-1, les co-agonistes GIP / GLP-1 et les triagonistes GIP / GLP-1 / glucagon. Ces médicaments aux effets hypoglycémiants et pondéraux puissants ont modifié radicalement notre prise en charge thérapeutique du diabète de type 2 et de l’obésité.</AbstractText><CopyrightInformation>© 2024 médecine/sciences – Inserm.</CopyrightInformation></OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>19</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>19</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>15</Hour><Minute>12</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39656981</ArticleId><ArticleId IdType="doi">10.1051/medsci/2024153</ArticleId><ArticleId IdType="pii">msc240165</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>https://www.has-sante.fr/jcms/p_3191108/fr/strategie-therapeutique-du-patient-vivant-avec-un-diabete-de-type-2</Citation></Reference><Reference><Citation>Fosse-Edorh S, Fagot-Campagna A, Detournay B, et al. 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Lancet 2022 ; 400 : 1869–81.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39656751</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>04</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>12</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Cost-utility and budget impact analysis of laparoscopic bariatric surgery for obesity with Type II Diabetes Mellitus in Thailand.</ArticleTitle><Pagination><StartPage>e0315336</StartPage><MedlinePgn>e0315336</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e0315336</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0315336</ELocationID><Abstract><AbstractText Label="UNLABELLED">Bariatric surgery is another treatment options for patients with obesity, who cannot achieve weight controlled by conservative non-surgical therapy. Although bariatric surgery provides clinical benefits for these patients, it is costly. This study aims to evaluate the cost-effectiveness of bariatric surgery, as compared to nonbariatric surgery, in patients with body mass index (BMI) ≥32.5 kg/m2 and type 2 diabetes mellitus (T2DM), and to estimate the budget impact of bariatric surgery in Thailand.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A Markov model was developed to estimate and compare total costs incurred and quality-adjusted life years (QALYs) gained between bariatric surgery and nonbariatric surgery over lifetime horizontal. Analysis was conducted under payer and societal perspectives. Costs and outcomes were discounted at an annual rate of 3%. The outcomes were presented as incremental cost- effectiveness ratio (ICER).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Under payer's perspective, bariatric surgery resulted in higher total lifetime cost (676,658.39 baht vs 574,683.38 baht) and QALYs gained (16.08 QALYs vs 14.78 QALYs), as compared to nonbariatric surgery, resulting in an ICER of 78,643.02 baht/QALY. Similarly, under the societal perspective, bariatric surgery resulted in higher total lifetime cost (1,451,923.83 baht vs 1,407,590.49 baht) and QALYs gained (16.08 QALYs vs 14.78 QALYs), as compared to nonbariatric surgery. Under societal perspective, ICER was estimated at 34,189.82 baht/QALY. A 5-year budget impact analysis indicated that bariatric surgery incurred the total budget of 223,821 million baht.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">At the cost-effectiveness threshold of 160,000 baht/QALY, bariatric surgery was a cost-effective strategy and should continue to be included in the benefit package for patients with obesity and T2DM.</AbstractText><CopyrightInformation>Copyright: © 2024 Noparatayaporn et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Noparatayaporn</LastName><ForeName>Prapaporn</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Mahidol University Health Technology Assessment (MUHTA) Graduate Program, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thavorncharoensap</LastName><ForeName>Montarat</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-8256-2167</Identifier><AffiliationInfo><Affiliation>Mahidol University Health Technology Assessment (MUHTA) Graduate Program, Bangkok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Social and Administrative Pharmacy Division, Department of Pharmacy, Faculty of Pharmacy, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chaikledkaew</LastName><ForeName>Usa</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Mahidol University Health Technology Assessment (MUHTA) Graduate Program, Bangkok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Social and Administrative Pharmacy Division, Department of Pharmacy, Faculty of Pharmacy, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Looareesuwan</LastName><ForeName>Panu</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Biostatistics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shantavasinkul</LastName><ForeName>Prapimporn Chattranukulchai</ForeName><Initials>PC</Initials><AffiliationInfo><Affiliation>Division of Nutrition and Biochemical Medicine, Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sumritpradit</LastName><ForeName>Preeda</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Trauma, Acute Care Surgery and Surgical Critical Care Unit, Department of Surgery, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thakkinstian</LastName><ForeName>Ammarin</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Mahidol University Health Technology Assessment (MUHTA) Graduate Program, Bangkok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Biostatistics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050110" MajorTopicYN="Y">Bariatric Surgery</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013785" MajorTopicYN="N" Type="Geographic">Thailand</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003362" MajorTopicYN="Y">Cost-Benefit Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="Y">Obesity</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019057" MajorTopicYN="Y">Quality-Adjusted Life Years</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008390" MajorTopicYN="Y">Markov Chains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010535" MajorTopicYN="N">Laparoscopy</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002017" MajorTopicYN="N">Budgets</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015992" MajorTopicYN="N">Body Mass Index</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>5</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>23</Day></PubMedPubDate><PubMedPubDate 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Obesity Reviews. 2020;21(8):e13028. doi: 10.1111/obr.13028</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/obr.13028</ArticleId><ArticleId IdType="pubmed">32497417</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39673731</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1520-7560</ISSN><JournalIssue CitedMedium="Internet"><Volume>41</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Diabetes/metabolism research and reviews</Title><ISOAbbreviation>Diabetes Metab Res Rev</ISOAbbreviation></Journal><ArticleTitle>Searching the Crystal Ball for Tailored GLP-1 Receptor Agonists Treatment in Type 2 Diabetes and Obesity.</ArticleTitle><Pagination><StartPage>e70017</StartPage><MedlinePgn>e70017</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/dmrr.70017</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Glucagon-like peptide 1 receptor agonists (RA) are novel agents used in the management of type 2 diabetes (T2D) and obesity. Although highly effective, the response to treatment may vary significantly among patients.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">This perspective review aims to summarise the current knowledge about markers of poor or good response to GLP-1 RA, highlighting the possibility of tailoring treatment strategies and reducing costs associated with T2D and obesity treatment.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A comprehensive literature search was conducted using PubMed, NCBI, and Scopus databases, focussing on studies published between 2016 and 2024 that evaluated factors influencing treatment outcomes with GLP-1 RA.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Several markers, including baseline HbA1c levels, ghrelin and glucose-dependent insulinotropic polypeptide (GIP) levels, specific gut microbiome composition, b-cell function, and genetic markers, were identified as factors associated with treatment response.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Understanding predictive markers of response to therapy can enhance precision-based medicine for the selection of patients eligible for GLP-1 RA, improving clinical outcomes and optimising diabetes management.</AbstractText><CopyrightInformation>© 2024 John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Saturnino</LastName><ForeName>Asia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Campus Bio-Medico University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maddaloni</LastName><ForeName>Ernesto</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0003-3844-9463</Identifier><AffiliationInfo><Affiliation>Sapienza University of Rome, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zampetti</LastName><ForeName>Simona</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Sapienza University of Rome, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buzzetti</LastName><ForeName>Raffaella</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0003-1490-6041</Identifier><AffiliationInfo><Affiliation>Sapienza University of Rome, Rome, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Diabetes Metab Res Rev</MedlineTA><NlmUniqueID>100883450</NlmUniqueID><ISSNLinking>1520-7552</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000593833">GLP1R protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="Y">Obesity</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057285" MajorTopicYN="N">Precision Medicine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>10</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>20</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>20</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>13</Hour><Minute>52</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39673731</ArticleId><ArticleId IdType="doi">10.1002/dmrr.70017</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>L. 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Meier, “GLP‐1 Receptor Agonists in the Treatment of Type 2 Diabetes – State‐Of‐The‐Art,” Molecular Metabolism 46, no. 46 (2021): 101102, https://doi.org/10.1016/j.molmet.2020.101102.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39673670</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1567-2387</ISSN><JournalIssue CitedMedium="Internet"><Volume>56</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>14</Day></PubDate></JournalIssue><Title>Journal of molecular histology</Title><ISOAbbreviation>J Mol Histol</ISOAbbreviation></Journal><ArticleTitle>Protective effects of ghrelin on pancreas in fructose diet and streptozotocin-induced diabetic rats.</ArticleTitle><Pagination><StartPage>43</StartPage><MedlinePgn>43</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10735-024-10329-8</ELocationID><Abstract><AbstractText>Ghrelin, which is widely expressed in central and peripheral tissues, has several metabolic effects. It has been suggested that these effects may include anti-inflammatory, anti-oxidant, and anti-apoptotic effects. Therefore, we aimed to investigate the effects of ghrelin administered to diabetic rats on DNA repair and apoptosis mechanisms, and differences in oxidative stress (OS) and pancreatic hormone levels in the pancreas. Twenty-one rats were randomly divided into three groups: control, type 2 diabetes mellitus (T2DM), and T2DM treated with ghrelin (T2DM + ghrelin). We examined PCNA and PARP-1 to evaluate the effect of ghrelin on DNA repair, caspase-3 and caspase-9 to evaluate its effect on apoptosis, and insulin and glucagon to evaluate its role in regulating glucose homeostasis by immunohistochemistry in diabetic rats. Malondialdehyde, glutathione, and protein carbonyl levels, as well as catalase, glutathione-S-transferase, and superoxide dismutase (SOD) activities, were measured spectrophotometrically to detect the ghrelin effect on OS. Homeostasis model assessment for insulin resistance (HOMA-IR) and pancreatic insulin levels were assessed by ELISA method. Ghrelin may be a potential regulator of apoptosis as it significantly reduced the number of caspase-3 and caspase-9 immunopositive cells (p < 0.0001). In addition, ghrelin treatment reduced OS by decreasing glutathione (p < 0.001), malondialdehyde, and protein carbonyl, as well as the activity of SOD (p < 0.05) in diabetic rats. The results suggest that ghrelin is a potential apoptotic regulator and may be considered as a therapeutic agent due to its significant ability to suppress OS in T2DM.</AbstractText><CopyrightInformation>© 2024. The Author(s), under exclusive licence to Springer Nature B.V.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Colak</LastName><ForeName>Dilara Kamer</ForeName><Initials>DK</Initials><Identifier Source="ORCID">0000-0003-4968-2826</Identifier><AffiliationInfo><Affiliation>Department of Medical Biology, Cerrahpaşa Faculty of Medicine, Istanbul University-Cerrahpaşa, Istanbul, Türkiye.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Coskun Yazici</LastName><ForeName>Zeynep Mine</ForeName><Initials>ZM</Initials><Identifier Source="ORCID">0000-0003-4791-6537</Identifier><AffiliationInfo><Affiliation>Department of Molecular Biology and Genetics, Faculty of Arts and Sciences, Demiroglu Bilim University, Istanbul, Türkiye.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bolkent</LastName><ForeName>Sema</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-8463-5561</Identifier><AffiliationInfo><Affiliation>Department of Medical Biology, Cerrahpaşa Faculty of Medicine, Istanbul University-Cerrahpaşa, Istanbul, Türkiye. bolkent@iuc.edu.tr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>J Mol Histol</MedlineTA><NlmUniqueID>101193653</NlmUniqueID><ISSNLinking>1567-2379</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054439">Ghrelin</NameOfSubstance></Chemical><Chemical><RegistryNumber>30237-26-4</RegistryNumber><NameOfSubstance UI="D005632">Fructose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>5W494URQ81</RegistryNumber><NameOfSubstance UI="D013311">Streptozocin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053453">Caspase 9</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020011">Protective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>4Y8F71G49Q</RegistryNumber><NameOfSubstance UI="D008315">Malondialdehyde</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-92-5</RegistryNumber><NameOfSubstance UI="D005934">Glucagon</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054439" MajorTopicYN="Y">Ghrelin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010179" MajorTopicYN="Y">Pancreas</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="Y">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005632" MajorTopicYN="N">Fructose</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013311" MajorTopicYN="N">Streptozocin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053453" MajorTopicYN="N">Caspase 9</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008315" MajorTopicYN="N">Malondialdehyde</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005934" MajorTopicYN="N">Glucagon</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Ghrelin</Keyword><Keyword MajorTopicYN="N">Oxidative stress</Keyword><Keyword MajorTopicYN="N">Pancreatic hormones</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>Declarations. 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Front Physiol 9:1308. https://doi.org/10.3389/fphys.2018.01308</Citation><ArticleIdList><ArticleId IdType="doi">10.3389/fphys.2018.01308</ArticleId><ArticleId IdType="pubmed">30298019</ArticleId><ArticleId IdType="pmc">6160589</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39673172</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2044-8287</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Feb</Month></PubDate></JournalIssue><Title>British journal of health psychology</Title><ISOAbbreviation>Br J Health Psychol</ISOAbbreviation></Journal><ArticleTitle>A network analysis to explore illness perceptions in Black adults with type 2 diabetes.</ArticleTitle><Pagination><StartPage>e12775</StartPage><MedlinePgn>e12775</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e12775</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1111/bjhp.12775</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">This study explores the structure of beliefs about type 2 diabetes among Black adults and informs potential targets to reframe negative beliefs and enhance diabetes self-management.</AbstractText><AbstractText Label="RESEARCH DESIGN AND METHODS" NlmCategory="METHODS">We applied network analysis to investigate the interrelated structure and clusters of beliefs about diabetes and identify specific items that could serve as behavioural targets. We obtained self-reported survey data from 170 Black adults with type 2 diabetes. Regularised partial correlation networks and a Gaussian graphical model were used to explore and visualise the interrelationship among 21 items of a culturally adapted Illness Perception Questionnaire-Revised.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Overwhelming negative emotions representing the current and long-term effects of diabetes were central to the illness perceptions network among Black adults, with feeling depressed having the highest node strength of centrality indices in the network. Four beliefs had a bridging effect with the central cluster: diabetes taking away the ability to enjoy food, diabetes keeping me away from the job I want, being poor contributed to my having diabetes, and I receive encouragement from friends and family.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In addition to highlighting the overwhelming feeling of diabetes, the illness perception network further differentiated the role of racial identity and social determinants of health as discrete, though both are related sociocultural influence constructs. To enhance self-management for Black adults with type 2 diabetes, this network informs promising intervention targets focused on culturally tailored education related to emotional regulation, internalised stigma and healthy food adaptation, and leveraging support to address social determinants of health.</AbstractText><CopyrightInformation>© 2024 The Author(s). British Journal of Health Psychology published by John Wiley & Sons Ltd on behalf of British Psychological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wen</LastName><ForeName>Meng-Jung</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Division of Social and Administrative Sciences in Pharmacy, School of Pharmacy, University of Wisconsin-Madison, Madison, Wisconsin, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zou</LastName><ForeName>Tongtong</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Educational Psychology, School of Education, University of Wisconsin-Madison, Madison, Wisconsin, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bolt</LastName><ForeName>Daniel M</ForeName><Initials>DM</Initials><AffiliationInfo><Affiliation>Department of Educational Psychology, School of Education, University of Wisconsin-Madison, Madison, Wisconsin, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shiyanbola</LastName><ForeName>Olayinka O</ForeName><Initials>OO</Initials><Identifier Source="ORCID">0000-0002-6018-2104</Identifier><AffiliationInfo><Affiliation>Department of Clinical Pharmacy, College of Pharmacy, University of Michigan, Ann Arbor, Michigan, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>KL2 TR000428</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 DK092926</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 TR000427</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Br J Health Psychol</MedlineTA><NlmUniqueID>9605409</NlmUniqueID><ISSNLinking>1359-107X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001741" MajorTopicYN="Y">Black or African American</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000208" MajorTopicYN="N">ethnology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007722" MajorTopicYN="Y">Health Knowledge, Attitudes, Practice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073278" MajorTopicYN="N">Self-Management</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011795" MajorTopicYN="N">Surveys and Questionnaires</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">African Americans</Keyword><Keyword MajorTopicYN="N">Black adults</Keyword><Keyword MajorTopicYN="N">diabetes</Keyword><Keyword MajorTopicYN="N">illness perceptions</Keyword><Keyword MajorTopicYN="N">network analysis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>12</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>20</Hour><Minute>7</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>20</Hour><Minute>6</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>2</Hour><Minute>13</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>14</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39673172</ArticleId><ArticleId IdType="pmc">PMC11645490</ArticleId><ArticleId IdType="doi">10.1111/bjhp.12775</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Abubakari, A.‐R. , Jones, M. 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The Diabetes Educator, 40(2), 231–239.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4692724</ArticleId><ArticleId IdType="pubmed">24478047</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39673064</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2050-6511</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>BMC pharmacology & toxicology</Title><ISOAbbreviation>BMC Pharmacol Toxicol</ISOAbbreviation></Journal><ArticleTitle>The effect of vildagliptin versus metformin on hepatic steatosis in type 2 diabetic patients: a randomized controlled trial.</ArticleTitle><Pagination><StartPage>94</StartPage><MedlinePgn>94</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">94</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s40360-024-00818-7</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The risk of hepatic steatosis (HS) is elevated in patients with type 2 diabetes mellitus (T2D). Antidiabetic medications may contribute to the prevention or treatment of HS. This study aimed to compare the effects of vildagliptin and metformin on hepatic steatosis in newly diagnosed T2D patients, using the Hepatic Steatosis Index (HSI) and ultrasound grading.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The study included 246 newly diagnosed T2D patients who were randomly assigned to two groups. The first group (117 patients) received 50 mg of vildagliptin orally twice daily. The second group (129 patients) received 500 mg of metformin orally twice daily with meals, and the dosage could be gradually increased by 500 mg per week, up to a maximum daily dose of 2000 mg. Baseline and 6-month follow-up assessments included fasting blood glucose (FBG), HbA1c, weight, body mass index (BMI), waist circumference (WC), hip circumference (HC), the Hepatic Steatosis Index (HSI), and hepatic steatosis grading via ultrasound.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Both groups showed significant improvements in FBG, HbA1c, weight, BMI, WC, HC, HSI, and ultrasound grading of hepatic steatosis from baseline to the 6-month follow-up (p < 0.001). The metformin group demonstrated significantly greater reductions in weight and BMI compared to the vildagliptin group (p = 0.001 and p = 0.009, respectively). However, there was no significant difference between the two groups in terms of hepatic steatosis improvement on ultrasound. Correlation analysis revealed that HSI was significantly associated with HbA1c, BMI, WC, and HC (p < 0.001 for all), as well as FBG (p = 0.008), but not with age. The lipid profile, particularly total cholesterol and LDL, was identified as a stronger predictor of hepatic steatosis, based on high AUC, sensitivity, and specificity values.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Both vildagliptin and metformin are effective in improving glycemic control in newly diagnosed T2D patients, as evidenced by reductions in FBG and HbA1c levels. Additionally, both drugs significantly reduced the HSI, body weight, and BMI, with metformin showing a more pronounced effect on weight and BMI. Both vildagliptin and metformin effectively decreased hepatic steatosis in T2D patients. Total cholesterol and LDL are important predictors of hepatic steatosis.</AbstractText><AbstractText Label="TRIAL REGISTRATION" NlmCategory="BACKGROUND">Trial Registration ID: UMIN000055121, registered on 30/07/2024 (retrospectively registered).</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mohamed</LastName><ForeName>Asmaa S</ForeName><Initials>AS</Initials><Identifier Source="ORCID">0000-0001-7755-2362</Identifier><AffiliationInfo><Affiliation>Clinical Pharmacy and Pharmacy Practice Department, Faculty of Pharmacy, Port said University, Port said, Egypt. Asmaa.Mohamed@pharm.psu.edu.eg.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahmad</LastName><ForeName>Hosam M</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Internal Medicine and Biomedical Chemistry Departments, Egypt Ministry of Health and Population, Minia, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharawy</LastName><ForeName>Mohammed A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Internal Medicine Department, Faculty of Medicine, Minia University, Minia, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamel</LastName><ForeName>Fatma M M</ForeName><Initials>FMM</Initials><AffiliationInfo><Affiliation>Internal Medicine Department, Faculty of Medicine, Minia University, Minia, Egypt.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Pharmacol Toxicol</MedlineTA><NlmUniqueID>101590449</NlmUniqueID><ISSNLinking>2050-6511</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>I6B4B2U96P</RegistryNumber><NameOfSubstance UI="D000077597">Vildagliptin</NameOfSubstance></Chemical><Chemical><RegistryNumber>9100L32L2N</RegistryNumber><NameOfSubstance UI="D008687">Metformin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009570">Nitriles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011759">Pyrrolidines</NameOfSubstance></Chemical><Chemical><RegistryNumber>PJY633525U</RegistryNumber><NameOfSubstance UI="D000218">Adamantane</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077597" MajorTopicYN="Y">Vildagliptin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008687" MajorTopicYN="Y">Metformin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005234" MajorTopicYN="Y">Fatty Liver</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009570" MajorTopicYN="N">Nitriles</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011759" MajorTopicYN="N">Pyrrolidines</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000218" MajorTopicYN="N">Adamantane</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Hepatic steatosis</Keyword><Keyword MajorTopicYN="N">Metformin</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword><Keyword MajorTopicYN="N">Vildagliptin</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: This study was approved by the ethics committee of Port Said University. Written informed consent was obtained from the study participants after describing the study’s goals and advantages. All study steps were performed in accordance with the Declaration of Helsinki. Human ethics: All study steps were performed in accordance with the Declaration of Helsinki. Consent for publication: Not applicable. 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J Family Med Prim Care. 2019;8(3):923–8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6482810</ArticleId><ArticleId IdType="pubmed">31041226</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39673018</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>09</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1708-0428</ISSN><JournalIssue CitedMedium="Internet"><Volume>35</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Obesity surgery</Title><ISOAbbreviation>Obes Surg</ISOAbbreviation></Journal><ArticleTitle>Prediction Model of Diabetes Remission at 1-Year after Sleeve Gastrectomy and Comparison with other Models.</ArticleTitle><Pagination><StartPage>249</StartPage><EndPage>256</EndPage><MedlinePgn>249-256</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11695-024-07634-2</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Although numerous prediction models are available for diabetes remission following metabolic bariatric surgery, few are based on sleeve gastrectomy (SG). This study aimed to establish a predictive model for type 2 diabetes mellitus (T2DM) remission following SG and evaluate the efficacy of existing predictive models.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Patient data were gathered from a cohort study titled "Longitudinal Study of Bariatric Surgery in Western China." The synthetic minority oversampling technique was implemented, with 70% randomly selected as the training set and the remaining 30% as the testing set. Univariate logistic regression was used to identify factors associated with T2DM remission. These were included in subsequent stepwise multivariate analyses. A nomogram was then constructed. It was evaluated using a receiver operating characteristic (ROC) curve, calibration plot, and decision curve analysis. Finally, eight pre-existing predictive models were validated.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Initially, 166 patients were enrolled with a T2DM remission rate of 89.2%. Univariate logistic regression indicated that male patients, T2DM duration exceeding 1 year, elevated fasting blood glucose levels, and higher HbA1c levels were less likely to achieve remission 1 year following SG. A nomogram was constructed using variables, including sex, T2DM duration, and HbA1c levels. The ROC curve indicated that the nomogram had higher accuracy (AUC = 0.826, 95%CI: 0.768-0.884). Moreover, the AUCs were 0.790 (95%CI: 0.692-0.887), 0.865 (95%CI: 0.774-0.956) and 0.813 (95%CI: 0.733-0.893) for the testing, externally validated, and raw datasets, respectively.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The nomogram exhibited high efficacy in predicting T2DM remission in Chinese patients who underwent SG.</AbstractText><CopyrightInformation>© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Hongmei</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>The Third People's Hospital of Chengdu, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Peisen</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>The Third People's Hospital of Chengdu, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Yi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>The Third People's Hospital of Chengdu, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Xiaolin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>The Third People's Hospital of Chengdu, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Bing</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>The Third People's Hospital of Chengdu, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Huawu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>The Third People's Hospital of Chengdu, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Jiahui</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Third People's Hospital of Chengdu, Chengdu, China. dr_jiahuiyu@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CSY-YV-01-2023-038</GrantID><Agency>The Third People's Hospital of Chengdu</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Obes Surg</MedlineTA><NlmUniqueID>9106714</NlmUniqueID><ISSNLinking>0960-8923</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005743" MajorTopicYN="Y">Gastrectomy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012074" MajorTopicYN="Y">Remission Induction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049451" MajorTopicYN="Y">Nomograms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009767" MajorTopicYN="Y">Obesity, Morbid</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002681" MajorTopicYN="N" Type="Geographic">China</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050110" MajorTopicYN="N">Bariatric Surgery</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012372" MajorTopicYN="N">ROC Curve</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Prediction model</Keyword><Keyword MajorTopicYN="N">Sleeve gastrectomy</Keyword><Keyword MajorTopicYN="N">T2DM remission</Keyword></KeywordList><CoiStatement>Declarations. 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Chin Med J (Engl). 2024;137(3):320–8.</Citation><ArticleIdList><ArticleId IdType="doi">10.1097/CM9.0000000000002718</ArticleId><ArticleId IdType="pubmed">37341649</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39672583</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>14</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2044-6055</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>12</Day></PubDate></JournalIssue><Title>BMJ open</Title><ISOAbbreviation>BMJ Open</ISOAbbreviation></Journal><ArticleTitle>Prevalence and characteristics of liver steatosis and fibrosis in type 2 diabetes mellitus (T2DM) patients: a cross-sectional study in populations of eastern China.</ArticleTitle><Pagination><StartPage>e087550</StartPage><MedlinePgn>e087550</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e087550</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjopen-2024-087550</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">To describe the prevalence, clinical characteristics and risk factors of liver steatosis and fibrosis in type 2 diabetes mellitus (T2DM) patients in eastern China.</AbstractText><AbstractText Label="DESIGN" NlmCategory="METHODS">A cross-sectional, multicentre study based on an ongoing cohort study.</AbstractText><AbstractText Label="SETTING" NlmCategory="METHODS">16 clinics in eastern China, including primary clinics to tertiary hospitals.</AbstractText><AbstractText Label="PARTICIPANTS" NlmCategory="METHODS">1816 patients with T2DM diagnosis who met the inclusion criteria were recruited into the study.</AbstractText><AbstractText Label="INTERVENTION" NlmCategory="METHODS">Participants underwent elastography examination.</AbstractText><AbstractText Label="MAIN OUTCOME MEASURES" NlmCategory="METHODS">Descriptive analysis was performed to calculate the prevalence and characteristics of liver steatosis and fibrosis. The correlated factors were analysed using single- and multivariate logistic regression analysis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The prevalence of liver steatosis in T2DM patients is 69.7%, with 46% moderate to severe steatosis. 34.6% and 6.7% of the patients were detected with liver fibrosis and cirrhosis. Steatosis patients were younger, had higher body mass index (BMI), higher levels of insulin resistance and more severe lipid metabolism disorders. Similar trends of differences were observed in patients with fibrosis. Female gender (OR=0.574, 95% CI 0.381 to 0.865), BMI (OR=1.491, 95% CI 1.375 to 1.616), disease duration, inflammation and serum lipid profile markers were risk factors of steatosis, while BMI (OR=1.204, 95% CI 1.137 to 1.275) and female gender (OR=0.672, 95% CI 0.470 to 0.961) were still the most significant predictors of liver fibrosis.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The prevalence of liver steatosis and fibrosis were high in patients with T2DM. Liver steatosis and fibrosis in these patients appeared to be more associated with lipid metabolism disorders and insulin resistance rather than glucose levels.</AbstractText><AbstractText Label="TRIAL REGISTRATION NUMBER" NlmCategory="BACKGROUND">Clinical trial: NCT05597709.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ Group.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Yu</LastName><ForeName>Hekai</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Su</LastName><ForeName>Xianghui</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, First Affiliated Hospital of Xinjiang Medical University, Xinjiang, Xinjiang, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Tao</LastName><ForeName>Wenxuan</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Weixia</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiaoyan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Qing</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Southeast University, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Zhuoxiao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Nanjing Gaochun Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xiaoqian</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Nanjing Central Hospital, Nanjing, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xinliang</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Kangda College of Nanjing Medical University, Lianyungang, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jia</LastName><ForeName>Dianrong</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Taizhou Jiangyan Hospital of Traditional Chinese Medicine, Taizhou, Jiangsu, China dr_liling@126.com jiadianrong-1111@163.com 15836364293@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Nanjing Gaochun Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu, China dr_liling@126.com jiadianrong-1111@163.com 15836364293@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Ling</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, School of Medicine, Southeast University Zhongda Hospital, Nanjing, Jiangsu, China dr_liling@126.com jiadianrong-1111@163.com 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Hepatology. 2023;78:1625–53. doi: 10.1097/HEP.0000000000000182.</Citation><ArticleIdList><ArticleId IdType="doi">10.1097/HEP.0000000000000182</ArticleId><ArticleId IdType="pmc">PMC10681123</ArticleId><ArticleId IdType="pubmed">36626642</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39672582</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>14</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2044-6055</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>12</Day></PubDate></JournalIssue><Title>BMJ open</Title><ISOAbbreviation>BMJ Open</ISOAbbreviation></Journal><ArticleTitle>Can SGLT-2 inhibitors improve cardiovascular outcomes and ensure safety for patients with type 2 diabetes and heart failure in Thailand? A real-world multicentre retrospective cohort study.</ArticleTitle><Pagination><StartPage>e090226</StartPage><MedlinePgn>e090226</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e090226</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjopen-2024-090226</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">To assess the real-world effectiveness and safety of sodium-glucose co-transporter-2 inhibitors (SGLT2i) on cardiovascular outcomes in patients with type 2 diabetes mellitus (T2D) and heart failure (HF) and to evaluate the associated risks of adverse events.</AbstractText><AbstractText Label="DESIGN" NlmCategory="METHODS">A retrospective cohort study using propensity score analysis to control confounding variables.</AbstractText><AbstractText Label="SETTING" NlmCategory="METHODS">Data were collected from the electronic health records of two large tertiary care hospitals in Thailand over a 12-year period (2010-2022).</AbstractText><AbstractText Label="PARTICIPANTS" NlmCategory="METHODS">Adults aged 18 years and older with a diagnosis of T2D and HF were included in the study. Patients who received SGLT2i for a minimum of 3 months were compared with those in a non-SGLT2i group. Participants with a diagnosis of HF that preceded their diagnosis of T2D were excluded from the analysis.</AbstractText><AbstractText Label="PRIMARY AND SECONDARY OUTCOME MEASURES" NlmCategory="METHODS">The primary outcome was heart failure hospitalisation (HFH). Secondary outcomes included non-fatal stroke, non-fatal myocardial infarction (MI), all-cause mortality and adverse events (urinary tract infections, hypoglycaemia and acute kidney injury).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">A total of 11 758 patients were included in the study, with a median follow-up of 2.44 (IQR: 0.72-5.02) years. After applying inverse probability of treatment weighting, covariates were balanced, ensuring the validity of the treatment effect model's assumptions. SGLT2i use was associated with a 59% reduction in HFH (HR 0.41, 95% CI 0.28 to 0.61), a 54% reduction in stroke (HR 0.46, 95% CI 0.33 to 0.63), a 51% reduction in MI (HR 0.49, 95% CI 0.36 to 0.67) and a 76% reduction in in-hospital all-cause mortality (HR 0.24, 95% CI 0.14 to 0.42). Additionally, SGLT2i use was associated with fewer adverse events, including lower rates of urinary tract infections and hypoglycaemia, compared with the non-SGLT2i group.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">SGLT2i significantly improved cardiovascular outcomes in patients with T2D and HF in a real-world clinical setting. These findings support the incorporation of SGLT2i in the management of high-risk patients with T2D and HF. Further research is warranted to explore long-term outcomes and barriers to SGLT2i prescription in routine practice.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kongmalai</LastName><ForeName>Tanawan</ForeName><Initials>T</Initials><Identifier Source="ORCID">0000-0002-1192-9267</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Siriraj Health Policy Unit, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Siriraj Research Data Management Unit, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tansawet</LastName><ForeName>Amarit</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-2040-7970</Identifier><AffiliationInfo><Affiliation>Department of Research and Medical Innovation, Faculty of Medicine Vajira Hospital, Navamindradhiraj University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pattanaprateep</LastName><ForeName>Oraluck</ForeName><Initials>O</Initials><Identifier Source="ORCID">0000-0001-9570-2635</Identifier><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Biostatistics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ratanatharathorn</LastName><ForeName>Cholatid</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Biostatistics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amornritvanich</LastName><ForeName>Porntep</ForeName><Initials>P</Initials><Identifier Source="ORCID">0009-0004-2970-4594</Identifier><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Biostatistics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Looareesuwan</LastName><ForeName>Panu</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0001-8179-9149</Identifier><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Biostatistics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boonwatcharapai</LastName><ForeName>Burin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Siriraj Informatics and Data Innovation Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khunakorncharatphong</LastName><ForeName>Anon</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Siriraj Health Policy Unit, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nimitphong</LastName><ForeName>Hataikarn</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Division of Endocrinology, Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srinonprasert</LastName><ForeName>Varalak</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Siriraj Health Policy Unit, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand Varalak.sri@mahidol.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Siriraj Research Data Management Unit, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Geriatric Medicine, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thakkinstian</LastName><ForeName>Ammarin</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Biostatistics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open</MedlineTA><NlmUniqueID>101552874</NlmUniqueID><ISSNLinking>2044-6055</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013785" MajorTopicYN="N" Type="Geographic">Thailand</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006760" MajorTopicYN="N">Hospitalization</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057216" MajorTopicYN="N">Propensity Score</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007003" MajorTopicYN="N">Hypoglycemia</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="N">Myocardial Infarction</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020521" MajorTopicYN="N">Stroke</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cardiovascular Disease</Keyword><Keyword MajorTopicYN="N">Diabetes Mellitus, Type 2</Keyword><Keyword MajorTopicYN="N">Drug Therapy</Keyword><Keyword MajorTopicYN="N">Heart failure</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>43</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>12</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39672582</ArticleId><ArticleId 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Cell physiology</Title><ISOAbbreviation>Am J Physiol Cell Physiol</ISOAbbreviation></Journal><ArticleTitle>Prevention of cardiovascular disease in women with type 2 diabetes: the role of incretin mimetics and sodium-glucose cotransporter-2 inhibitors.</ArticleTitle><Pagination><StartPage>C315</StartPage><EndPage>C322</EndPage><MedlinePgn>C315-C322</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpcell.00765.2024</ELocationID><Abstract><AbstractText>Cardiovascular disease (CVD) is the leading cause of death among individuals with type 2 diabetes (T2D), with women experiencing a disproportionate risk of events compared with men. Women have an amplified burden of cardiovascular risk factors once T2D is diagnosed. Incretin mimetics now plays a central role in managing cardiovascular risk by improving glycemic control, promoting weight loss, and potentially exerting direct cardioprotective effects. Similarly, sodium-glucose cotransporter-2 inhibitors contribute to CVD prevention through various nonglucose-lowering mechanisms. Both classes of medications are integral to personalized treatment strategies aimed at addressing the heightened cardiovascular risk faced by women with diabetes. This mini-review addresses possible mechanisms underlying the increased cardiovascular risk and explores the role of incretin mimetics and SGLT2 inhibitors in mitigating CVD in women with T2D. Emphasizing personalized and sex-specific approaches in diabetes care is crucial for optimizing treatment outcomes and improving cardiovascular health.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ibrahim</LastName><ForeName>Eiman</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri, United States.</Affiliation><Identifier Source="ROR">https://ror.org/02ymw8z06</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Burken</LastName><ForeName>Mya</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri, United States.</Affiliation><Identifier Source="ROR">https://ror.org/02ymw8z06</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lastra</LastName><ForeName>Guido</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0001-9205-1021</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri, United States.</Affiliation><Identifier Source="ROR">https://ror.org/02ymw8z06</Identifier></AffiliationInfo><AffiliationInfo><Affiliation>Harry S. Truman Memorial Veterans' Hospital, Columbia, Missouri, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manrique-Acevedo</LastName><ForeName>Camila</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0001-9341-404X</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri, United States.</Affiliation><Identifier Source="ROR">https://ror.org/02ymw8z06</Identifier></AffiliationInfo><AffiliationInfo><Affiliation>Harry S. Truman Memorial Veterans' Hospital, Columbia, Missouri, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>NextGen Precision Health, University of Missouri, Columbia, Missouri, United States.</Affiliation><Identifier Source="ROR">https://ror.org/02ymw8z06</Identifier></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>I01 CX002399</GrantID><Acronym>CX</Acronym><Agency>CSRD VA</Agency><Country>United States</Country></Grant><Grant><GrantID>R01HL142770</GrantID><Agency>HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)</Agency><Country/></Grant><Grant><GrantID>R01AG082413</GrantID><Agency>HHS | NIH | National Institute on Aging (NIA)</Agency><Country/></Grant><Grant><GrantID>1I01CX002399</GrantID><Agency>U.S. Department of Veterans Affairs (VA)</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Cell Physiol</MedlineTA><NlmUniqueID>100901225</NlmUniqueID><ISSNLinking>0363-6143</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054795">Incretins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054795" MajorTopicYN="Y">Incretins</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000082742" MajorTopicYN="N">Heart Disease Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="N">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">SGLT2 inhibitors</Keyword><Keyword MajorTopicYN="N">cardiovascular disease</Keyword><Keyword MajorTopicYN="N">diabetes</Keyword><Keyword MajorTopicYN="N">incretin mimetics</Keyword><Keyword MajorTopicYN="N">sex differences</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>10</Day><Hour>18</Hour><Minute>20</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39672547</ArticleId><ArticleId IdType="doi">10.1152/ajpcell.00765.2024</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39672082</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>06</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-1983</ISSN><JournalIssue CitedMedium="Internet"><Volume>44</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Clinical nutrition (Edinburgh, Scotland)</Title><ISOAbbreviation>Clin Nutr</ISOAbbreviation></Journal><ArticleTitle>Biomarkers of oxidation, inflammation and intestinal permeability in persons with diabetes mellitus with parenteral nutrition: A multicenter randomized trial.</ArticleTitle><Pagination><StartPage>155</StartPage><EndPage>164</EndPage><MedlinePgn>155-164</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.clnu.2024.11.044</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0261-5614(24)00441-2</ELocationID><Abstract><AbstractText Label="BACKGROUND AND AIMS" NlmCategory="OBJECTIVE">Parenteral nutrition (PN) composition could play a role in the management of systemic inflammatory response and intestinal barrier disruption. We aimed to evaluate changes in biomarkers of inflammation, oxidative status and intestinal permeability in patients with type 2 diabetes mellitus (T2DM) who received different PN lipid formulas.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">This was a prospective study, including 94 patients with T2DM who received omega (n)-3 polyunsaturated fatty acids (PUFA)-enriched PN, a mixture of medium and long chain triglycerides (MCT/LCT) PN, or an olive oil-based PN. Serum levels of biomarkers of oxidative status, intestinal permeability and inflammation biomarkers were determined at day 1 and day 5 after PN initiation. Registered under ClinicalTrials.gov Identifier no. NCT02706119.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">At day 5 after the onset of PN, the MCT/LCT group had a significant reduction of 2 proinflammatory cytokines [interleukin (IL)-15, IL-17A], elevation of the anti-inflammatory cytokine IL-13 and increase of zonulin and indoxylsulfate. The olive oil group showed a statistically significant reduction of 5 proinflammatory cytokines [IL-1β, IL-17A, IL-6, cytokine-leukemia inhibitory factor (LIF) and tumor necrosis factor alpha (TNF-α)] and reduced concentrations of the anti-inflammatory cytokine IL-1RA, while the n-3 PUFA-enriched group presented a statistically significant reduction of 8 proinflammatory cytokines (interferon-gamma, IL-1β, IL-15, IL-17A, IL-6, LIF, monocyte chemoattractant protein 1, and TNF-α). In the between-group comparisons, indoxylsulfate significantly increased in the MCT/LCT group compared to the n-3 PUFA-enriched group, while 8-isoprostane and indoxylsulfate significantly increased in the MCT/LCT group compared to the other groups and superoxide dismutase significantly decreased in the MCT/LCT group compared to the other groups.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">In patients with T2DM, PN lipid composition exerts a profound impact on proinflammatory, prooxidative and intestinal permeability biomarkers.</AbstractText><CopyrightInformation>Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Soria-Utrilla</LastName><ForeName>Virginia</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Regional Universitario de Málaga, Instituto de Investigación Biomédica de Málaga (IBIMA)-BIONAND Platform, Málaga, Spain; Department of Medicine and Dermatology, Faculty of Medicine, University of Malaga, Malaga, Spain. Electronic address: virginiasoriau@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sasso</LastName><ForeName>Corina Verónica</ForeName><Initials>CV</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Regional Universitario de Málaga, Instituto de Investigación Biomédica de Málaga (IBIMA)-BIONAND Platform, Málaga, Spain; Department of Medicine and Dermatology, Faculty of Medicine, University of Malaga, Malaga, Spain. 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Electronic address: agmanzanares2010@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bretón-Lesmes</LastName><ForeName>Irene</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Universitario Gregorio Marañón, Madrid, Spain. Electronic address: irenebreton@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Serrano-Aguayo</LastName><ForeName>Pilar</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Universitario Virgen del Rocío, Sevilla, Spain. Electronic address: piagua@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pérez-Ferre</LastName><ForeName>Natalia</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Universitario Clínico San Carlos, Madrid, Spain. Electronic address: nataliaferre79@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>López-Gómez</LastName><ForeName>Juan José</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Clínico Universitario de Valladolid, Valladolid, Spain. Electronic address: jjlopez161282@hotmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olivares-Alcolea</LastName><ForeName>Josefina</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Universitario Son Espases, Palma de Mallorca, Spain. Electronic address: jolivares@hsll.es.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moreno-Martínez</LastName><ForeName>Macarena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Complejo Hospitalario Universitario de Jaén, Jaén, Spain. Electronic address: mmorenomtnez@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tejera-Pérez</LastName><ForeName>Cristina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Complejo Hospitalario Universitario de Ferrol, A Coruña, Spain; Epigenomics in Endocrinology and Nutrition Group, Epigenomics Unit, Instituto de Investigacion Sanitaria de Santiago de Compostela (IDIS), Complejo Hospitalario Universitario de Santiago de Compostela, Santiago de Compostela, Spain. Electronic address: cristinatejera.mui@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>García-Arias</LastName><ForeName>Sara</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital El Bierzo, Ponferrada, León, Spain. Electronic address: sara_ga85@hotmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abad-González</LastName><ForeName>Ángel Luis</ForeName><Initials>ÁL</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital General Universitario Doctor Balmis, Alicante, Spain; Instituto de Investigación Sanitaria y Biomédica de Alicante (ISABIAL), Spain. Electronic address: angeluis1024@ono.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alhambra-Expósito</LastName><ForeName>María Rosa</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Universitario Reina Sofía, Córdoba, Spain; Instituto Maimónides de investigación biomédica translacional (IMIBIC), Córdoba, Spain. Electronic address: mralhambra@hotamail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zugasti-Murillo</LastName><ForeName>Ana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Universitario de Navarra, Pamplona, Spain. Electronic address: azugas@hotmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parra-Barona</LastName><ForeName>Juan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital de Mérida, Mérida, Spain. Electronic address: juanparrabarona@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Torrejón-Jaramillo</LastName><ForeName>Sara</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital de Sant Joan Despí Moisès Broggi, Barcelona, Spain. Electronic address: sara.torrejon@sanitatintegral.org.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abuin</LastName><ForeName>José</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Regional Universitario de Málaga, Instituto de Investigación Biomédica de Málaga (IBIMA)-BIONAND Platform, Málaga, Spain; Department of Medicine and Dermatology, Faculty of Medicine, University of Malaga, Malaga, Spain. Electronic address: jose.abuin.fdez@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fernández-García</LastName><ForeName>José Carlos</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Regional Universitario de Málaga, Instituto de Investigación Biomédica de Málaga (IBIMA)-BIONAND Platform, Málaga, Spain; Department of Medicine and Dermatology, Faculty of Medicine, University of Malaga, Malaga, Spain. Electronic address: jcfernandez@uma.es.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olveira</LastName><ForeName>Gabriel</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Hospital Regional Universitario de Málaga, Instituto de Investigación Biomédica de Málaga (IBIMA)-BIONAND Platform, Málaga, Spain; Department of Medicine and Dermatology, Faculty of Medicine, University of Malaga, Malaga, Spain; Centro de Investigación Biomédica en Red (CIBER) de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Málaga, Spain. Electronic address: gabolvfus@uma.es.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>Nutrition Area of the Spanish Society of Endocrinology and Nutrition (SEEN)</CollectiveName></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName><AccessionNumberList><AccessionNumber>NCT02706119</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Clin Nutr</MedlineTA><NlmUniqueID>8309603</NlmUniqueID><ISSNLinking>0261-5614</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015525">Fatty Acids, Omega-3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000069463">Olive Oil</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014280">Triglycerides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C408043">zonulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006242">Haptoglobins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011498">Protein Precursors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="Y">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010288" MajorTopicYN="Y">Parenteral Nutrition</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="Y">Inflammation</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="Y">Cytokines</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010539" MajorTopicYN="Y">Permeability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015525" MajorTopicYN="Y">Fatty Acids, Omega-3</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069463" MajorTopicYN="Y">Olive Oil</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014280" MajorTopicYN="Y">Triglycerides</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007413" MajorTopicYN="N">Intestinal Mucosa</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000095644" MajorTopicYN="N">Intestinal Barrier Function</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006242" MajorTopicYN="N">Haptoglobins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011498" MajorTopicYN="N">Protein Precursors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Intestinal permeability</Keyword><Keyword MajorTopicYN="N">Oxidative status</Keyword><Keyword MajorTopicYN="N">Parenteral nutrition</Keyword></KeywordList><CoiStatement>Conflict of interest The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>7</Day><Hour>0</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>18</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39672082</ArticleId><ArticleId IdType="doi">10.1016/j.clnu.2024.11.044</ArticleId><ArticleId IdType="pii">S0261-5614(24)00441-2</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39671462</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>12</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Glycemic control and bacterial infectious risk in type 2 diabetes: A retrospective cohort from a primary care database.</ArticleTitle><Pagination><StartPage>e0314287</StartPage><MedlinePgn>e0314287</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e0314287</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0314287</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">The prevalence of diabetes was estimated at 5.3% of the French population in 2020. People with type 2 diabetes have an increased risk of infection. Currently, there is no consensus on the impact of glycemic control on infectious risk. The objective was to evaluate whether glycemic control and diabetes severity were associated with infectious risk in type 2 diabetes.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">We designed a multicenter retrospective cohort study using data from a French primary care database. Data were collected from January 2012 to January 2022. Glycemic control was estimated by the threshold of glycated hemoglobin and diabetes severity by the number, and the type, of antidiabetic treatments. Infectious risk was evaluated by the mean of antibiotic prescriptions per year.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Among 59,020 patients, 1959 patients were included in the final analysis. The threshold of glycated hemoglobin was not associated with the mean of antibiotic prescriptions per year (ANOVA p = 0.228). Secondary analyses did not show an association between the number, or the type, of antidiabetic treatments and the mean of antibiotic prescriptions per year (p = 0.53 and p = 0.018, respectively). No association was observed between glycemic control, diabetes severity and infectious risk in patients with type 2 diabetes. This is the first European study using data from primary care to examine bacterial infectious risk in patients with type 2 diabetes, demonstrating the possibilities offered by the use of databases in primary care research.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Long-term glycemic control was not associated with bacterial infectious risk in patients with type 2 diabetes.</AbstractText><CopyrightInformation>Copyright: © 2024 Lemoine et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lemoine</LastName><ForeName>Edouard</ForeName><Initials>E</Initials><Identifier Source="ORCID">0009-0006-1120-5492</Identifier><AffiliationInfo><Affiliation>Department of General Practice, UNIROUEN, Normandie Université, Rouen, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dusenne</LastName><ForeName>Mikaël</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical Information and Informatics, CHU Rouen, Rouen, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schuers</LastName><ForeName>Matthieu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of General Practice, UNIROUEN, Normandie Université, Rouen, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Information and Informatics, CHU Rouen, Rouen, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Medical Informatics and e-Health Knowledge Engineering Laboratory, INSERM, U1142, LIMICS, Sorbonne University, Paris, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000900">Anti-Bacterial Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011320" MajorTopicYN="Y">Primary Health Care</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000085002" MajorTopicYN="Y">Glycemic Control</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016208" MajorTopicYN="Y">Databases, Factual</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001424" MajorTopicYN="N">Bacterial Infections</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000900" MajorTopicYN="N">Anti-Bacterial Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005602" MajorTopicYN="N" Type="Geographic">France</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>10</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>7</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>6</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>13</Hour><Minute>44</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>13</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39671462</ArticleId><ArticleId IdType="pmc">PMC11642988</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0314287</ArticleId><ArticleId IdType="pii">PONE-D-23-29894</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Home, Resources, diabetes L with, Acknowledgement, FAQs, Contact, et al. 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Br J Gen Pract. févr 2015;65(631):54–5. doi: 10.3399/bjgp15X683353</Citation><ArticleIdList><ArticleId IdType="doi">10.3399/bjgp15X683353</ArticleId><ArticleId IdType="pmc">PMC4325440</ArticleId><ArticleId IdType="pubmed">25624277</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39671339</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>213</Issue><PubDate><Year>2024</Year><Month>Nov</Month><Day>29</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/67189</ELocationID><Abstract><AbstractText>The underlying pathophysiological mechanisms of diabetic cardiomyopathy (DbCM), a leading cause of mortality among patients with type 2 diabetes mellitus (T2DM), remain poorly understood. The myocardial toxicity associated with T2DM is attributed to factors such as lipotoxicity, glucotoxicity, oxidative stress, reduced cardiac efficiency, and lipoapoptosis. Compared to rats, mice offer greater accessibility, cost-effectiveness, and broader applicability for animal experiments. Insulin resistance and impaired insulin secretion are crucial factors in the pathophysiology of T2DM. We introduce a novel nongenetic murine model that replicates the progression of human DbCM induced by a combination of high-fat diet (HFD) feeding and streptozotocin (STZ) injection. In this study, we used wild-type C57BL/6J mice, administering an HFD regimen for 12 weeks, followed by intraperitoneal injections of STZ for an additional 12 weeks to induce characteristic manifestations of T2DM. We conducted oral glucose tolerance tests and measured serum insulin concentrations to confirm the development of insulin resistance and insufficient insulin secretion. Cardiac structure and function were rigorously assessed through noninvasive transthoracic echocardiography. Pathological characteristics were evaluated through Masson's trichrome staining and wheat germ agglutinin (WGA) staining, revealing pathological features related to DbCM. Therefore, we provide a robust and versatile method for establishing a nongenetic murine model of DbCM.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Xu</LastName><ForeName>Yanjiani</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University; Laboratory of Cardiac Structure and Function, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University; Cardiac Structure and Function Research Key Laboratory of Sichuan Province, West China Hospital, Sichuan University.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Zhang</LastName><ForeName>Jialiang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University; Laboratory of Cardiac Structure and Function, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University; Cardiac Structure and Function Research Key Laboratory of Sichuan Province, West China Hospital, Sichuan University; zjl094@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University; Laboratory of Cardiac Structure and Function, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University; Cardiac Structure and Function Research Key Laboratory of Sichuan Province, West China Hospital, Sichuan University.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yaoyu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University; Laboratory of Cardiac Structure and Function, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University; Cardiac Structure and Function Research Key Laboratory of Sichuan Province, West China Hospital, Sichuan University.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Fangyang</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University; Laboratory of Cardiac Structure and Function, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University; Cardiac Structure and Function Research Key Laboratory of Sichuan Province, West China Hospital, Sichuan University; fyhuang1989@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Mao</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University; Laboratory of Cardiac Structure and Function, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University; Cardiac Structure and Function Research Key Laboratory of Sichuan Province, West China Hospital, Sichuan University; hmaochen@vip.sina.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D059040">Video-Audio Media</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Vis Exp</MedlineTA><NlmUniqueID>101313252</NlmUniqueID><ISSNLinking>1940-087X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>5W494URQ81</RegistryNumber><NameOfSubstance UI="D013311">Streptozocin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058065" MajorTopicYN="Y">Diabetic Cardiomyopathies</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="Y">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="Y">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013311" MajorTopicYN="N">Streptozocin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>7</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>6</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>13</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39671339</ArticleId><ArticleId IdType="doi">10.3791/67189</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39671241</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>04</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2050-084X</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><PubDate><Year>2024</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>eLife</Title><ISOAbbreviation>Elife</ISOAbbreviation></Journal><ArticleTitle>Genetic inactivation of zinc transporter SLC39A5 improves liver function and hyperglycemia in obesogenic settings.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">RP90419</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.7554/eLife.90419</ELocationID><Abstract><AbstractText>Recent studies have revealed a role for zinc in insulin secretion and glucose homeostasis. Randomized placebo-controlled zinc supplementation trials have demonstrated improved glycemic traits in patients with type II diabetes (T2D). Moreover, rare loss-of-function variants in the zinc efflux transporter <i>SLC30A8</i> reduce T2D risk. Despite this accumulated evidence, a mechanistic understanding of how zinc influences systemic glucose homeostasis and consequently T2D risk remains unclear. To further explore the relationship between zinc and metabolic traits, we searched the exome database of the Regeneron Genetics Center-Geisinger Health System DiscovEHR cohort for genes that regulate zinc levels and associate with changes in metabolic traits. We then explored our main finding using in vitro and in vivo models. We identified rare loss-of-function (LOF) variants (MAF <1%) in <i>Solute Carrier Family 39, Member 5</i> (<i>SLC39A5</i>) associated with increased circulating zinc (p=4.9 × 10<sup>-4</sup>). Trans-ancestry meta-analysis across four studies exhibited a nominal association of <i>SLC39A5</i> LOF variants with decreased T2D risk. To explore the mechanisms underlying these associations, we generated mice lacking <i>Slc39a5. Slc39a5<sup>-/-</sup></i> mice display improved liver function and reduced hyperglycemia when challenged with congenital or diet-induced obesity. These improvements result from elevated hepatic zinc levels and concomitant activation of hepatic AMPK and AKT signaling, in part due to zinc-mediated inhibition of hepatic protein phosphatase activity. Furthermore, under conditions of diet-induced non-alcoholic steatohepatitis (NASH), <i>Slc39a5<sup>-/-</sup></i> mice display significantly attenuated fibrosis and inflammation. Taken together, these results suggest SLC39A5 as a potential therapeutic target for non-alcoholic fatty liver disease (NAFLD) due to metabolic derangements including T2D.</AbstractText><CopyrightInformation>© 2023, Chim et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chim</LastName><ForeName>Shek Man</ForeName><Initials>SM</Initials><Identifier Source="ORCID">0000-0002-5116-8394</Identifier><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Howell</LastName><ForeName>Kristen</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dronzek</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Weizhen</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Van Hout</LastName><ForeName>Cristopher</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferreira</LastName><ForeName>Manuel A R</ForeName><Initials>MAR</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Bin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brydges</LastName><ForeName>Susannah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Regeneron Pharmaceuticals, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arunachalam</LastName><ForeName>Vinayagam</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marcketta</LastName><ForeName>Anthony</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Locke</LastName><ForeName>Adam E</ForeName><Initials>AE</Initials><Identifier Source="ORCID">0000-0001-6227-198X</Identifier><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bovijn</LastName><ForeName>Jonas</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Verweij</LastName><ForeName>Niek</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>De</LastName><ForeName>Tanima</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lotta</LastName><ForeName>Luca</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mitnaul</LastName><ForeName>Lyndon</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>LeBlanc</LastName><ForeName>Michelle</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Center</LastName><ForeName>Regeneron Genetics</ForeName><Initials>RG</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carey</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>Geisinger Health System, Danville, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Melander</LastName><ForeName>Olle</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shuldiner</LastName><ForeName>Alan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karalis</LastName><ForeName>Katia</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Economides</LastName><ForeName>Aris N</ForeName><Initials>AN</Initials><Identifier Source="ORCID">0000-0002-6508-8942</Identifier><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Regeneron Pharmaceuticals, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nistala</LastName><ForeName>Harikiran</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0003-4928-7527</Identifier><AffiliationInfo><Affiliation>Regeneron Genetics Center, New York, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>DiscovEHR collaboration</CollectiveName></Author><Author ValidYN="Y"><CollectiveName>Regeneron Genetics Center</CollectiveName></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Elife</MedlineTA><NlmUniqueID>101579614</NlmUniqueID><ISSNLinking>2050-084X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>J41CSQ7QDS</RegistryNumber><NameOfSubstance UI="D015032">Zinc</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D027682">Cation Transport Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="UpdateOf"><RefSource>doi: 10.1101/2021.12.08.21267440</RefSource></CommentsCorrections><CommentsCorrections RefType="UpdateOf"><RefSource>doi: 10.7554/eLife.90419.1</RefSource></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006943" MajorTopicYN="Y">Hyperglycemia</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="Y">Liver</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015032" MajorTopicYN="Y">Zinc</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D027682" MajorTopicYN="Y">Cation Transport Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="Y">Obesity</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">NAFLD</Keyword><Keyword MajorTopicYN="N">Type II diabetes</Keyword><Keyword MajorTopicYN="N">genetics</Keyword><Keyword MajorTopicYN="N">genomics</Keyword><Keyword MajorTopicYN="N">human</Keyword><Keyword MajorTopicYN="N">mouse</Keyword><Keyword MajorTopicYN="N">zinc transporter</Keyword></KeywordList><CoiStatement>SC, KH, JD, WW, MF, BY, AL, SB, VA, AM, AL, JB, NV, TD, LM, ML, RC, AS, AE, HN full-time employee of the Regeneron Genetics Center or Regeneron Pharmaceuticals Inc and hold stock options/restricted stock as part of compensation, CV, DC, OM, KK No competing interests declared, LL full-time employee of the Regeneron Genetics Center or Regeneron Pharmaceuticals Inc and hold stock options/restricted stock as part of compensation.full-time employee of the Regeneron Genetics Center or Regeneron Pharmaceuticals Inc and hold stock options/restricted stock as part of compensation</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>6</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>12</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>11</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate 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Ultra-high-performance liquid chromatography-high-resolution-mass-spectrometry detected lipidomics and metabolomics profiles. DME patients received ≥3 anti-VEGF treatments, categorized into strong and weak response groups. Machine learning (ML) screened prospective metabolic features, developing prediction models.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Key metabolic features identified in the metabolomics and lipidomics datasets included n-acetyl isoleucine (odds ratio [OR] = 1.635), cis-aconitic acid (OR = 3.296), and ophthalmic acid (OR = 0.836) for DR. For early-DR, n-acetyl isoleucine (OR = 1.791) and decaethylene glycol (PEG-10) (OR = 0.170) were identified as key markers. L-kynurenine (OR = 0.875), niacinamide (OR = 0.843), and linoleoyl ethanolamine (OR = 0.941) were identified as significant indicators for DME. Trigonelline (OR = 1.441) and 4-methylcatechol-2-sulfate (OR = 1.121) emerged as predictors for strong response to anti-VEGF. Predictive models achieved R² values of 99.9%, 97.7%, 93.9%, and 98.4% for DR, early-DR, DME, and strong response groups in the calibration set, respectively, and validated well with R² values of 96.3%, 96.8%, 79.9%, and 96.3%.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">This research used ML to identify differential metabolic features from metabolomics and lipidomics datasets in DR patients. It implies that metabolic indicators can effectively predict early disease progression and potential weak responders to anti-VEGF therapy in DME eyes.</AbstractText><AbstractText Label="TRANSLATIONAL RELEVANCE" NlmCategory="UNASSIGNED">The identified metabolic indicators may aid in predicting the early progression of DR and optimizing therapeutic strategies for DME.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pang</LastName><ForeName>Yuhui</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luo</LastName><ForeName>Chaokun</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Qingruo</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiongze</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liao</LastName><ForeName>Nanying</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Yuying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mi</LastName><ForeName>Lan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gan</LastName><ForeName>Yuhong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Yongyue</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wen</LastName><ForeName>Feng</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Hui</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Transl Vis Sci Technol</MedlineTA><NlmUniqueID>101595919</NlmUniqueID><ISSNLinking>2164-2591</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020533">Angiogenesis Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467484">VEGFA protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003930" MajorTopicYN="Y">Diabetic Retinopathy</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069550" MajorTopicYN="Y">Machine Learning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008269" MajorTopicYN="Y">Macular Edema</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020533" MajorTopicYN="Y">Angiogenesis Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="Y">Vascular Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001082" MajorTopicYN="Y">Aqueous Humor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055432" MajorTopicYN="N">Metabolomics</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000081362" MajorTopicYN="N">Lipidomics</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002851" MajorTopicYN="N">Chromatography, High Pressure Liquid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000095028" MajorTopicYN="N">Multiomics</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Disclosure: <b>Y. Pang</b>, None; <b>C. Luo</b>, None; <b>Q. Zhang</b>, None; <b>X. Zhang</b>, None; <b>N. Liao</b>, None; <b>Y. Ji</b>, None; <b>L. Mi</b>, None; <b>Y. Gan</b>, None; <b>Y. Su</b>, None; <b>F. Wen</b>, None; <b>H. 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Detection of diabetic retinopathy from ultra-widefield scanning laser ophthalmoscope images: a multicenter deep learning analysis. Ophthalmol Retina. 2021; 5: 1097–1106.</Citation><ArticleIdList><ArticleId IdType="pubmed">33540169</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39670902</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>16</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1853-0605</ISSN><JournalIssue CitedMedium="Internet"><Volume>81</Volume><Issue>4</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>13</Day></PubDate></JournalIssue><Title>Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina)</Title><ISOAbbreviation>Rev Fac Cien Med Univ Nac Cordoba</ISOAbbreviation></Journal><ArticleTitle>[Impact of educational intervention in a population with type 2 diabetes mellitus].</ArticleTitle><Pagination><StartPage>752</StartPage><EndPage>767</EndPage><MedlinePgn>752-767</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.31053/1853.0605.v81.n4.44579</ELocationID><Abstract><AbstractText Label="INTRODUCTION">The complications associated with the chronic pathophysiological process of type 2 diabetes mellitus (T2DM) have a significant impact on the affected population. The Diabetes Knowledge Questionnaire (DKQ-24) determines the level of knowledge about diabetes, providing health professionals with information to carry out useful educational interventions and prevent both acute and chronic complications of the disease</AbstractText><AbstractText Label="OBJECTIVE">To assess the long-term effect of implementing a hospital-based therapeutic diabetes education model (self-care and knowledge) on patients with type 2 diabetes mellitus (T2DM) in a population from southern Colombia.</AbstractText><AbstractText Label="MATERIALS AND METHODS">Longitudinal study, prospective type, conducted on 60 hospitalized T2DM patients. The DKQ-24 was used for pre-assessment, and after 90 days, it was administered again, along with the collection of biometric variables. The intervention consisted of 5 sessions of therapeutic diabetes education in hospital settings.</AbstractText><AbstractText Label="RESULTS">The average results according to the DKQ-2 questionnaire pre-intervention (10.13±3.28) and post-intervention (20.13±2.77) showed significant differences (p<0.000). The biometric profile indicated significant differences (p<0.000) during pre and post-intervention, except for systolic blood pressure (p=0.275). The Cronbach's alpha for the DKQ 24 had an adequate value of 0.86. The intraclass correlation coefficient (ICC) for average measures was 0.860, considered "good" (p<0.000).</AbstractText><AbstractText Label="CONCLUSIONS">The diabetes educational intervention demonstrated significant changes in basic knowledge levels regarding the disease, glycemic control, and complication prevention, improving the patient's biometric profile and highlighting its importance.</AbstractText><CopyrightInformation>Universidad Nacional de Córdoba</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tafurt Cardona</LastName><ForeName>Yaliana</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Fundación Universitaria de Navarra.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ramón Collazos</LastName><ForeName>Rober Andrés</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Fundación Universitaria de Navarra.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Murillo Cumber</LastName><ForeName>Camilo Alexander</ForeName><Initials>CA</Initials><AffiliationInfo><Affiliation>Fundación Universitaria de Navarra.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ortiz Tique</LastName><ForeName>Juan Pablo</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>Fundación Universitaria de Navarra.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mendoza Perez</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Universidad Autónoma de Chiapas.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peralta-Pineda</LastName><ForeName>Edison</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Universidad Autónoma de Chiapas.</Affiliation></AffiliationInfo></Author></AuthorList><Language>spa</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Impacto de la intervención educativa en una población con Diabetes Mellitus tipo 2.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Argentina</Country><MedlineTA>Rev Fac Cien Med Univ Nac Cordoba</MedlineTA><NlmUniqueID>8303003</NlmUniqueID><ISSNLinking>0014-6722</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010353" MajorTopicYN="Y">Patient Education as Topic</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011795" MajorTopicYN="N">Surveys and Questionnaires</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003105" MajorTopicYN="N" Type="Geographic">Colombia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007722" MajorTopicYN="Y">Health Knowledge, Attitudes, Practice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012648" MajorTopicYN="N">Self Care</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="spa"><AbstractText Label="INTRODUCCIÓN">Las complicaciones asociadas al proceso fisiopatológico crónico de la diabetes mellitus tipo 2 (DM2) inciden enormemente en la población que la padece. El Diabetes Knowledge Questionnaire (DKQ-24), determina el nivel de conocimientos sobre diabetes, proporcionando información a los profesionales de la salud, para realizar intervenciones educativas útiles y prevenir complicaciones agudas y crónicas de la enfermedad.</AbstractText><AbstractText Label="OBJETIVOS">Evaluar el efecto de la aplicación de un modelo de educación terapéutica diabetológica hospitalario (autocuidado y conocimiento) a largo plazo en pacientes con diabetes mellitus tipo 2 (DM2) en una población del sur de Colombia.  Materiales y métodos: Estudio longitudinal prospectivo, realizado en 60 pacientes con DM2 hospitalizados. Se utilizó el cuestionario DKQ-24 como evaluación previa y posterior a 90 días se aplicó de nuevo junto con la toma de las variables biométricas. Se realizo la intervención en 5 sesiones educativas de educación terapéutica diabetológica en ámbitos hospitalarios.</AbstractText><AbstractText Label="RESULTADOS">Los resultados promedios según el cuestionario DKQ-2 pre (10,13±3,28) y posintervención (20,13±2,77) presentaron diferencias significativas (p<0.000). Según el perfil biométrico indico diferencias significativas (p<0.000) durante la pre y posintervención, excepto para la presión sistólica (p= 0,275). El alfa de Cronbach para el DKQ 24 tuvo un valor adecuado de 0,86. El coeficiente de correlación intraclase (ICC) para las medidas promedio fue de 0,860, considerado "bueno" (p<0.000).</AbstractText><AbstractText Label="CONCLUSIÓN">La intervención educativa diabetológica mostró cambios importantes en los niveles de conocimiento básico sobre la enfermedad, control glicémico y la prevención de complicaciones, mejorando el perfil biométrico en el paciente, evidenciando su importancia.</AbstractText><CopyrightInformation>Universidad Nacional de Córdoba</CopyrightInformation></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword><Keyword MajorTopicYN="N">educational intervention</Keyword><Keyword MajorTopicYN="N">knowledge</Keyword><Keyword MajorTopicYN="N">complications</Keyword><Keyword MajorTopicYN="N">bioimpedance</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>3</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>12</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>12</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>10</Hour><Minute>30</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39670902</ArticleId><ArticleId IdType="doi">10.31053/1853.0605.v81.n4.44579</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39670387</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2335-6936</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><PubDate><Year>2025</Year></PubDate></JournalIssue><Title>Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing</Title><ISOAbbreviation>Pac Symp Biocomput</ISOAbbreviation></Journal><ArticleTitle>Cross-Species Modeling Identifies Gene Signatures in Type 2 Diabetes Mouse Models Predictive of Inflammatory and Estrogen Signaling Pathways Associated with Alzheimer's Disease Outcomes in Humans.</ArticleTitle><Pagination><StartPage>426</StartPage><EndPage>440</EndPage><MedlinePgn>426-440</MedlinePgn></Pagination><Abstract><AbstractText>Alzheimer's disease (AD), the predominant form of dementia, is influenced by several risk factors, including type 2 diabetes (T2D), a metabolic disorder characterized by the dysregulation of blood sugar levels. Despite mouse and human studies reporting this connection between T2D and AD, the mechanism by which T2D contributes to AD pathobiology is not well understood. A challenge in understanding mechanistic links between these conditions is that evidence between mouse and human experimental models must be synthesized, but translating between these systems is difficult due to evolutionary distance, physiological differences, and human heterogeneity. To address this, we employed a computational framework called translatable components regression (TransComp-R) to overcome discrepancies between pre-clinical and clinical studies using omics data. Here, we developed a novel extension of TransComp-R for multi-disease modeling to analyze transcriptomic data from brain samples of mouse models of AD, T2D, and simultaneous occurrence of both disease (ADxT2D) and postmortem human brain data to identify enriched pathways predictive of human AD status. Our TransComp-R model identified inflammatory and estrogen signaling pathways encoded by mouse principal components derived from models of T2D and ADxT2D, but not AD alone, predicted with human AD outcomes. The same mouse PCs predictive of human AD outcomes were able to capture sex-dependent differences in human AD biology, including significant effects unique to female patients, despite the TransComp-R being derived from data from only male mice. We demonstrated that our approach identifies biological pathways of interest at the intersection of the complex etiologies of AD and T2D which may guide future studies into pathogenesis and therapeutic development for patients with T2D-associated AD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ball</LastName><ForeName>Brendan K</ForeName><Initials>BK</Initials><AffiliationInfo><Affiliation>Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Proctor</LastName><ForeName>Elizabeth A</ForeName><Initials>EA</Initials></Author><Author ValidYN="Y"><LastName>Brubaker</LastName><ForeName>Douglas K</ForeName><Initials>DK</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pac Symp Biocomput</MedlineTA><NlmUniqueID>9711271</NlmUniqueID><ISSNLinking>2335-6928</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004967">Estrogens</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="Y">Alzheimer Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019295" MajorTopicYN="Y">Computational Biology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="Y">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004967" MajorTopicYN="Y">Estrogens</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013045" MajorTopicYN="N">Species Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>12</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>11</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>5</Hour><Minute>43</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39670387</ArticleId><ArticleId IdType="pii">9789819807024_0031</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39669492</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>Association between waist circumference or weight change after smoking cessation and incidence of cardiovascular disease or all-cause death in Korean adults with type 2 diabetes.</ArticleTitle><Pagination><StartPage>1493663</StartPage><MedlinePgn>1493663</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1493663</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1493663</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">To investigate the association among smoking cessation, weight or waist circumference change post-cessation, and cardiovascular disease (CVD) or all-cause death among patients with type 2 Diabetes (T2D).</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="UNASSIGNED">This retrospective cohort study included 32,142 patients with T2D classified according to changes in smoking status, post-cessation weight, and waist circumference. Especially for recent or long-term quitters, participants who changed from current to none/former smoker or from non-smoker to former smoker were defined as recent quitters, and those who changed from former to none/former smoker were defined as long-term quitters. CVD or all-cause death risk was evaluated.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 5,845 participants were newly diagnosed with CVD, and 3,723 died during follow-up. After adjusting for potential confounding factors, compared with current smokers, the hazard ratios (HRs) for CVD were 0.94 (95% confidence interval [CI]: 0.85-1.03), 0.82 (95% CI: 0.74-0.90), and 0.82 (95% CI: 0.75-0.90) for recent quitters, long-term quitters, non-smokers, respectively; 0.88 (95% CI: 0.78-0.99), 0.68 (95% CI: 0.57-0.81), and 0.82 (95% CI: 0.67-1.00) for long-term quitters with no waist circumference gain, long-term quitters with waist circumference gain of 0.1-5.0 cm, and long-term quitters with waist circumference gain ≥5.0 cm, respectively; and 0.79 (95% CI: 0.71-0.89), 0.85 (95% CI: 0.74-0.98), and 0.84 (95% CI: 0.60-1.17) for long-term quitters with no weight gain, long-term quitters with weight gain of 2-5 kg, and long-term quitters with weight gain ≥5 kg, respectively. Similar associations were observed for all-cause death.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">Patients with T2D should maintain their weight and waist circumference after long-term smoking cessation to prevent CVD. It is more important for them to maintain weight rather than waist circumference to prevent all-cause death.</AbstractText><CopyrightInformation>Copyright © 2024 Lee, Shin and Choi.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Heajung</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Statistics and Data Science, Yonsei University, Seoul, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shin</LastName><ForeName>Jaeyong</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Preventive Medicine, Yonsei University, Seoul, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Jae Woo</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Health Insurance Research Institute, National Health Insurance Service, Wonju, Republic of Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016540" MajorTopicYN="Y">Smoking Cessation</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055105" MajorTopicYN="Y">Waist Circumference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056910" MajorTopicYN="N" Type="Geographic">Republic of Korea</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002423" MajorTopicYN="N">Cause of Death</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012907" MajorTopicYN="N">Smoking</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001835" MajorTopicYN="N">Body Weight</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cardiovascular disease</Keyword><Keyword MajorTopicYN="N">mortality</Keyword><Keyword MajorTopicYN="N">smoking cessation</Keyword><Keyword MajorTopicYN="N">waist change</Keyword><Keyword MajorTopicYN="N">weight change</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>11</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate 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However, the role of GDF15 as a biomarker of health outcomes in obese men from different racial/ethnic background has not been evaluated. The objective of this study was to investigate the racial/ethnic differences on the relationship between GDF15 and markers of glucometabolic status, hormonal profile, body composition and bone mineral density (BMD) in obese men. One hundred ninety-three obese men from diverse racial/ethnic backgrounds were enrolled. BMD and body composition were measured by dual energy X-ray absorptiometry. Serum GDF15, osteocalcin, C-terminal telopeptide, sclerostin, adiponectin, leptin, estradiol, testosterone, follicle-stimulating hormone, luteinizing hormone, 25-hydroxyvitamin D, lipid profile, and hemoglobin A1C (A1C) were measured. Non-African Americans (NAA) had significantly higher GDF15 level than African Americans (AA). Level was also higher in patients with type 2 diabetes (T2DM). In both the groups GDF15 correlated with A1C and lean mass. However. GDF15 correlated  with body fat, LDL total cholesterol and femoral neck BMD only in NAA and with appendicular lean mass only in AA. Ethnicity, total cholesterol and T2DM were found to be independent predictors of GDF15. We conclude that GDF15 may influence glucometabolic status, body composition and bone parameters which may affect cardiovascular risk and osteoporosis  between races.</AbstractText><CopyrightInformation>Published 2024. This article is a U.S. Government work and is in the public domain in the USA. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bathina</LastName><ForeName>Siresha</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-1092-5600</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Michael E. De Bakey Veterans Affairs (VA) Medical Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lopez</LastName><ForeName>Virginia Fuenmayor</ForeName><Initials>VF</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Michael E. De Bakey Veterans Affairs (VA) Medical Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Prado</LastName><ForeName>Mia</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Michael E. De Bakey Veterans Affairs (VA) Medical Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ballato</LastName><ForeName>Elliot</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Colleluori</LastName><ForeName>Georgia</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tetlay</LastName><ForeName>Maryam</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Villareal</LastName><ForeName>Dennis Tan</ForeName><Initials>DT</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Michael E. De Bakey Veterans Affairs (VA) Medical Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mediwala</LastName><ForeName>Sanjay</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Michael E. De Bakey Veterans Affairs (VA) Medical Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Rui</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Michael E. De Bakey Veterans Affairs (VA) Medical Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qualls</LastName><ForeName>Clifford</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Mathematics and Statistics, University of New Mexico, Albuquerque, New Mexico, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Armamento-Villareal</LastName><ForeName>Reina</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Division of Endocrinology Diabetes and Metabolism at Baylor College of Medicine, Houston, Texas, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Michael E. De Bakey Veterans Affairs (VA) Medical Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HD093047</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HD093047</GrantID><Acronym>GF</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Physiol Rep</MedlineTA><NlmUniqueID>101607800</NlmUniqueID><ISSNLinking>2051-817X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D055436">Growth Differentiation Factor 15</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C526140">GDF15 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="Y">Obesity</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000208" MajorTopicYN="N">ethnology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015519" MajorTopicYN="Y">Bone Density</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055436" MajorTopicYN="Y">Growth Differentiation Factor 15</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001823" MajorTopicYN="N">Body Composition</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000208" MajorTopicYN="N">ethnology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001741" MajorTopicYN="N">Black or African American</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000095223" MajorTopicYN="N">White</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">A1C</Keyword><Keyword MajorTopicYN="N">Cardiovascular risk</Keyword><Keyword MajorTopicYN="N">Cholesterol</Keyword><Keyword MajorTopicYN="N">GDF15</Keyword><Keyword MajorTopicYN="N">Obesity</Keyword></KeywordList><CoiStatement>The authors declare no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>11</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>11</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>2</Hour><Minute>12</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>12</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39668628</ArticleId><ArticleId IdType="pmc">PMC11638490</ArticleId><ArticleId IdType="doi">10.14814/phy2.70124</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Adela, R. , & Banerjee, S. 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Two competing guilds, associated with high-fiber vs. control diets, correlated with healthy biomarkers. The potential of this approach was further verified across 15 diseases in 26 studies.</AbstractText><CopyrightInformation>Copyright © 2024. Published by Elsevier Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gomes</LastName><ForeName>Antonio L C</ForeName><Initials>ALC</Initials><AffiliationInfo><Affiliation>Department of Hematology and Hematopoietic Cell Transplantation, City of Hope, Duarte, CA 91010, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jenq</LastName><ForeName>Robert R</ForeName><Initials>RR</Initials><AffiliationInfo><Affiliation>Department of Hematology and Hematopoietic Cell Transplantation, City of Hope, Duarte, CA 91010, USA. Electronic address: rjenq@coh.org.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cell Host Microbe</MedlineTA><NlmUniqueID>101302316</NlmUniqueID><ISSNLinking>1931-3128</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004043">Dietary Fiber</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069196" MajorTopicYN="N">Gastrointestinal Microbiome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001419" MajorTopicYN="N">Bacteria</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000145" MajorTopicYN="N">classification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D064307" MajorTopicYN="N">Microbiota</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004043" MajorTopicYN="N">Dietary Fiber</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004032" MajorTopicYN="N">Diet</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Declaration of interests R.R.J. is part of the scientific advisory board of Seres therapeutics, MaaT Pharma, Prolacta, and Postbiotics Plus. R.R.J. holds patent royalties at Seres therapeutics and stock options at Seres Therapeutics and Postbiotics Plus. A.L.C.G. has stock options for Xbiome Inc.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>11</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>18</Hour><Minute>19</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39667342</ArticleId><ArticleId IdType="doi">10.1016/j.chom.2024.11.010</ArticleId><ArticleId IdType="pii">S1931-3128(24)00441-4</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39666780</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>12</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>12</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Analysis of rare coding variants in 470,000 exome-sequenced subjects characterises contributions to risk of type 2 diabetes.</ArticleTitle><Pagination><StartPage>e0311827</StartPage><MedlinePgn>e0311827</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e0311827</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0311827</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">To follow up results from an earlier study using an extended sample of 470,000 exome-sequenced subjects to identify genes associated with type 2 diabetes (T2D) and to characterise the distribution of rare variants in these genes.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">Exome sequence data for 470,000 UK Biobank participants was analysed using a combined phenotype for T2D obtained from diagnostic and prescription data. Gene-wise weighted burden analysis of rare coding variants in the new cohort of 270,000 samples was carried out for the 32 genes previously significant with uncorrected p < 0.001 along with 7 other genes previously implicated in T2D. Follow-up studies of GCK, GIGYF1, HNF1A and HNF4A used the full sample of 470,000 to investigate the effects of different categories of variant.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">No novel genes were identified as exome wide significant. Rare loss of function (LOF) variants in GCK exerted a very large effect on T2D risk but more common (though still very rare) nonsynonymous variants classified as probably damaging by PolyPhen on average approximately doubled risk. Rare variants in the other three genes also had large effects on risk.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In spite of the very large sample size, no novel genes are implicated. Coding variants with an identifiable effect are collectively too rare be generally useful for guiding treatment choices for most patients. The finding that some nonsynonymous variants in GCK affect T2D risk is novel but not unexpected and does not have obvious practical implications. This research has been conducted using the UK Biobank Resource.</AbstractText><CopyrightInformation>Copyright: © 2024 David Curtis. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Curtis</LastName><ForeName>David</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-4089-9183</Identifier><AffiliationInfo><Affiliation>UCL, UCL Genetics Institute, London, United Kingdom.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="Y">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073359" MajorTopicYN="Y">Exome Sequencing</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059472" MajorTopicYN="Y">Exome</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014644" MajorTopicYN="N">Genetic Variation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The author has declared no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>9</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>18</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>18</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>13</Hour><Minute>55</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>12</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39666780</ArticleId><ArticleId IdType="pmc">PMC11637267</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0311827</ArticleId><ArticleId IdType="pii">PONE-D-24-23535</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Curtis D.
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This paper summarizes the evidence and implications of the use of the new CGM system, FreeStyle Libre 2 (FSL2). A global review of the literature on the use of FSL2 in people with DM was performed. All types of studies were included. The evidence is presented qualitatively together with expert clinical opinion. FSL2 is an integrated CGM system with real-time glucose readings (no scanning required) and customizable alarms. In studies of subjects aged 2 years and older with DM1 or DM2, the overall mean absolute relative difference for FSL2 was 8.2%, with a high degree of clinical accuracy. Compared to blood monitoring in DM1, studies show higher time within range, lower time below range and lower time above range at 4, 8 and 12 weeks of FSL2 use. These results were confirmed in observational studies in DM, where the majority of FSL2 users reported greater satisfaction with treatment and a significant improvement in quality of life. In concluded, Including the FSL2 system in the management of people with DM would also reduce the risks associated with DM complications, improving the prognosis of this population and allowing for the appropriate use of healthcare resources.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Litwak</LastName><ForeName>León</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Servicio de Endocrinología, Metabolismo y Medicina Nuclear, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. E-mail: leon.litwak@hospitalitaliano.org.ar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ré</LastName><ForeName>Matías</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Unidad de Diabetes, Hospital San Juan de Dios de La Plata, Buenos Aires, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Proietti</LastName><ForeName>Adrián</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Servicio de Endocrinología, Diabetes y Tecnología aplicada, Kynet-Integral, Buenos Aires, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dain</LastName><ForeName>Alejandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Servicio de Diabetes y Nutrición, Clínica Universitaria Reina Fabiola, Córdoba, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Flores</LastName><ForeName>Adriana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Servicio Nutrición y Diabetes, Fundación Hospitalaria. Buenos Aires, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Figueroa</LastName><ForeName>Shairine</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Medical Affairs, Abbott Diabetes Care, Bogotá, Colombia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barbieri</LastName><ForeName>Douglas E</ForeName><Initials>DE</Initials><AffiliationInfo><Affiliation>Medical Affairs, Abbott Diabetes Care, São Paulo, Brasil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>spa</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D004740">English Abstract</PublicationType></PublicationTypeList><VernacularTitle>Avances en el monitoreo continuo de glucosa: evidencia de una nueva generación de tecnología.</VernacularTitle></Article><MedlineJournalInfo><Country>Argentina</Country><MedlineTA>Medicina (B Aires)</MedlineTA><NlmUniqueID>0204271</NlmUniqueID><ISSNLinking>0025-7680</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015190" MajorTopicYN="Y">Blood Glucose Self-Monitoring</DescriptorName><QualifierName UI="Q000295" MajorTopicYN="N">instrumentation</QualifierName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="N">Diabetes Mellitus</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011788" MajorTopicYN="N">Quality of Life</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="N">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000095583" MajorTopicYN="N">Continuous Glucose Monitoring</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="spa"><AbstractText>El monitoreo continuo de glucosa (MCG) proporciona información completa y dinámica para guiar el tratamiento de la diabetes mellitus (DM). Este documento sintetiza la evidencia e implicancias del uso del FreeStyle Libre 2 (FSL2), un sistema integrado de MCG con lecturas de glucosa en tiempo real (sin necesidad de escaneo) y alarmas personalizables. Se realizó una revisión global de la literatura que incluyó todo tipo de estudios y se presentó la evidencia de manera cualitativa junto con la opinión de expertos clínicos. Se identificaron estudios en sujetos a partir de los 2 años de edad con DM1/DM2, que han registrado una diferencia media relativa absoluta global del 8.2% para FSL2, con un alto grado de exactitud clínica. En comparación con la monitorización sanguínea en DM1, los ensayos muestran mayor tiempo dentro del rango, menor tiempo por debajo del rango y menor tiempo por encima del rango, a 4, 8 y 12 semanas de uso del FSL2. Estos resultados se han confirmado en estudios observacionales en DM, en los que la mayoría de los usuarios de FSL2 reportaron mayor satisfacción con el tratamiento y mejor calidad de vida. En conclusión, la inclusión del sistema FSL2 en el manejo de la DM reduciría los riesgos asociados a las complicaciones de la DM, mejorando el pronóstico de esta población y permitiendo un uso adecuado de los recursos sanitarios.</AbstractText></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">FreeStyle Libre 2</Keyword><Keyword MajorTopicYN="N">alarm</Keyword><Keyword MajorTopicYN="N">blood glucose control</Keyword><Keyword MajorTopicYN="N">continuous glucose monitoring</Keyword><Keyword MajorTopicYN="N">type 1 diabetes mellitus</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>18</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>18</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>12</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39666416</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39665019</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>12</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>Threshold effect of atherogenic index of plasma on type 2 diabetes mellitus and modification by uric acid in normal-weight adults with hypertension.</ArticleTitle><Pagination><StartPage>1495340</StartPage><MedlinePgn>1495340</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1495340</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1495340</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">The association between atherogenic index of plasma (AIP) and type 2 diabetes mellitus (T2DM) in normal-weight individuals with hypertension remains unclear. This study seeks to elucidate this relationship in normal-weight adults with hypertension.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">This cross-sectional study included 8,258 normal-weight adults with hypertension from the China Hypertension Registry Study. The AIP was calculated as log10 (triglycerides/high-density lipoprotein cholesterol). The multivariate logistic regression, generalized additive model, smooth fitting curve, sensitivity analyses, two-part logistic regression, and subgroup analyses were conducted to detect the correlation between AIP and T2DM.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">The mean age of the study population was 64.89 ± 8.97 years, with an overall prevalence of T2DM of 15.55%. Multivariate logistic regression analyses indicated that there was a positive and independent relationship between AIP and T2DM (OR: 3.73; 95% CI: 2.82, 4.94). Threshold effect analysis identified a J-shaped association between AIP and T2DM, with an inflection point at 0. Additionally, an interaction between hyperuricemia and AIP was observed (<i>P</i> for interaction = 0.034).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">In normal-weight adults with hypertension, there was a J-shaped association between AIP and T2DM, with an inflection point at 0. the correlation between AIP and T2DM was more pronounced in individuals with hyperuricemia compared to those with normal uric acid.</AbstractText><CopyrightInformation>Copyright © 2024 Tao, Wang, Zhou, Zhu, Yu, Bao, Li and Cheng.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tao</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Jiangxi Provincial Cardiovascular Disease Clinical Medical Research Center, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Tao</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Jiangxi Provincial Cardiovascular Disease Clinical Medical Research Center, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Center for Prevention and Treatment of Cardiovascular Diseases, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Wei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Jiangxi Provincial Cardiovascular Disease Clinical Medical Research Center, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Center for Prevention and Treatment of Cardiovascular Diseases, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Lingjuan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Jiangxi Provincial Cardiovascular Disease Clinical Medical Research Center, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Center for Prevention and Treatment of Cardiovascular Diseases, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Chao</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Jiangxi Provincial Cardiovascular Disease Clinical Medical Research Center, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Center for Prevention and Treatment of Cardiovascular Diseases, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bao</LastName><ForeName>Huihui</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Center for Prevention and Treatment of Cardiovascular Diseases, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Juxiang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Jiangxi Provincial Cardiovascular Disease Clinical Medical Research Center, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Xiaoshu</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Center for Prevention and Treatment of Cardiovascular Diseases, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>268B43MJ25</RegistryNumber><NameOfSubstance UI="D014527">Uric Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014280">Triglycerides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008076">Cholesterol, HDL</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014527" MajorTopicYN="Y">Uric Acid</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="Y">Hypertension</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050197" MajorTopicYN="Y">Atherosclerosis</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002681" MajorTopicYN="N" Type="Geographic">China</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D033461" MajorTopicYN="N">Hyperuricemia</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014280" MajorTopicYN="N">Triglycerides</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008076" MajorTopicYN="N">Cholesterol, HDL</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">atherogenic index of plasma</Keyword><Keyword MajorTopicYN="N">hypertension</Keyword><Keyword MajorTopicYN="N">threshold effect</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword><Keyword MajorTopicYN="N">uric acid modification</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>11</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>11</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>4</Hour><Minute>59</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>1</Month><Day>1</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39665019</ArticleId><ArticleId IdType="pmc">PMC11631599</ArticleId><ArticleId IdType="doi">10.3389/fendo.2024.1495340</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Collaborators GBDD . 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This study aimed to investigate the association of socioeconomic deprivation and ethnicity on the risk of diabetes in Birmingham.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">Data were included from 108,514 NHS Health Checks conducted in Birmingham between 2018 and 2023. Attributable fraction and multinomial logistic regression were used to estimate the number of events avoidable and the prevalence odds ratios (POR) of determinants respectively.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Attributable fraction analysis estimated that 64% of diabetes and 44% of pre-diabetes cases could be attributed to socioeconomic deprivation. Specifically, if Asian attendees in the least deprived areas had the same risk as White individuals in the least deprived areas, there would have been 1,056 fewer cases of diabetes and 2,226 fewer cases of pre-diabetes. Diabetes was significantly associated with Asian ethnicity (POR = 5.43, <i>p</i> < 0.001), Black ethnicity (POR = 3.15, <i>p</i> < 0.001) and Mixed ethnicity (POR = 2.79, <i>p</i> < 0.001). Pre-diabetes was also significantly associated with Asian ethnicity (POR = 3.06, <i>p</i> < 0.001), Black ethnicity (POR = 2.70, <i>p</i> < 0.001) and Mixed ethnicity (POR = 2.21, <i>p</i> < 0.001). The interaction effects between ethnicity and deprivation posed a greater risk of diabetes, especially for Asian attendees in the first (POR = 9.34, <i>p</i> < 0.001) and second (POR = 6.24, <i>p</i> < 0.001) most deprived quintiles.</AbstractText><AbstractText Label="DISCUSSION" NlmCategory="UNASSIGNED">The present findings demonstrate the association of ethnicity and socioeconomic deprivation on the risk of diabetes and pre-diabetes. It underscores the necessity for targeted interventions and policies to address these inequalities.</AbstractText><CopyrightInformation>Copyright © 2024 Au-Yeung, Ellis, Dallaway, Riley, Varney and Howell-Jones.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Au-Yeung</LastName><ForeName>Chung Him</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>Public Health, Birmingham City Council, Birmingham, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ellis</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Public Health, Birmingham City Council, Birmingham, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dallaway</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>School of Health and Society, Faculty of Education, Health and Wellbeing, University of Wolverhampton, Wolverhampton, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riley</LastName><ForeName>Jenny</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Public Health, Birmingham City Council, Birmingham, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Varney</LastName><ForeName>Justin</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Public Health, Birmingham City Council, Birmingham, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Howell-Jones</LastName><ForeName>Rebecca</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Public Health, Birmingham City Council, Birmingham, United Kingdom.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Public Health</MedlineTA><NlmUniqueID>101616579</NlmUniqueID><ISSNLinking>2296-2565</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012959" MajorTopicYN="Y">Socioeconomic Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013222" MajorTopicYN="Y">State Medicine</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005006" MajorTopicYN="Y">Ethnicity</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015995" MajorTopicYN="N">Prevalence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054624" MajorTopicYN="N">Health Status Disparities</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">body mass index</Keyword><Keyword MajorTopicYN="N">glycated hemoglobin A1c</Keyword><Keyword MajorTopicYN="N">health inequities</Keyword><Keyword MajorTopicYN="N">logistic models</Keyword><Keyword MajorTopicYN="N">primary health care</Keyword><Keyword MajorTopicYN="N">social determinants of health</Keyword><Keyword MajorTopicYN="N">socioeconomic factors</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>7</Day></PubMedPubDate><PubMedPubDate 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(2011) 2:320–32. 10.1504/IJBHR.2011.043414</Citation><ArticleIdList><ArticleId IdType="doi">10.1504/IJBHR.2011.043414</ArticleId><ArticleId IdType="pmc">PMC4224297</ArticleId><ArticleId IdType="pubmed">25383095</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39663847</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>20</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1744-7658</ISSN><JournalIssue CitedMedium="Internet"><Volume>33</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Expert opinion on investigational drugs</Title><ISOAbbreviation>Expert Opin Investig Drugs</ISOAbbreviation></Journal><ArticleTitle>Survodutide in MASH: bridging the gap between hepatic and systemic metabolic dysfunction.</ArticleTitle><Pagination><StartPage>1167</StartPage><EndPage>1176</EndPage><MedlinePgn>1167-1176</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/13543784.2024.2441865</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="UNASSIGNED">Glucagon-like peptide-1 receptor (GLP-1 R) agonists have demonstrated remarkable effectiveness in the treatment of obesity and type 2 diabetes. Although these agents provide beneficial effects for metabolic dysfunction-associated steatohepatitis (MASH) through their glucose-lowering and weight-reducing properties, their efficacy in promoting fibrosis regression remains unproven. Survodutide, an investigational dual agonist that simultaneously targets both the glucagon receptor (GCGR) and GLP-1 R, has emerged as a promising therapeutic candidate for the comprehensive management of obesity and MASH. By engaging these two critical receptors, this drug has the potential to offer a broad spectrum of metabolic benefits, addressing multiple pathogenic mechanisms underlying these interrelated disorders.</AbstractText><AbstractText Label="AREAS COVERED" NlmCategory="UNASSIGNED">This review examines the pharmacological profile, clinical efficacy, and safety data of survodutide derived from phase 1 and 2 clinical trials.</AbstractText><AbstractText Label="EXPERT OPINION" NlmCategory="UNASSIGNED">Survodutide's dual agonism of the GCGR and GLP-1 R may surpass the efficacy of selective GLP-1 R agonists, demonstrating significant potential in resolving MASH and promoting fibrosis regression. The drug is generally well tolerated, with primarily manageable gastrointestinal adverse effects. As survodutide progresses through phase 3 clinical development, its potential to provide a more effective and holistic approach to treating MASH and its comorbidities may significantly improve patient outcomes and quality of life.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kaya</LastName><ForeName>Eda</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Medicine, Knappschaftskrankenhaus Bochum, Ruhr University, Bochum, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Hepatology, The Global NASH Council, Washington, DC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yilmaz</LastName><ForeName>Yusuf</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Hepatology, The Global NASH Council, Washington, DC, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Gastroenterology, School of Medicine, Recep Tayyip Erdogan University, Rize, Türkiye.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alkhouri</LastName><ForeName>Naim</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Hepatology, The Global NASH Council, Washington, DC, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Hepatology, Arizona Liver Health, Chandler, Arizona, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Opin Investig Drugs</MedlineTA><NlmUniqueID>9434197</NlmUniqueID><ISSNLinking>1354-3784</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018027">Receptors, Glucagon</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C585906">2-(2,6-dimethyl-4-(3-(4-(methylthio)phenyl)-3-oxo-1-propenyl)phenoxyl)-2-methylpropanoic acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011422">Propionates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047188">Chalcones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="Y">Obesity</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005234" MajorTopicYN="Y">Fatty Liver</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018027" MajorTopicYN="N">Receptors, Glucagon</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076722" MajorTopicYN="N">Drug Development</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011422" MajorTopicYN="N">Propionates</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D047188" MajorTopicYN="N">Chalcones</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Metabolic dysfunction-associated steatotic liver disease</Keyword><Keyword MajorTopicYN="N">diabetes</Keyword><Keyword MajorTopicYN="N">fibrosis</Keyword><Keyword MajorTopicYN="N">metabolic disorders, comorbidities</Keyword><Keyword MajorTopicYN="N">metabolic dysfunction-associated steatohepatitis</Keyword><Keyword MajorTopicYN="N">obesity</Keyword><Keyword MajorTopicYN="N">survodutide</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>20</Day><Hour>12</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>3</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39663847</ArticleId><ArticleId IdType="doi">10.1080/13543784.2024.2441865</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39663585</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>01</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1521-0758</ISSN><JournalIssue CitedMedium="Internet"><Volume>49</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month><Day>02</Day></PubDate></JournalIssue><Title>Ultrastructural pathology</Title><ISOAbbreviation>Ultrastruct Pathol</ISOAbbreviation></Journal><ArticleTitle>Metformin ameliorates diabetes-induced hepatic ultrastructural damage and the immune biomarker CD86 and inflammation in rats.</ArticleTitle><Pagination><StartPage>58</StartPage><EndPage>66</EndPage><MedlinePgn>58-66</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/01913123.2024.2440479</ELocationID><Abstract><AbstractText>Diabetes is a known inducer of hepatic ultrastructural alterations, and the expression of the immune biomarker that involves in T-cell immunity, cluster of differentiation 86 (CD86) is increased in diabetic patients with liver cirrhosis. The antidiabetic drug metformin has not previously been used to protect against type 2 diabetes mellitus (T2DM)-induced alternations in hepatic ultrastructure and the induction of the hepatic CD86/inflammation axis in diabetic animal models induced by streptozotocin and a high fat diet. To test our hypotheses, T2DM was induced in rats (model group) and the protective animals were treated with the antidiabetic drug metformin (200 mg/kg) until being sacrificed at week 12. A profound ultrastructural damage to the hepatocytes and liver tissue injury was induced by T2DM as demonstrated by hepatocytes with dark shrunken irregular nuclei, rarefied cytoplasm with lipid droplets, mitochondria with disrupted cristae, as well as depletion of glycogen granules and damaged of liver architecture, which were effectively (<i>p</i> < .0001) protected with metformin. Metformin also suppressed diabetes-induced hepatic gene expression of CD86 and inflammation as well as glycemia and liver injury markers. Furthermore, a significant correlation between hepatocyte damage and CD86, inflammation, glycemia, and biomarkers of liver injury was observed. These findings demonstrate that diabetes is associated with the induction of the hepatic CD86/inflammation axis and hepatocyte ultrastructural alterations while being protected by metformin.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alshahrani</LastName><ForeName>Mohammad Y</ForeName><Initials>MY</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al Amri</LastName><ForeName>Fahad S</ForeName><Initials>FS</Initials><AffiliationInfo><Affiliation>Department of Surgery, College of Medicine, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alzahrani</LastName><ForeName>Mohammed A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, College of Medicine, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alshahrani</LastName><ForeName>Abdulaziz S</ForeName><Initials>AS</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, College of Medicine, Najran University, Najran, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abdel Kader</LastName><ForeName>Dina H</ForeName><Initials>DH</Initials><AffiliationInfo><Affiliation>Department of Medical Histology, Kasr Al-Aini Faculty of Medicine, Cairo University, Cairo, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Almasabi</LastName><ForeName>Faris</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zafrah</LastName><ForeName>Hind</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dallak</LastName><ForeName>Mohammad</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Osman</LastName><ForeName>Osama M</ForeName><Initials>OM</Initials><AffiliationInfo><Affiliation>Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Ani</LastName><ForeName>Bahjat</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alzamil</LastName><ForeName>Norah M</ForeName><Initials>NM</Initials><AffiliationInfo><Affiliation>Department of Family and Community Medicine, College of Medicine, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Ultrastruct Pathol</MedlineTA><NlmUniqueID>8002867</NlmUniqueID><ISSNLinking>0191-3123</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9100L32L2N</RegistryNumber><NameOfSubstance UI="D008687">Metformin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051940">B7-2 Antigen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008687" MajorTopicYN="Y">Metformin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="Y">Biomarkers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051940" MajorTopicYN="Y">B7-2 Antigen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="Y">Liver</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">CD86</Keyword><Keyword MajorTopicYN="N">diabetes</Keyword><Keyword MajorTopicYN="N">hepatocyte ultrastructure</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">metformin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>1</Day><Hour>21</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>0</Hour><Minute>33</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39663585</ArticleId><ArticleId IdType="doi">10.1080/01913123.2024.2440479</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39662975</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>20</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>15</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">2169-575X</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>20</Day></PubDate></JournalIssue><Title>Global health, science and practice</Title><ISOAbbreviation>Glob Health Sci Pract</ISOAbbreviation></Journal><ArticleTitle>Service Delivery Redesign for Noncommunicable Disease Management: Assessment of Needs and Solutions Through a Co-Creation Process in Argentina.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e2400208</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.9745/GHSP-D-24-00208</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">In Argentina, the implementation of a national strategy to reduce the prevalence of noncommunicable diseases (NCDs) has been hampered by challenges at the provincial level. We aimed to design a new model of care for NCDs at the primary care level by conducting a multimodal system assessment and co-design of potential solutions in the province of Mendoza.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We carried out a mixed-methods study with 7 components: evaluation of patterns of care, patient focus groups, cross-sectional standardized population-based phone survey, an electronic cohort follow-up of patients with type 2 diabetes, in-depth interviews with stakeholders, a knowledge test for health care providers on chronic condition management, and a Delphi consensus to provide recommendations from stakeholders.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Focus group and in-depth interviews revealed access to primary health care for NCDs was associated with problems with long waiting times and time-consuming procedures for referral to laboratory tests, hospital care, and provision of medication. Mental health care services were particularly limited. Survey respondents (N=1,190) were predominantly covered through public (41%) or social security sectors (54%); 41% fell in the lowest income group. Contact with the health system was high (5.7 annual visits), but 19.7% reported unmet health care needs. Public sector providers perceived they provided high-quality care despite insufficient material and human resources. Within the social security sector, the main challenge was insufficient staff, particularly affecting mental health care. Health care providers showed a higher percentage of correct answers to depression-related questions, but worse results were seen in hypertension and diabetes care. Actions supported by evidence and expert agreement were identified for implementation to guide future system changes.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Our research highlights the potential for Argentina's primary care system to initiate transformative, system-level changes aimed at improving health outcomes. We propose an innovative methodological assessment and co-design for improving primary care.</AbstractText><CopyrightInformation>© Mazzoni et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mazzoni</LastName><ForeName>Agustina</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute for Clinical Effectiveness and Health Policy, Buenos Aires, Argentina. amazzoni@iecs.org.ar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roberti</LastName><ForeName>Javier</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute for Clinical Effectiveness and Health Policy, Buenos Aires, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guglielmino</LastName><ForeName>Marina</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute for Clinical Effectiveness and Health Policy, Buenos Aires, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nadal</LastName><ForeName>Ana María</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Ministry of Health of Mendoza Province, Mendoza, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mazzaresi</LastName><ForeName>Yanina</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Ministry of Health of Mendoza Province, Mendoza, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Falaschi</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Ministry of Health of Mendoza Province, Mendoza, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>García</LastName><ForeName>Patricia J</ForeName><Initials>PJ</Initials><AffiliationInfo><Affiliation>Universidad Peruana Cayetano Heredia, Lima, Peru.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Espinoza-Pajuelo</LastName><ForeName>Laura</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Universidad Peruana Cayetano Heredia, Lima, Peru.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Medina-Ranilla</LastName><ForeName>Jesús</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Universidad Peruana Cayetano Heredia, Lima, Peru.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leslie</LastName><ForeName>Hannah H</ForeName><Initials>HH</Initials><AffiliationInfo><Affiliation>Division of Prevention Science, University of California, San Francisco, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Portillo</LastName><ForeName>Juan Manuel Gómez</ForeName><Initials>JMG</Initials><AffiliationInfo><Affiliation>Obra Social de Empleados Públicos de Mendoza, Mendoza, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Masier</LastName><ForeName>María Gabriela</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>Obra Social de Empleados Públicos de Mendoza, Mendoza, Argentina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>García-Elorrio</LastName><ForeName>Ezequiel</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institute for Clinical Effectiveness and Health Policy, Buenos Aires, Argentina.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Glob Health Sci Pract</MedlineTA><NlmUniqueID>101624414</NlmUniqueID><ISSNLinking>2169-575X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001118" MajorTopicYN="N" Type="Geographic">Argentina</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073296" MajorTopicYN="Y">Noncommunicable Diseases</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011320" MajorTopicYN="Y">Primary Health Care</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003695" MajorTopicYN="N">Delivery of Health Care</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017144" MajorTopicYN="N">Focus Groups</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019468" MajorTopicYN="N">Disease Management</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006297" MajorTopicYN="N">Health Services Accessibility</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020380" MajorTopicYN="N">Needs 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Int J Qual Health Care. 2023;35(4):mzad083. 10.1093/intqhc/mzad083.</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/intqhc/mzad083</ArticleId><ArticleId IdType="pubmed">37875010</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39662122</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2212-5353</ISSN><JournalIssue CitedMedium="Internet"><Volume>63</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Respiratory investigation</Title><ISOAbbreviation>Respir Investig</ISOAbbreviation></Journal><ArticleTitle>Sodium-glucose co-transporter-2 inhibitors versus dipeptidyl peptidase-4 inhibitors on in-hospital mortality following pneumonia without heart failure: A retrospective cohort study of older adults with diabetes.</ArticleTitle><Pagination><StartPage>88</StartPage><EndPage>93</EndPage><MedlinePgn>88-93</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.resinv.2024.11.016</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S2212-5345(24)00185-0</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Sodium-glucose co-transporter-2 inhibitors (SGLT2i) may contribute to better clinical outcomes in adults with diabetes and pneumonia owing to their potential anti-inflammatory effects. To investigate whether SGLT2i are associated with lower in-hospital mortality following pneumonia without heart failure than dipeptidyl peptidase-4 inhibitors (DPP-4i).</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Using the Japanese Diagnosis Procedure Combination database, we retrospectively identified patients with diabetes aged ≥65 years treated with SGLT2i or DPP-4i who were admitted and managed for pneumonia from April 2016 to October 2020. We then compared in-hospital mortality, the need for mechanical ventilation, and discharges to locations (other than home) between the SGLT2i and DPP-4i groups using multivariable logistic regression analyses fitted with generalized estimating equations.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We analyzed the data of 27,334 patients (mean age, 78.8 years; male, 71.2%), including 535 and 26,799 patients regularly treated with SGLT2i and DPP-4i, respectively. No significant differences were observed between the SGLT2i and DPP-4i groups in in-hospital mortality rate (3.4% vs. 5.9%; odds ratio [OR], 0.64; 95% confidence interval [CI], 0.40-1.05), the need for mechanical ventilation (1.5% vs. 1.8%; OR, 0.78; 95%Cl, 0.39-1.59), and discharge to locations other than home (8.1% vs. 14.1%; OR, 0.72; 95%Cl, 0.51-1.02). The association between the diabetic treatment and in-hospital mortality remained insignificant across weight subgroups (underweight: OR, 0.47; 95%Cl, 0.13-1.67; normal weight: OR, 0.66; 95%Cl, 0.34-1.25; and overweight/obesity: OR 1.06; 95%Cl, 0.43-2.65).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Regular SGLT2i use in patients with diabetes admitted with pneumonia without heart failure may not be associated with improved in-hospital mortality outcomes compared with DPP-4i use.</AbstractText><CopyrightInformation>Copyright © 2024 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Maki</LastName><ForeName>Hiroki</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Health Economics, School of Public Health, The University of Tokyo, Tokyo, Japan; Department of Pharmacy, Kofu City Regional Medical Center, Yamanashi, Japan. Electronic address: makih1210@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Isogai</LastName><ForeName>Toshiaki</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Health Economics, School of Public Health, The University of Tokyo, Tokyo, Japan; Department of Cardiology, Tokyo Metropolitan Tama Medical Center, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Michihata</LastName><ForeName>Nobuaki</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Health Economics, School of Public Health, The University of Tokyo, Tokyo, Japan; Cancer Prevention Center, Chiba Cancer Center Research Institute, Chiba, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsui</LastName><ForeName>Hiroki</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Health Services Research, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fushimi</LastName><ForeName>Kiyohide</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Health Policy and Informatics, Tokyo Medical and Dental University Graduate School of Medicine and Dental Science, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yasunaga</LastName><ForeName>Hideo</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Clinical Epidemiology and Health Economics, School of Public Health, The University of Tokyo, Tokyo, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Respir Investig</MedlineTA><NlmUniqueID>101581124</NlmUniqueID><ISSNLinking>2212-5345</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017052" MajorTopicYN="Y">Hospital Mortality</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011014" MajorTopicYN="Y">Pneumonia</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054873" MajorTopicYN="Y">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012121" MajorTopicYN="N">Respiration, Artificial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="N">Diabetes Mellitus</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DPP-4 inhibitor</Keyword><Keyword MajorTopicYN="N">Diabetes mellitus</Keyword><Keyword MajorTopicYN="N">Pneumonia</Keyword><Keyword MajorTopicYN="N">SGLT2 inhibitor</Keyword></KeywordList><CoiStatement>Conflict of interest The authors have no conflict of interest to declare.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>4</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>9</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>12</Day><Hour>15</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>18</Hour><Minute>32</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39662122</ArticleId><ArticleId IdType="doi">10.1016/j.resinv.2024.11.016</ArticleId><ArticleId IdType="pii">S2212-5345(24)00185-0</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39661889</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>11</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0043-5147</ISSN><JournalIssue CitedMedium="Print"><Volume>77</Volume><Issue>10</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Wiadomosci lekarskie (Warsaw, Poland : 1960)</Title><ISOAbbreviation>Wiad Lek</ISOAbbreviation></Journal><ArticleTitle>Effectiveness of the quercetin use in patients with COVID-19 with concomitant type 2 diabetes mellitus.</ArticleTitle><Pagination><StartPage>1962</StartPage><EndPage>1968</EndPage><MedlinePgn>1962-1968</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.36740/WLek/191875</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Aim: To conduct a comparative analysis of the effectiveness of basic therapy and basic therapy with the inclusion of quercetin in patients with COVID-19 with concomitant type 2 diabetes.</AbstractText><AbstractText Label="PATIENTS AND METHODS" NlmCategory="METHODS">Materials and Methods: There were examined 60 patients with COVID-19 with concomitant T2DM. Upon admission into the hospital and again after 10 days, serum levels of interleukin-6, C-reactive protein, procalcitonin, ferritin, endothelin-1 were determined, and capillaroscopy of the nail plate was performed. Patients of the group I (30) against the background of protocol therapy received 0.5 g of quercetin intravenously once a day for 10 days. Patients of the group II (30) received to basic therapy.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Results: After the treatment in patients of the group I general weakness decreased, body temperature normalized, improved saturation indicators, the level of acute-phase parameters (interleukin-6, CRP and ferritin) significantly decreased, a positive effect of quercetin on the level of D-dimer in blood serum was noted, indices of pericapillary edema and hemosiderin deposition significantly decreased, indices diameter of the arterial part of the capillary and capillary network density significantly increased.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Conclusions: The use of quercetin against the background of basic therapy in patients with COVID-19 and concomitant T2DM reliably reduces the level of acute-phase indices, has an important clinical significance for reducing endothelial dysfunction and for preventing thrombotic complications.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tylishchak</LastName><ForeName>Zoriana</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pryshliak</LastName><ForeName>Oleksandra</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boichuk</LastName><ForeName>Oleksandr</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fedorov</LastName><ForeName>Sergiy</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Protsyk</LastName><ForeName>Andrii</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kobryn</LastName><ForeName>Taras</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miziuk</LastName><ForeName>Ruslan</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Poland</Country><MedlineTA>Wiad Lek</MedlineTA><NlmUniqueID>9705467</NlmUniqueID><ISSNLinking>0043-5147</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9IKM0I5T1E</RegistryNumber><NameOfSubstance UI="D011794">Quercetin</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-41-4</RegistryNumber><NameOfSubstance UI="D002097">C-Reactive Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-73-2</RegistryNumber><NameOfSubstance UI="D005293">Ferritins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011794" MajorTopicYN="Y">Quercetin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000093485" MajorTopicYN="N">COVID-19 Drug Treatment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002097" MajorTopicYN="N">C-Reactive Protein</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005293" MajorTopicYN="N">Ferritins</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">respiratory insufficiency</Keyword><Keyword MajorTopicYN="N">D-dimer</Keyword><Keyword MajorTopicYN="N">capillaroscopy</Keyword><Keyword MajorTopicYN="N">endothelin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>18</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>18</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>15</Hour><Minute>53</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39661889</ArticleId><ArticleId IdType="doi">10.36740/WLek/191875</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39661800</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>11</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1678-4170</ISSN><JournalIssue CitedMedium="Internet"><Volume>121</Volume><Issue>11</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Arquivos brasileiros de cardiologia</Title><ISOAbbreviation>Arq Bras Cardiol</ISOAbbreviation></Journal><ArticleTitle>Cluster of Physical Inactivity and Other Risk Factors and Diabesity in Quilombol Adults.</ArticleTitle><Pagination><StartPage>e20230715</StartPage><MedlinePgn>e20230715</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e20230715</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.36660/abc.20230715</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0066-782X2024001100309</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Diabesity is a condition characterized by the coexistence of type 02 diabetes and obesity. The causes are multifactorial, resulting from a complex interaction of genetic and behavioral factors. Among the behavioral factors, there are physical inactivity, inadequate eating habits and excessive consumption of alcohol and tobacco.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To investigate the clustering of physical inactivity and other risk factors and the association between risk factor combinations and the presence of diabesity in quilombola adults.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Cross-sectional study involving a sample of 332 middle-aged and older adults (≥ 50 years) selected among participants in the "Epidemiological Profile of Quilombolas in Bahia" study. Data were collected by interview and anthropometric assessment. Descriptive statistics, cluster analysis, and multinomial logistic regression procedures were used for data analysis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The highest prevalence of clustering was identified for the combinations of regular alcohol consumption in the absence of the other factors (O/E=14.2; 95%CI 0.87-1.15), followed by regular alcohol and tobacco consumption (O/E=10.3; 95%CI 0.64-0.95) and regular consumption of alcohol, tobacco and foods high in sugar and fat (O/E=6.8; 95%CI= 1.31-1.75). Unadjusted analysis revealed an association between physical inactivity in the absence of the other factors (OR=0.82; 95%CI 0.78-0.86) and diabesity.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Alcohol consumption was the most prevalent factor among the largest combinations evaluated. Furthermore, the presence of physical inactivity without the other behaviors analyzed and the absence of all behaviors were associated with diabesity only in unadjusted analysis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Santana</LastName><ForeName>Poliana Pereira</ForeName><Initials>PP</Initials><Identifier Source="ORCID">0000-0003-1086-4593</Identifier><AffiliationInfo><Affiliation>Universidade Estadual do Sudoeste da Bahia, Programa de Pós-Graduação em Educação Física UESB/UESC, Jequié, BA - Brasil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dos Santos</LastName><ForeName>Clarice Alves</ForeName><Initials>CA</Initials><Identifier Source="ORCID">0000-0002-2730-5117</Identifier><AffiliationInfo><Affiliation>Universidade Estadual do Sudoeste da Bahia, Programa de Pós-Graduação em Educação Física UESB/UESC, Jequié, BA - Brasil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Universidade Estadual do Sudoeste da Bahia, Departamento de Ciências Biológicas, Jequié, BA - Brasil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mussi</LastName><ForeName>Ricardo Franklin de Freitas</ForeName><Initials>RFF</Initials><Identifier Source="ORCID">0000-0003-1515-9121</Identifier><AffiliationInfo><Affiliation>Universidade do Estado da Bahia, Programa de Pós-Graduação em Ensino, Linguagem e Sociedade, Caitité, BA - Brasil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Munaro</LastName><ForeName>Hector Luiz Rodrigues</ForeName><Initials>HLR</Initials><Identifier Source="ORCID">0000-0002-6421-1718</Identifier><AffiliationInfo><Affiliation>Universidade Estadual do Sudoeste da Bahia, Programa de Pós-Graduação em Educação Física UESB/UESC, Jequié, BA - Brasil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Universidade Estadual do Sudoeste da Bahia, Departamento de Saúde, Jequié, BA - Brasil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rocha</LastName><ForeName>Saulo Vasconcelos</ForeName><Initials>SV</Initials><Identifier Source="ORCID">0000-0001-8655-5151</Identifier><AffiliationInfo><Affiliation>Universidade Estadual do Sudoeste da Bahia, Programa de Pós-Graduação em Educação Física UESB/UESC, Jequié, BA - Brasil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Universidade Estadual do Sudoeste da Bahia, Departamento de Saúde II, Jequié, BA - Brasil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Universidade Estadual de Feira de Santana, Programa de Pós-Graduação em Saúde Coletiva, Feira de Santana, BA - Brasil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>por</Language><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Cluster de Inatividade Física e Outros Fatores de Risco na Diabesidade em Adultos Quilombolas.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Brazil</Country><MedlineTA>Arq Bras Cardiol</MedlineTA><NlmUniqueID>0421031</NlmUniqueID><ISSNLinking>0066-782X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057185" MajorTopicYN="Y">Sedentary Behavior</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016000" MajorTopicYN="N">Cluster Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001938" MajorTopicYN="N" Type="Geographic">Brazil</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000428" MajorTopicYN="Y">Alcohol Drinking</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012959" MajorTopicYN="N">Socioeconomic Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012907" MajorTopicYN="N">Smoking</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005247" MajorTopicYN="N">Feeding Behavior</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064424" MajorTopicYN="N">Tobacco Use</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015995" MajorTopicYN="N">Prevalence</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="por"><AbstractText Label="FUNDAMENTO" NlmCategory="OBJECTIVE">A diabesidade é uma condição caracterizada pela coexistência de diabetes tipo 02 e obesidade. As causas são multifatoriais, resultantes de uma complexa interação de fatores genéticos e comportamentais. Entre os fatores comportamentais, destacam-se a inatividade física, os hábitos alimentares inadequados e o consumo excessivo de álcool e tabaco.</AbstractText><AbstractText Label="OBJETIVO" NlmCategory="OBJECTIVE">Investigar o agrupamento (clustering) da inatividade física e outros fatores de risco e a associação entre as combinações de fatores de risco e a presença de diabesidade em adultos quilombolas.</AbstractText><AbstractText Label="MÉTODOS" NlmCategory="UNASSIGNED">Trata-se de estudo transversal com amostra composta por 332 adultos de meia idade e idosos (idade ≥ 50 anos), selecionados entre os participantes do estudo "Perfil epidemiológico dos quilombolas baianos". Os dados foram obtidos por meio de entrevistas e avaliação antropométrica. Para a análise dos dados, foram utilizadas estatísticas descritivas, análise de cluster e procedimentos de regressão logística multinominal.</AbstractText><AbstractText Label="RESULTADO" NlmCategory="RESULTS">A maior prevalência de agrupamento foi identificada para as combinações de consumo regular de álcool sem a presença dos demais fatores (O/E=14,2; IC95%= 0,87-1,15), seguido de consumo regular de álcool e tabaco (O/E=10,3; IC95%= 0,64-0,95) e consumo regular de álcool, tabaco e alimentos ricos em açúcar e gorduras (O/E=6,8; IC95%= 1,31-1,75). Na análise bruta, foram observadas associações entre inatividade física sem a presença dos demais fatores (OR= 0,82 IC95%= 0,78-0,86) e diabesidade.</AbstractText><AbstractText Label="CONCLUSÃO" NlmCategory="UNASSIGNED">O consumo de álcool foi o fator mais prevalente nas maiores combinações avaliadas. Além disso, inatividade física, sem os outros comportamentos analisados, e a ausência de todos os comportamentos associaram-se à diabesidade apenas na análise bruta.</AbstractText></OtherAbstract><OtherAbstract Type="Publisher" Language="eng"><AbstractText Label="BACKGROUND:">Diabesity is a condition characterized by the coexistence of type 02 diabetes and obesity. The causes are multifactorial, resulting from a complex interaction of genetic and behavioral factors. Among the behavioral factors, there are physical inactivity, inadequate eating habits and excessive consumption of alcohol and tobacco.</AbstractText><AbstractText Label="OBJECTIVE:">To investigate the clustering of physical inactivity and other risk factors and the association between risk factor combinations and the presence of diabesity in quilombola adults.</AbstractText><AbstractText Label="METHODS:">Cross-sectional study involving a sample of 332 middle-aged and older adults (≥ 50 years) selected among participants in the "Epidemiological Profile of Quilombolas in Bahia" study. Data were collected by interview and anthropometric assessment. Descriptive statistics, cluster analysis, and multinomial logistic regression procedures were used for data analysis.</AbstractText><AbstractText Label="RESULTS:">The highest prevalence of clustering was identified for the combinations of regular alcohol consumption in the absence of the other factors (O/E=14.2; 95%CI 0.87-1.15), followed by regular alcohol and tobacco consumption (O/E=10.3; 95%CI 0.64-0.95) and regular consumption of alcohol, tobacco and foods high in sugar and fat (O/E=6.8; 95%CI= 1.31-1.75). Unadjusted analysis revealed an association between physical inactivity in the absence of the other factors (OR=0.82; 95%CI 0.78-0.86) and diabesity.</AbstractText><AbstractText Label="CONCLUSION:">Alcohol consumption was the most prevalent factor among the largest combinations evaluated. Furthermore, the presence of physical inactivity without the other behaviors analyzed and the absence of all behaviors were associated with diabesity only in unadjusted analysis.</AbstractText></OtherAbstract><CoiStatement><b>Potencial conflito de interesse:</b> Não há conflito com o presente artigo</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>11</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>8</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>18</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>18</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>15</Hour><Minute>43</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>11</Month><Day>13</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39661800</ArticleId><ArticleId IdType="pmc">PMC11634302</ArticleId><ArticleId IdType="doi">10.36660/abc.20230715</ArticleId><ArticleId IdType="pii">S0066-782X2024001100309</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Guarisco G, Leonetti F. 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Although hypertrophic cardiomyopathy (HCM) and DM rarely co-occur, particularly in older individuals, the impact of DM on cardiac function and outcomes in individuals with HCM remains insufficiently understood.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A total of 421 HCM patients were included and followed up in a prospective cohort study (mean 68.7 months). In the diabetic HCM group (n = 47), patients had a mean age of 47 ± 17 years, and 31 (66%) were male, while the non-diabetic HCM group (n = 374) had a mean age of 44 ± 14 years, and 246 (65%) were male. At study entry, all patients underwent echocardiographic evaluation, encompassing left ventricular (LV) regional and global longitudinal strain (GLS), as well as strain rate (SR) analysis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">In diabetic HCM, there was a greater prevalence of hypertension (p < 0.0001), while the ratio of septal to posterior wall thickness (PWT) (p < 0.003) and E' value were lower (p < 0.009) compared to non-diabetic HCM. No significant difference between groups in NYHA class or cardiac phenotype. Diabetic HCM exhibited notable reductions in GLS (p < 0.02), systolic SR (SRsys) (p < 0.04), and early diastolic SR (SRe) p < 0.006. Additionally, there was a significant inverse correlation between LVGLS and HbA1c levels (r = -0.58, p < 0.0001), and the duration of diabetes (r = -0.39, p < 0.006). Hospitalization rates were greater in the diabetic HCM than in the non-diabetic group (44.7% vs.19.5%, p < 0.001). Among all demographic characteristics, phenotypic data, conventional echocardiographic measurements, and LV mechanics, diabetes emerged as the sole determinant of hospitalization among HCM patients. The presence of diabetes nearly tripled the odds of hospitalization (odds ratio: 2.813 [1.448-5.465], p < 0.002). However, diabetes did not negatively affect long-term survival, and age remained the only independent predictor of all-cause mortality.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In HCM, T2DM is linked to more deterioration of cardiac mechanics and contributes to unfavorable consequences by frequent hospitalization on its own, independent of age, comorbidities, or phenotype.</AbstractText><CopyrightInformation>© 2024 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Badran</LastName><ForeName>Hala Mahfouz</ForeName><Initials>HM</Initials><Identifier Source="ORCID">0000-0001-5231-750X</Identifier><AffiliationInfo><Affiliation>Cardiology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Helmy</LastName><ForeName>John Anis</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Cardiology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>Nagalaa Fahem</ForeName><Initials>NF</Initials><AffiliationInfo><Affiliation>Cardiology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yacoub</LastName><ForeName>Magdi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiovascular surgery, Faculty of Medicine, Imperial College, London, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Echocardiography</MedlineTA><NlmUniqueID>8511187</NlmUniqueID><ISSNLinking>0742-2822</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002312" MajorTopicYN="Y">Cardiomyopathy, Hypertrophic</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="Y">Echocardiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018487" MajorTopicYN="N">Ventricular Dysfunction, Left</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">diabetes mellitus</Keyword><Keyword MajorTopicYN="N">hypertrophic cardiomyopathy</Keyword><Keyword MajorTopicYN="N">left ventricular mechanics</Keyword><Keyword MajorTopicYN="N">vector velocity imaging</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>10</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>12</Hour><Minute>36</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>12</Hour><Minute>35</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>10</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39661017</ArticleId><ArticleId IdType="doi">10.1111/echo.70048</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>B. 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Physical training is recommended as a treatment for type 2 diabetes mellitus (T2DM); however, its effects on the concentrations of these hormones/enzymes are not well known. Thus, the present study aimed to evaluate the effects of combined training (CT) on the concentrations of hormones/enzymes with insulinotropic actions in individuals with T2DM and overweight. Individuals of both sexes with T2DM (age 51.73 ± 4.19 years; body mass index [BMI] 29.46 ± 3.39 kg/m<sup>2</sup>) were randomly distributed in the control group (CG, n = 17) and the combined training group (CTG, n = 17). The CT consisted of strength followed by erobic training, 3 times/week, for 16 weeks. Functional variables, body composition, and serum biochemical analyses (clinical markers, GLP-1, GIP, DPP-4, amylin/IAPP, and IDE) were evaluated. The CTG showed a decrease in GLP-1 (pre: 32.8 ± 12.1, post: 28.4 ± 13.5, and p = 0.04) in the group/time analysis. In the evaluation of the Δ% of variation, CTG presented a decrease for GLP-1 (-9.3%; p = 0.03) and amylin/IAPP (-13.4%; p < 0.01), in addition to an increase for DPP-4 (6.2%; p = 0.04) enzyme. CT decreases the baseline levels of important hormones with insulinotropic actions in individuals with T2DM and overweight. The improvement in overall metabolism provided by CT must be the main reason for these effects. These results broaden the understanding of the effects and relationships between CT and glucose metabolism.</AbstractText><CopyrightInformation>© 2024 The Authors. European Journal of Sport Science published by Wiley‐VCH GmbH on behalf of European College of Sport Science.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bonfante</LastName><ForeName>Ivan Luiz Padilha</ForeName><Initials>ILP</Initials><Identifier Source="ORCID">0000-0001-6278-4611</Identifier><AffiliationInfo><Affiliation>Laboratory of Exercise Physiology, Faculty of Physical Education, University of Campinas, Campinas, Brazil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Federal Institute of Education, Science and Technology of São Paulo, Hortolândia Campus, Hortolândia, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duft</LastName><ForeName>Renata Garbellini</ForeName><Initials>RG</Initials><AffiliationInfo><Affiliation>Laboratory of Exercise Physiology, Faculty of Physical Education, University of Campinas, Campinas, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mateus</LastName><ForeName>Keryma Chaves da Silva</ForeName><Initials>KCDS</Initials><AffiliationInfo><Affiliation>Laboratory of Exercise Physiology, Faculty of Physical Education, University of Campinas, Campinas, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Trombeta</LastName><ForeName>Joice Cristina Dos Santos</ForeName><Initials>JCDS</Initials><AffiliationInfo><Affiliation>Laboratory of Exercise Physiology, Faculty of Physical Education, University of Campinas, Campinas, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chacon-Mikahil</LastName><ForeName>Mara Patricia Traina</ForeName><Initials>MPT</Initials><AffiliationInfo><Affiliation>Laboratory of Exercise Physiology, Faculty of Physical Education, University of Campinas, Campinas, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Velloso</LastName><ForeName>Licio Augusto</ForeName><Initials>LA</Initials><AffiliationInfo><Affiliation>Laboratory of Cell Signaling, Department of Internal Medicine, University of Campinas, Campinas, São Paulo, Brazil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Obesity and Comorbidities Research Center, University of Campinas, Campinas, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cavaglieri</LastName><ForeName>Cláudia Regina</ForeName><Initials>CR</Initials><AffiliationInfo><Affiliation>Laboratory of Exercise Physiology, Faculty of Physical Education, University of Campinas, Campinas, Brazil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>001</GrantID><Agency>Coordination for the Improvement of Higher Education Personnel</Agency><Country/></Grant><Grant><GrantID>2016/08751-3</GrantID><Agency>São Paulo Research Foundation</Agency><Country/></Grant><Grant><GrantID>303571/2018-7</GrantID><Agency>National Council for Scientific and Technological Development</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Eur J Sport Sci</MedlineTA><NlmUniqueID>101146739</NlmUniqueID><ISSNLinking>1536-7290</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>89750-14-1</RegistryNumber><NameOfSubstance UI="D052216">Glucagon-Like Peptide 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>59392-49-3</RegistryNumber><NameOfSubstance UI="D005749">Gastric Inhibitory Polypeptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058228">Islet Amyloid Polypeptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054795">Incretins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050177" MajorTopicYN="Y">Overweight</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052216" MajorTopicYN="N">Glucagon-Like Peptide 1</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005749" MajorTopicYN="N">Gastric Inhibitory Polypeptide</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055070" MajorTopicYN="N">Resistance Training</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058228" MajorTopicYN="N">Islet Amyloid Polypeptide</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054795" MajorTopicYN="N">Incretins</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015992" MajorTopicYN="N">Body Mass Index</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">amylin/islet amyloid polypeptide (IAPP)</Keyword><Keyword MajorTopicYN="N">combined training</Keyword><Keyword MajorTopicYN="N">dipeptidyl peptidase‐4 (DPP‐4)</Keyword><Keyword MajorTopicYN="N">glucagon‐like peptide‐1 (GLP‐1)</Keyword><Keyword MajorTopicYN="N">glucose‐dependent insulinotropic polypeptide (GIP)</Keyword><Keyword MajorTopicYN="N">insulin‐degrading enzyme (IDE)</Keyword></KeywordList><CoiStatement>The authors declare no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2023</Year><Month>10</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>4</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2023</Year><Month>11</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>12</Hour><Minute>36</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>12</Hour><Minute>35</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>10</Hour><Minute>3</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>1</Month><Day>30</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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Our aim is to study the correlation between serum glycated hemoglobin level (HbA1c) and the hearing thresholds in diabetic patients.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">A case-control study was conducted in the Audio-Vestibular Medicine Unit, xxxx University on 82 subjects. The subjects were divided into 2 groups: the first group consisted of 42 diabetic patients and the second group consisted of 40 healthy subjects. All the participants underwent a pure tone audiogram and speech audiometric evaluation. All participants also underwent diabetes laboratory assessments, including fasting blood glucose serum level and serum HbA1c level. The average hearing threshold at frequencies from 250 Hz to 16 000 Hz in both groups was calculated and correlated to different variables.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Diabetic patients showed higher hearing thresholds than those of the control group, with an increasing tendency of elevation of the hearing threshold levels toward the higher frequencies in both groups. There was no statistically significant difference in the hearing thresholds between patients with diabetes < 5 years (20 subjects) and those with a duration of ≤ 5 years (22 subjects). Also, there was no statistically significant difference in the average hearing thresholds among type 2 diabetic patients based on fasting blood sugar level results, except at 16 000 Hz.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Poor glycemic control status [Hb A1c ≥ 7%] is significantly associated with elevated hearing thresholds.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>ElSherif</LastName><ForeName>Mayada</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology, Audiovestibular Medicine Unit, Alexandria University Faculty of Medicine, Alexandria, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fathey El Sayed Mahfouz</LastName><ForeName>Aya</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology, Audiovestibular Medicine Unit, Alexandria University Faculty of Medicine, Alexandria, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohamed Gaber Amin</LastName><ForeName>Noha</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Alexandria University Faculty of Medicine, Alexandria, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saad Kozou</LastName><ForeName>Hesham</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology, Audiovestibular Medicine Unit, Alexandria University Faculty of Medicine, Alexandria, Egypt.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Turkey</Country><MedlineTA>J Int Adv Otol</MedlineTA><NlmUniqueID>101522982</NlmUniqueID><ISSNLinking>1308-7649</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001301" MajorTopicYN="Y">Audiometry, Pure-Tone</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D034381" MajorTopicYN="N">Hearing Loss</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001309" MajorTopicYN="N">Auditory Threshold</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Hearing loss</Keyword><Keyword MajorTopicYN="N">glycated hemoglobin</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement><b>Declaration of Interests:</b> The authors have no conflicts of interest to declare.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate 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Internet J Otorhinolaryngol. 2003;3(1):1 10.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39660687</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>11</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1369-7625</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Health expectations : an international journal of public participation in health care and health policy</Title><ISOAbbreviation>Health Expect</ISOAbbreviation></Journal><ArticleTitle>Social Determinants as Mediators of the Emotional State of People With Type 2 Diabetes and/or Hypertension During the COVID-19 Pandemic in Ecuador and Spain.</ArticleTitle><Pagination><StartPage>e70123</StartPage><MedlinePgn>e70123</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e70123</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1111/hex.70123</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">We aimed to explore the impact of the COVID-19 pandemic and the resulting restrictions on the emotional state of people with type 2 diabetes mellitus (T2DM) and/or hypertension in Ecuador and Spain. Given the differences in sociopolitical and socioeconomic contexts between these two countries, the research focused on how these diverse environments and their management of social policies and pandemic strategies influenced the emotional well-being of individuals with chronic illnesses.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We conducted 36 semi-structured telephone interviews between August and December 2020 with adults diagnosed with T2DM and/or hypertension (19 in Ecuador, 17 in Spain). The interviews were recorded, anonymized and transcribed for thematic analysis. This approach allowed us to systematically identify and analyse themes related to the participants' emotional experiences during the pandemic.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The results revealed a significant deterioration in the emotional state of participants, attributable to the stress generated by the health crisis and concerns related to their chronic illnesses. The situation elicited a range of emotions among participants, from boredom and apathy to fear, uncertainty and depression. The study highlighted how the impact on emotional well-being was shaped by the interplay between conjunctural determinants (measures to control COVID-19 infections) and structural factors driving inequalities (social class, gender, ethnicity).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">We developed a conceptual framework illustrating how measures to control COVID-19 infections directly influenced economic, health and social determinants, which interacted with pre-existing inequalities and had a differential impact on individuals' emotional well-being. This framework can be useful for designing more effective and equitable social policies during future health crises, ensuring they address social needs and safeguard psychological and emotional well-being, particularly among vulnerable groups such as those with chronic illnesses.</AbstractText><AbstractText Label="PATIENT AND PUBLIC CONTRIBUTION" NlmCategory="UNASSIGNED">Thirty-six participants diagnosed with T2DM and/or hypertension (19 in Ecuador, 17 in Spain) contributed to the study by sharing their emotional experiences during the pandemic. Their detailed accounts enriched the research by providing valuable insights into how the pandemic affected their emotional well-being. There was no additional involvement or contribution from the public in the design, conduct, analysis or interpretation of the study, nor in the preparation of the manuscript.</AbstractText><CopyrightInformation>© 2024 The Author(s). Health Expectations published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sanchís-Ramón</LastName><ForeName>María José</ForeName><Initials>MJ</Initials><Identifier Source="ORCID">0000-0002-2046-4342</Identifier><AffiliationInfo><Affiliation>Departamento de Salud Pública, Universidad Miguel Hernández de Elche, Sant Joan d'Alacant, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chilet-Rosell</LastName><ForeName>Elisa</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Departamento de Salud Pública, Universidad Miguel Hernández de Elche, Sant Joan d'Alacant, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red, Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peralta</LastName><ForeName>Andrés</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Instituto de Salud Pública, Pontificia Universidad Católica del Ecuador, Quito, Ecuador.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Puig-García</LastName><ForeName>Marta</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Departamento de Salud Pública, Universidad Miguel Hernández de Elche, Sant Joan d'Alacant, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red, Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rivadeneira</LastName><ForeName>María Fernanda</ForeName><Initials>MF</Initials><AffiliationInfo><Affiliation>Instituto de Salud Pública, Pontificia Universidad Católica del Ecuador, Quito, Ecuador.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caicedo</LastName><ForeName>Cintia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Centro de Epidemiologia Comunitaria y Medicina Tropical (CECOMET), Esmeraldas, Ecuador.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Benazizi-Dahbi</LastName><ForeName>Ikram</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Departamento de Salud Pública, Universidad Miguel Hernández de Elche, Sant Joan d'Alacant, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lumbreras</LastName><ForeName>Blanca</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Departamento de Salud Pública, Universidad Miguel Hernández de Elche, Sant Joan d'Alacant, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red, Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nicols</LastName><ForeName>Montse</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Centro de Salud de Alzira, Valencia, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cebrián</LastName><ForeName>Ana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centro de Salud Cartagena Casco, Murcia, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ricart</LastName><ForeName>Wifredo</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Fundació Institut d'Investigaciò Biomèdica de Girona- IDIBGI, Girona, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red Obesidad y Nutrición (CIBEROBN), Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lopez-Miras</LastName><ForeName>Ester</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Unitat de Diabetis, Endocrinologia i Nutrició (UDENTG) Departament de Salut Generalitat de Catalunya.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parker</LastName><ForeName>Lucy A</ForeName><Initials>LA</Initials><AffiliationInfo><Affiliation>Departamento de Salud Pública, Universidad Miguel Hernández de Elche, Sant Joan d'Alacant, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red, Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>This work was supported by the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (Grant number 804761).</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Health Expect</MedlineTA><NlmUniqueID>9815926</NlmUniqueID><ISSNLinking>1369-6513</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004484" MajorTopicYN="N" Type="Geographic">Ecuador</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013030" MajorTopicYN="N" Type="Geographic">Spain</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064890" MajorTopicYN="Y">Social Determinants of Health</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="Y">Hypertension</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004644" MajorTopicYN="N">Emotions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007407" MajorTopicYN="N">Interviews as 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Given the strong genetic underpinnings of T2D, research has explored the connection between mitochondrial DNA haplogroups, specific variants, and the risk and comorbidities of T2D. For example, haplogroups F, D, M9, and N9a have been linked to an elevated risk of T2D across various populations. Additionally, specific mitochondrial DNA variants, such as the rare mtDNA 3243 A>G and the more prevalent mtDNA 16189 T>C, have also been implicated in heightened T2D risk. Notably, these associations vary among different populations. Given the high incidence of T2D in the Gulf Cooperation Council countries, this study investigates the correlation between T2D and mitochondrial haplogroups and variants in Arab populations from the Gulf region.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">This analysis involved mitochondrial haplogroup and variant testing in a cohort of 1,112 native Kuwaiti and Qatari individuals, comprising 685 T2D patients and 427 controls. Complete mitochondrial genomes were derived from whole exome sequencing data to examine the associations between T2D and haplogroups and mitochondrial DNA variants.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">The analysis revealed a significant protective effect of haplogroup H against T2D (odds ratio [OR] = 0.65; P = 0.022). This protective association persisted when adjusted for age, sex, body mass index (BMI) and population group, with an OR of 0.607 (P = 0.021). Furthermore, specific mitochondrial variants showed significant associations with T2D risk after adjustment for relevant covariates, and some variants were exclusively found in T2D patients.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Our findings confirm that the maternal haplogroup H, previously identified as protective against obesity in Kuwaiti Arabs, also serves as a protective factor against T2D in Arabs from the Gulf region. The study also identifies mitochondrial DNA variants that either increase or decrease the risk of T2D, underscoring their role in cellular energy metabolism.</AbstractText><CopyrightInformation>Copyright © 2024 Dashti, Ali, Alsaleh, John, Nizam, Thanaraj and Al-Mulla.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dashti</LastName><ForeName>Mohammed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Genetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait City, Kuwait.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ali</LastName><ForeName>Naser M</ForeName><Initials>NM</Initials><AffiliationInfo><Affiliation>Department of Medical Laboratories, Ahmadi Hospital, Kuwait Oil Company (KOC), Ahmadi, Kuwait.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alsaleh</LastName><ForeName>Hussain</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Saad Al-Abdullah Academy for Security Sciences, Ministry of Interior, Shuwaikh, Kuwait.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>John</LastName><ForeName>Sumi Elsa</ForeName><Initials>SE</Initials><AffiliationInfo><Affiliation>Genetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait City, Kuwait.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nizam</LastName><ForeName>Rasheeba</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Genetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait City, Kuwait.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thanaraj</LastName><ForeName>Thangavel Alphonse</ForeName><Initials>TA</Initials><AffiliationInfo><Affiliation>Genetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait City, Kuwait.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Mulla</LastName><ForeName>Fahd</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Genetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait City, Kuwait.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004272">DNA, Mitochondrial</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018912" MajorTopicYN="Y">Arabs</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006239" MajorTopicYN="Y">Haplotypes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004272" MajorTopicYN="Y">DNA, Mitochondrial</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011780" MajorTopicYN="N" Type="Geographic">Qatar</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007730" MajorTopicYN="N" Type="Geographic">Kuwait</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Arab</Keyword><Keyword MajorTopicYN="N">haplogroups</Keyword><Keyword MajorTopicYN="N">mitochondria</Keyword><Keyword MajorTopicYN="N">mtDNA variants</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>11</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate 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Glycemic control alone cannot effectively prevent or alleviate DCM. <b>Methods:</b> Herein, we concentrated on the variations in levels of metabolites between DCM and T2D patients without cardiomyopathy phenotype. In high-fat diet/low-dose streptozotocin-induced T2D and leptin receptor-deficient diabetic mouse models, we investigated the effect of altering branched-chain amino acids (BCAAs) levels on DCM. <b>Results:</b> We discovered that the levels of plasma BCAAs are notably lower in 15 DCM patients compared to 19 T2D patients who do not exhibit cardiomyopathy phenotype, using nuclear magnetic resonance analysis. This finding was further validated in two additional batches of samples, 123 DCM patients and 129 T2D patients based on the BCAA assay kit, and 30 DCM patients and 30 T2D patients based on the LC-MS/MS method, respectively. Moreover, it is verified that BCAA deficiency aggravated, whereas BCAA supplementation alleviated cardiomyopathy phenotypes in diabetic mice. Furthermore, BCAA deficiency promoted cardiac fibroblast activation by stimulating autophagy in DCM mice. Mechanistically, BCAA deficiency activated autophagy via the AMPK-ULK1 signaling pathway in cardiac fibroblasts. Using pharmacological approaches, we validated our findings that autophagy inhibition relieved, whereas autophagy activation aggravated, DCM phenotypes. <b>Conclusions:</b> Taken together, we describe a novel perspective wherein BCAA supplementation may serve as a potential therapeutic agent to mitigate DCM and fibrosis. Our findings provide insights for the development of preventive measures for DCM.</AbstractText><CopyrightInformation>© The author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Ze-Yu</ForeName><Initials>ZY</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Kai</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anesthesiology and Perioperative Medicine, Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Zhi-Yan</ForeName><Initials>ZY</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology and Perioperative Medicine, Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ke</LastName><ForeName>Yu-Fan</ForeName><Initials>YF</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cai</LastName><ForeName>Ke</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Rui</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tao</LastName><ForeName>Hui</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anesthesiology and Perioperative Medicine, Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Jian-Yuan</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Institute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>International Human Phenome Institutes (Shanghai), Shanghai 200433, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>10</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Australia</Country><MedlineTA>Theranostics</MedlineTA><NlmUniqueID>101552395</NlmUniqueID><ISSNLinking>1838-7640</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000597">Amino Acids, Branched-Chain</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000597" MajorTopicYN="Y">Amino Acids, Branched-Chain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058065" MajorTopicYN="Y">Diabetic Cardiomyopathies</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005347" MajorTopicYN="Y">Fibroblasts</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">Branched-chain amino acid</Keyword><Keyword MajorTopicYN="N">Cardiac fibroblasts</Keyword><Keyword MajorTopicYN="N">Cardiac fibrosis</Keyword><Keyword MajorTopicYN="N">Diabetic cardiomyopathy</Keyword></KeywordList><CoiStatement>Competing Interests: The authors have declared that no competing interest exists.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>11</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate 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Nature. 2016;531:523–7.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4854628</ArticleId><ArticleId IdType="pubmed">26982722</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39658979</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>11</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0030-9982</ISSN><JournalIssue CitedMedium="Internet"><Volume>74</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>JPMA. The Journal of the Pakistan Medical Association</Title><ISOAbbreviation>J Pak Med Assoc</ISOAbbreviation></Journal><ArticleTitle>Vitamin D status of patients visiting a private endocrinology clinic: a retrospective analysis from Karachi, Pakistan.</ArticleTitle><Pagination><StartPage>2107</StartPage><EndPage>2113</EndPage><MedlinePgn>2107-2113</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.47391/JPMA.11117</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To estimate the burden of vitamin D deficiency and its association with chronic diseases in patients visiting a private endocrinology clinic in an urban setting.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The retrospective study was conducted at the Medicell Institute of Diabetes Endocrinology & Metabolism, Karachi, and comprised medical records of adult patients of either gender between January 2000 and December 2019.Vitamin D status of the patients and its association with various chronic disorders were investigated. Data was analysed using SPSS 21.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Of the 2,854 patients with mean age 40.87±15.1 years, 2,302(80.7%) were females, and 552(19.3%) were males. There were 1055(37%) patients with vitamin D deficiency, 1,040(36.7%) with severe deficiency, 462(16.2%) with insufficiency, 295(10.3%) with normal status, and 2(0.1%) with vitamin D toxicity. Vitamin D deficiency was observed more frequently in those aged<40 years, and the deficiency was significantly related to type 2 diabetes, impaired glucose tolerance, dyslipidaemia and autoimmune disorders (p<0.05).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The burden of vitamin Deficiency was found to be alarmingly high at a private endocrine and medicine clinic serving a middle and upper socioeconomic class population in an urban setting.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ahsan</LastName><ForeName>Tasnim</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Medicell Institute of Diabetes, Endocrinology and Metabolism (MIDEM), OMI Hospital.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghaus</LastName><ForeName>Saima</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Medicell Institute of Diabetes, Endocrinology and Metabolism (MIDEM), Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sohail</LastName><ForeName>Erum</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Medicell Institute of Diabetes, Endocrinology and Metabolism (MIDEM), Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aijaz</LastName><ForeName>Wasfa</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Medicell Institute of Diabetes, Endocrinology and Metabolism (MIDEM), Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Erum</LastName><ForeName>Uzma</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Medicell Institute of Diabetes, Endocrinology and Metabolism (MIDEM), Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jaffri</LastName><ForeName>Samar Abbas</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>Medicell Institute of Diabetes, Endocrinology and Metabolism (MIDEM), Karachi, Pakistan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Pakistan</Country><MedlineTA>J Pak Med Assoc</MedlineTA><NlmUniqueID>7501162</NlmUniqueID><ISSNLinking>0030-9982</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>1406-16-2</RegistryNumber><NameOfSubstance UI="D014807">Vitamin D</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014808" MajorTopicYN="Y">Vitamin D Deficiency</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010154" MajorTopicYN="N" Type="Geographic">Pakistan</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050171" MajorTopicYN="N">Dyslipidemias</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014807" MajorTopicYN="N">Vitamin D</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001327" MajorTopicYN="N">Autoimmune Diseases</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018149" MajorTopicYN="N">Glucose Intolerance</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Vitamin D deficiency, Metabolic disorder, Diabetes mellitus, Hypertension.</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>1</Hour><Minute>33</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39658979</ArticleId><ArticleId IdType="doi">10.47391/JPMA.11117</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39658973</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>11</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0030-9982</ISSN><JournalIssue CitedMedium="Internet"><Volume>74</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>JPMA. The Journal of the Pakistan Medical Association</Title><ISOAbbreviation>J Pak Med Assoc</ISOAbbreviation></Journal><ArticleTitle>Comparison of ketoacidosis in type 1 and 2 diabetic patients with and without concurrent COVID-19 and determining the factors affecting their treatment and survival: a retrospective cohort study.</ArticleTitle><Pagination><StartPage>2072</StartPage><EndPage>2077</EndPage><MedlinePgn>2072-2077</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.47391/JPMA.9651</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="UNASSIGNED">To assess the incidence of diabetic ketoacidosis in coronavirus disease-2019 patients and their survival rate, and to compare their outcomes with diabetic ketoacidosis patients without coronavirus disease-2019.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The retrospective cohort study was conducted at Aga Khan University Hospital, Karachi, and comprised data March 1, 2020, to March 31, 2021, related to patients. who had diabetic ketoacidosis with coronavirus disease- 2019 in group A, and those who had diabetic ketoacidosis without coronavirus disease-2019 in group B. Data included age, gender, duration and type of diabetes and the final outcome. Data was analysed using SPSS 25.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Of the 120 patients, 40(33.3%) were in group A; 21(52.5%) males and 19(47.5%) females, with 22(55%) aged 45-64 years. There were 80(66.6%) patients in group B; 42(52.5%) males and 38(47.5%) females, with 36(45%) aged <45 years (p>0.05). The mortality was higher in group A patients13(32.5%) compared to those in group B 10(12.5%) (p<0.05). The data analysis was performed with the Statistical Package for Social Sciences (SPSS), V.25. Survival analysis showed that age, dyslipidaemia, history of cardiac revascularisation, acute respiratory distress syndrome, ventilator requirement, and severity of coronavirus disease-2019 were significantly associated with mortality (p<0.05).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Patients of diabetic ketoacidosis with coronavirus disease-2019 had poor survival outcomes compared to diabetic ketoacidosis patients without coronavirus disease-2019.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>Asma</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Badini</LastName><ForeName>Kaleemullah</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khalid</LastName><ForeName>Farah</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sohail</LastName><ForeName>Sahlah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Salik</LastName><ForeName>Muhammad</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Pakistan</Country><MedlineTA>J Pak Med Assoc</MedlineTA><NlmUniqueID>7501162</NlmUniqueID><ISSNLinking>0030-9982</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016883" MajorTopicYN="Y">Diabetic Ketoacidosis</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010154" MajorTopicYN="N" Type="Geographic">Pakistan</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="Y">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015996" MajorTopicYN="N">Survival Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes mellitus, Diabetic ketoacidosis, COVID-19, Mechanical ventilator, Acidosis.</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>1</Hour><Minute>33</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39658973</ArticleId><ArticleId IdType="doi">10.47391/JPMA.9651</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39658957</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0253-9772</ISSN><JournalIssue CitedMedium="Print"><Volume>46</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Yi chuan = Hereditas</Title><ISOAbbreviation>Yi Chuan</ISOAbbreviation></Journal><ArticleTitle>The mechanism and related research progress of GLP-1 receptor agonists in treating Alzheimer's disease.</ArticleTitle><Pagination><StartPage>1017</StartPage><EndPage>1027</EndPage><MedlinePgn>1017-1027</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.16288/j.yczz.24-178</ELocationID><Abstract><AbstractText>GLP-1 receptor agonists are primarily used clinically for the treatment of type 2 diabetes and have the potential for weight loss, while they are currently expanding their horizons in the treatment of hypertension, non-alcoholic liver disease, depression, and neurodegenerative diseases. In particular, in the treatment of Alzheimer's disease, a large number of animal models and a handful of clinical studies have demonstrated the potential efficacy of GLP-1 receptor agonists, making it highly probable that they will become a new entrant in the drug list for Alzheimer's disease. At present, the research on the mechanism of GLP-1 receptor agonist in the treatment of Alzheimer's disease is mainly based on in-depth analysis of the pathogenesis of Alzheimer's disease and exploration of the mechanism of its comorbidity with diabetes. This article mainly reviews the latest advances in the mechanism of GLP-1 receptor agonists in the treatment of Alzheimer's disease, introduces the latest achievements in animal studies and clinical studies, and aims to provide reference for the subsequent relevant basic research and clinical application.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Xiao-Cheng</ForeName><Initials>XC</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yi-Wen</ForeName><Initials>YW</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Hong-Wen</ForeName><Initials>HW</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Yi Chuan</MedlineTA><NlmUniqueID>9436478</NlmUniqueID><ISSNLinking>0253-9772</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="Y">Alzheimer Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><AbstractText>GLP-1受体激动剂在临床上主要用于2型糖尿病的降糖治疗，并具有潜在的减重作用，而目前也开始尝试应用于治疗高血压、非酒精性肝病、抑郁症及神经退行性疾病等病症。尤其在阿尔茨海默症的治疗方面，大量的动物模型及一些临床研究已经展现了GLP-1受体激动剂潜在的疗效，它有很大可能成为治疗阿尔茨海默症药物谱的新秀。目前关于GLP-1受体激动剂治疗阿尔茨海默症的机制的研究，主要基于深入剖析阿尔茨海默症的致病机理，以及探索其与糖尿病的共病机制等方面展开。本文主要综述了GLP-1受体激动剂在治疗阿尔茨海默症的机制方面的最新进展，并介绍了目前在动物研究及临床研究中的最新成果，以期为后续GLP-1受体激动剂治疗阿尔茨海默症的基础研究和临床应用提供参考。.</AbstractText></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alzheimer’s disease</Keyword><Keyword MajorTopicYN="N">GLP-1 receptor agonists</Keyword><Keyword MajorTopicYN="N">pharmacology</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>11</Day><Hour>1</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39658957</ArticleId><ArticleId IdType="doi">10.16288/j.yczz.24-178</ArticleId><ArticleId IdType="pii">24-178</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39656459</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2574-3805</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>02</Day></PubDate></JournalIssue><Title>JAMA network open</Title><ISOAbbreviation>JAMA Netw Open</ISOAbbreviation></Journal><ArticleTitle>Glycemic Control With Layperson-Delivered Telephone Calls vs Usual Care for Patients With Diabetes: A Randomized Clinical Trial.</ArticleTitle><Pagination><StartPage>e2448809</StartPage><MedlinePgn>e2448809</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e2448809</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1001/jamanetworkopen.2024.48809</ELocationID><Abstract><AbstractText Label="IMPORTANCE" NlmCategory="UNASSIGNED">Diabetes is associated with emotional distress and poor mental health, especially for individuals with low income, hindering patients' ability to manage their condition. The health care system's workforce constraints limit its capacity to holistically support patients.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">To assess the effectiveness of layperson-delivered empathetic engagement over the telephone in helping improve glycemic management for patients with diabetes.</AbstractText><AbstractText Label="DESIGN, SETTING, AND PARTICIPANTS" NlmCategory="UNASSIGNED">This parallel-arm randomized clinical trial with blinded outcome assessment was conducted from February 12, 2022, to April 15, 2023, with final measurements on November 18, 2023, among 260 patients with uncontrolled diabetes from a federally qualified health center in Austin, Texas, engaging telephonically from home.</AbstractText><AbstractText Label="INTERVENTION" NlmCategory="UNASSIGNED">Patients assigned to the intervention group received empathy-oriented telephone calls by community-hired laypeople for 6 months, while those assigned to the control group received usual care. Patients were stratified by baseline score (≥5 vs <5) on the depressive symptom scale of the 9-item Patient Health Questionnaire (PHQ-9).</AbstractText><AbstractText Label="MAIN OUTCOMES AND MEASURES" NlmCategory="UNASSIGNED">The primary outcome was hemoglobin A1c level at baseline, 3 months, and 6 months, assessed for interaction between time and trial arm. Secondary outcomes were self-perceptions of managing diabetes, diabetes-related behaviors and distress, and mental health symptoms (measured via surveys). Analysis was performed on an intention-to-treat basis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Of 260 participants (mean [SD] age, 49.5 [10.1] years; 163 of 259 women [62.9%]; 176 of 203 [86.7%] with annual income <$40 000) enrolled, 6 withdrew. At 6 months, 204 of 254 (80.3%; intervention, 109 of 127 [85.8%] and control, 95 of 127 [74.8%]) returned for measurements. Participants in the intervention group had statistically significant mean (SD) decreases in hemoglobin A1c level at 6 months (from 10.0% [1.9%] to 9.3% [2.0%]) compared with those in the control group (from 9.8% [1.6%] to 9.7% [2.3%]) (P = .004). The within-person change in hemoglobin A1c level was -0.7% (95% CI, -1.0% to -0.4%) for the intervention group and 0.02% (95% CI, -0.4% to 0.4%) for the control group. For the subgroup with a PHQ-9 score of 5 or more at baseline (38.1% [99 of 260]), the within-person change in hemoglobin A1c was -1.1% (95% CI, -1.8% to -0.5%) for the intervention group and 0.1% (95% CI, -0.7% to 0.8%; P = .004) for the control group. For the subgroup with a PHQ-9 score less than 5, the within-person change in hemoglobin A1c was -0.4% (95% CI, -0.8% to -0.1%) for the intervention group and -0.02% (95% CI, -0.5% to 0.5%; P = .21) for the control group. At 6 months, 91.7% of the participants (99 of 108) responded that the program was very or extremely beneficial.</AbstractText><AbstractText Label="CONCLUSIONS AND RELEVANCE" NlmCategory="UNASSIGNED">In this randomized clinical trial of telephone-based layperson-delivered empathetic engagement, patients with diabetes and low income achieved clinically meaningful improvements in glycemic control. With workforce constraints, layperson-delivered programs for diabetes show promise.</AbstractText><AbstractText Label="TRIAL REGISTRATION" NlmCategory="UNASSIGNED">ClinicalTrials.gov Identifier: NCT05173675.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kahlon</LastName><ForeName>Maninder K</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aksan</LastName><ForeName>Nazan S</ForeName><Initials>NS</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aubrey</LastName><ForeName>Rhonda</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Clark</LastName><ForeName>Nicole</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cowley-Morillo</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>DuBois</LastName><ForeName>Carolina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garcia</LastName><ForeName>Carlos</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guerra</LastName><ForeName>Julia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pereira</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sither</LastName><ForeName>Mathew</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tomlinson</LastName><ForeName>Steven</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Seminary of the Southwest, Austin, Texas.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valenzuela</LastName><ForeName>Sandy</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Population Health, Dell Medical School, The University of Texas at Austin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valdez</LastName><ForeName>M Renee</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Lone Star Circle of Care, Georgetown, Texas.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName><AccessionNumberList><AccessionNumber>NCT05173675</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>JAMA Netw Open</MedlineTA><NlmUniqueID>101729235</NlmUniqueID><ISSNLinking>2574-3805</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>doi: 10.1001/jamanetworkopen.2024.48740</RefSource></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013689" MajorTopicYN="Y">Telephone</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000085002" MajorTopicYN="Y">Glycemic Control</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013781" MajorTopicYN="N" Type="Geographic">Texas</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="N">Diabetes Mellitus</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement><b>Conflict of Interest Disclosures:</b> Dr Kahlon reported receiving grants from the Michael & Susan Dell Foundation and the United Health Foundation outside the submitted work; and being the founder (unpaid) of a Texas LLC, with an active Medicaid contract, to scale the model presented here. Ms Aubrey reported being a cofounder (unpaid) of a Texas LLC, with an active Medicaid contract, to scale the model presented here. Dr Tomlinson reported receiving personal fees from Sandoz, Johnson & Johnson, and 3M outside the submitted work. 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Hyperglycaemia-induced oxidative stress and endoplasmic reticulum (ER) stress enhances inflammatory disorders, leading to further pancreatic β cell dysfunction. These changes trigger autophagy activation, which recycles cytoplasmic components and injured organelles. Autophagy regulates pancreatic β cell functions by different mechanisms. Though the exact role of autophagy in T2DM is not completely elucidated, that could be beneficial or detrimental. Therefore, this review aims to discuss the exact role of autophagy in the pathogenesis of T2DM.</AbstractText><CopyrightInformation>© 2024 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alanazi</LastName><ForeName>Yousef Abud</ForeName><Initials>YA</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, College of Medicine, Majmaah University, Majmaah, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Kuraishy</LastName><ForeName>Haydar M</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Gareeb</LastName><ForeName>Ali I</ForeName><Initials>AI</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alexiou</LastName><ForeName>Athanasios</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-2206-7236</Identifier><AffiliationInfo><Affiliation>University Centre for Research & Development, Chandigarh University, Mohali, Punjab, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Research & Development, Funogen, Athens, Greece.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Papadakis</LastName><ForeName>Marios</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Wuppertal, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bahaa</LastName><ForeName>Mostafa M</ForeName><Initials>MM</Initials><Identifier Source="ORCID">0000-0003-3332-4573</Identifier><AffiliationInfo><Affiliation>Pharmacy Practice Department, Faculty of Pharmacy, Horus University, New Damietta, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Negm</LastName><ForeName>Walaa A</ForeName><Initials>WA</Initials><AffiliationInfo><Affiliation>Department of Pharmacognosy, Faculty of Pharmacy, Tanta University, Tanta, Egypt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>AlAnazi</LastName><ForeName>Faisal Holil</ForeName><Initials>FH</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, College of Medicine, Majmaah University, Majmaah, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alrouji</LastName><ForeName>Mohammed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Shaqra University, Shaqra, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Batiha</LastName><ForeName>Gaber El-Saber</ForeName><Initials>GE</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, AlBeheira, Egypt.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Universität Witten/Herdecke</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Cell Mol Med</MedlineTA><NlmUniqueID>101083777</NlmUniqueID><ISSNLinking>1582-1838</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050417" MajorTopicYN="Y">Insulin-Secreting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059865" MajorTopicYN="Y">Endoplasmic Reticulum Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="Y">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006943" MajorTopicYN="N">Hyperglycemia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">pancreatic β cell</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>The authors declare no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>12</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>12</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate 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A systematic search was performed in the PubMed, Embase, Scopus, and Web of Science databases. Meta-analysis of 31 studies with 2594 patients showed that urine albumin-to-creatinine ratio (UACR) was significantly reduced with a mean difference of - 28.19 mg/g (95% CI - 41.17, - 15.21, P-value < 0.001). In addition, subgroup analysis of studies showed a significant decrease after Roux-en-Y gastric bypass (RYGB) but not after sleeve gastrectomy (SG). These results suggest that MBS may lead to better kidney function and improvement in DN.</AbstractText><CopyrightInformation>© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Einafshar</LastName><ForeName>Negar</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Innovative Medical Research Center, Faculty of Medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Islamic Republic of Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Esparham</LastName><ForeName>Ali</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moghani</LastName><ForeName>Mahta Shari'at</ForeName><Initials>MS</Initials><AffiliationInfo><Affiliation>Innovative Medical Research Center, Faculty of Medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Islamic Republic of Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Radboy</LastName><ForeName>Mahsa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Innovative Medical Research Center, Faculty of Medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Islamic Republic of Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghamari</LastName><ForeName>Mohammad Javad</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Faculty of Medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Islamic Republic of Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zandbaf</LastName><ForeName>Tooraj</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Faculty of Medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Islamic Republic of Iran. tooraj.zandbaf@gmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D000078182">Systematic Review</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Obes Surg</MedlineTA><NlmUniqueID>9106714</NlmUniqueID><ISSNLinking>0960-8923</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>AYI8EX34EU</RegistryNumber><NameOfSubstance UI="D003404">Creatinine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003928" MajorTopicYN="Y">Diabetic Nephropathies</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050110" MajorTopicYN="Y">Bariatric Surgery</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009767" MajorTopicYN="N">Obesity, Morbid</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015390" MajorTopicYN="N">Gastric Bypass</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005743" MajorTopicYN="N">Gastrectomy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000419" MajorTopicYN="N">Albuminuria</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003404" MajorTopicYN="N">Creatinine</DescriptorName><QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Albuminuria</Keyword><Keyword MajorTopicYN="N">Diabetes mellitus</Keyword><Keyword MajorTopicYN="N">Metabolic and bariatric surgery</Keyword><Keyword MajorTopicYN="N">Nephropathy</Keyword><Keyword MajorTopicYN="N">Urinary albumin excretion</Keyword></KeywordList><CoiStatement>Declarations. 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This dual burden poses significant challenges for TB control efforts. However, there is a lack of reliable laboratory tools to identify individuals at higher risk, and the immunological mechanisms underlying this susceptibility are poorly understood. In this study, we utilized the mycobacterial growth inhibition assay (MGIA) to assess immune response capacity against <i>Mycobacterium tuberculosis</i> (<i>M.tb</i>) in TB infection (TBI) in individuals with type 2 DM (T2DM) (<i>n</i> = 11) compared to those without type 2 DM (NDM) (<i>n</i> = 23). Additionally, we measured various cytokines using multiplex ELISA to understand the immune profile. Our findings revealed that TBI-T2DM individuals exhibited a lower capacity to inhibit <i>M.tb</i> growth compared to TBI-NDM, as evidenced by MGIA results (<i>P</i> = 0.0029). Cytokine analysis further demonstrated diminished production of key cytokines involved in protection, including type 1 (IFNγ, TNFα, IL-2), type 17 (IL-17A), and proinflammatory (IL-1α, IL-1β, IL-6, IL-12p70) cytokines in the TBI-T2DM group compared to TBI-NDM, upon <i>M.tb</i> infection. These findings suggest that MGIA holds promise as an <i>in vitro</i> marker for assessing <i>M.tb</i> immunological control in TBI individuals, particularly those with T2DM. The observed cytokine profile in TBI-T2DM individuals indicates a compromised immune response against <i>M.tb</i> activation, potentially explaining the heightened risk of active TB in this population.</AbstractText><AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">This study is important because it sheds light on the impaired immune response in individuals with type 2 diabetes mellitus (T2DM) who are infected with Mycobacterium tuberculosis (M.tb), offering critical insights into why they are at higher risk of developing active tuberculosis (TB). By demonstrating that T2DM individuals exhibit a weakened ability to control M.tb growth and a compromised cytokine profile, the research underscores the need for better diagnostic tools, such as the mycobacterial growth inhibition assay (MGIA), to identify those at greater risk of progression to active TB. The findings also highlight the importance of integrated care strategies for managing both T2DM and TB, particularly in TB-endemic regions, and point to the need for further research to develop more effective interventions tailored to this vulnerable population.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dasan</LastName><ForeName>Bindu</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of ICER, National Institute of Health-National Institute of Allergy and Infectious Diseases-International Center for Excellence in Research, Chennai, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rajamanickam</LastName><ForeName>Anuradha</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-8143-5502</Identifier><AffiliationInfo><Affiliation>Department of ICER, National Institute of Health-National Institute of Allergy and Infectious Diseases-International Center for Excellence in Research, Chennai, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pandiarajan</LastName><ForeName>Arul Nancy</ForeName><Initials>AN</Initials><AffiliationInfo><Affiliation>Department of ICER, National Institute of Health-National Institute of Allergy and Infectious Diseases-International Center for Excellence in Research, Chennai, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shanmugam</LastName><ForeName>Sivakumar</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Bacteriology, ICMR-National Institute for Research in Tuberculosis, Chennai, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nott</LastName><ForeName>Sujatha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Infectious Diseases, Dignity Health, Chandler, Arizona, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Babu</LastName><ForeName>Subash</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-9783-8042</Identifier><AffiliationInfo><Affiliation>Department of ICER, National Institute of Health-National Institute of Allergy and Infectious Diseases-International Center for Excellence in Research, Chennai, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>HHS | NIH | NIAID | Division of Intramural Research (DIR, NIAID)</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Microbiol Spectr</MedlineTA><NlmUniqueID>101634614</NlmUniqueID><ISSNLinking>2165-0497</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="Y">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009169" MajorTopicYN="Y">Mycobacterium tuberculosis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014376" MajorTopicYN="Y">Tuberculosis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004198" MajorTopicYN="N">Disease Susceptibility</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">TB infection</Keyword><Keyword MajorTopicYN="N">cytokines</Keyword><Keyword MajorTopicYN="N">mycobacterial growth inhibition assay</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>9</Day><Hour>6</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>12</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>9</Hour><Minute>14</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>10</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39656000</ArticleId><ArticleId IdType="pmc">PMC11705871</ArticleId><ArticleId IdType="doi">10.1128/spectrum.01445-24</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>
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Antibiotics (Basel) 9:21. doi:10.3390/antibiotics9010021</Citation><ArticleIdList><ArticleId IdType="doi">10.3390/antibiotics9010021</ArticleId><ArticleId IdType="pmc">PMC7168302</ArticleId><ArticleId IdType="pubmed">31936156</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39655712</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1098-2299</ISSN><JournalIssue CitedMedium="Internet"><Volume>85</Volume><Issue>8</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Drug development research</Title><ISOAbbreviation>Drug Dev Res</ISOAbbreviation></Journal><ArticleTitle>Does Metabolic Manager Show Encouraging Outcomes in Alzheimer's?: Challenges and Opportunity for Protein Tyrosine Phosphatase 1b Inhibitors.</ArticleTitle><Pagination><StartPage>e70026</StartPage><MedlinePgn>e70026</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/ddr.70026</ELocationID><Abstract><AbstractText>Protein tyrosine phosphatase 1b (PTP1b) is a member of the protein tyrosine phosphatase (PTP) enzyme group and encoded as PTP1N gene. Studies have evidenced an overexpression of the PTP1b enzyme in metabolic syndrome, anxiety, schizophrenia, neurodegeneration, and neuroinflammation. PTP1b inhibitor negatively regulates insulin and leptin pathways and has been explored as an antidiabetic agent in various clinical trials. Notably, the preclinical studies have shown that recuperating metabolic dysfunction and dyshomeostasis can reverse cognition and could be a possible approach to mitigate multifaceted Alzheimer's disease (AD). PTP1b inhibitor thus has attracted attention in neuroscience, though the development is limited to the preclinical stage, and its exploration in large clinical trials is warranted. This review provides an insight on the development of PTP1b inhibitors from different sources in diabesity. The crosstalk between metabolic dysfunction and insulin insensitivity in AD and type-2 diabetes has also been highlighted. Furthermore, this review presents the significance of PTP1b inhibition in AD based on pathophysiological facets, and recent evidences from preclinical and clinical studies.</AbstractText><CopyrightInformation>© 2024 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Singh</LastName><ForeName>Ritu</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, Banasthali Vidyapith, Banasthali, Rajasthan, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jain</LastName><ForeName>Smita</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, Banasthali Vidyapith, Banasthali, Rajasthan, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paliwal</LastName><ForeName>Vartika</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, Banasthali Vidyapith, Banasthali, Rajasthan, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Verma</LastName><ForeName>Kanika</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Division of Cardiology, LSU Health Sciences Center Shreveport, Louisiana, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paliwal</LastName><ForeName>Sarvesh</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-5247-2021</Identifier><AffiliationInfo><Affiliation>Department of Pharmacy, Banasthali Vidyapith, Banasthali, Rajasthan, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Swapnil</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-2639-7096</Identifier><AffiliationInfo><Affiliation>Department of Pharmacy, Banasthali Vidyapith, Banasthali, Rajasthan, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Drug Dev Res</MedlineTA><NlmUniqueID>8204468</NlmUniqueID><ISSNLinking>0272-4391</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 3.1.3.48</RegistryNumber><NameOfSubstance UI="D054562">Protein Tyrosine Phosphatase, Non-Receptor Type 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.48</RegistryNumber><NameOfSubstance UI="C516607">PTPN1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="Y">Alzheimer Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054562" MajorTopicYN="Y">Protein Tyrosine Phosphatase, Non-Receptor Type 1</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004791" MajorTopicYN="Y">Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">metabolic syndrome</Keyword><Keyword MajorTopicYN="N">neurodegeneration</Keyword><Keyword MajorTopicYN="N">neuroinflammation</Keyword><Keyword MajorTopicYN="N">oxidative stress</Keyword><Keyword MajorTopicYN="N">protein tyrosine phosphatase 1b enzyme</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>10</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>5</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>12</Hour><Minute>28</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>12</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>7</Hour><Minute>4</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39655712</ArticleId><ArticleId 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Previous research has suggested a role for neuropeptides in regulating bone metabolism; however, the contribution of the neuropeptide Neurotensin (NT), which is thoroughly implicated in T2D and cardiovascular disease, has not been investigated in this context.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To study the relationship between circulating levels of the NT precursor proneurotensin (proNT) and bone mineralisation in T2D women.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">This is a cross-sectional investigation with a longitudinal prospective phase, involving 126 women with T2D who underwent bone density scans and had proNT levels measured. Biomarkers of bone metabolism and inflammation were also assessed. Data on bone mineral density (BMD) after 12 months were available for 49 patients.</AbstractText><AbstractText Label="MAIN OUTCOME MEASURE" NlmCategory="METHODS">Plasma proNT levels in relation to BMD.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">32% of the participants had osteopenia/osteoporosis and exhibited higher proNT than those with normal BMD (200.8 ± 113.7 vs. 161.6 ± 108.8 pg/mL; p = 0.013). ProNT inversely correlated with femur BMD and T-score (p < 0.01) and was associated with degraded bone architecture (TBS, p = 0.02), and higher OPN, P1NP, TNF-α and IL-1β levels. Baseline proNT correlated with further BMD reduction at the 12-month follow-up, independently of potential confounders (p = 0.02).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In women with T2D, greater proNT levels are associated with impaired bone mineralisation and predict mineral density decline overtime. ProNT could potentially serve as a diagnostic tool for identifying patients at higher risk of osteopenia/osteoporosis, suggesting a significant connection between this neuropeptide and bone metabolism in diabetes.</AbstractText><CopyrightInformation>© 2024 The Author(s). Diabetes/Metabolism Research and Reviews published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Barchetta</LastName><ForeName>Ilaria</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dule</LastName><ForeName>Sara</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-5089-6963</Identifier><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cimini</LastName><ForeName>Flavia Agata</ForeName><Initials>FA</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sentinelli</LastName><ForeName>Federica</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine, Public Health, Life and Environmental Sciences (MeSVA), University of L'Aquila, L'Aquila, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oldani</LastName><ForeName>Alessandro</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Passarella</LastName><ForeName>Giulia</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Filardi</LastName><ForeName>Tiziana</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Venditti</LastName><ForeName>Vittorio</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bleve</LastName><ForeName>Enrico</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Romagnoli</LastName><ForeName>Elisabetta</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morano</LastName><ForeName>Susanna</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lenzi</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Melander</LastName><ForeName>Olle</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Skåne University Hospital, Malmö, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baroni</LastName><ForeName>Marco Giorgio</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine, Public Health, Life and Environmental Sciences (MeSVA), University of L'Aquila, L'Aquila, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Neuroendocrinology and Metabolic Diseases, IRCCS Neuromed, Pozzilli, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cavallo</LastName><ForeName>Maria Gisella</ForeName><Initials>MG</Initials><Identifier Source="ORCID">0000-0001-6630-8049</Identifier><AffiliationInfo><Affiliation>Department of Experimental Medicine, Sapienza University, Rome, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Agenzia Italian Medicines Agency, Ministero della Salute</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Diabetes Metab Res Rev</MedlineTA><NlmUniqueID>100883450</NlmUniqueID><ISSNLinking>1520-7552</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>39379-15-2</RegistryNumber><NameOfSubstance UI="D009496">Neurotensin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C411471">proneurotensin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011498">Protein Precursors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015519" MajorTopicYN="Y">Bone Density</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="Y">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017698" MajorTopicYN="Y">Postmenopause</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009496" MajorTopicYN="Y">Neurotensin</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011498" MajorTopicYN="Y">Protein Precursors</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015663" MajorTopicYN="N">Osteoporosis, Postmenopausal</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001851" MajorTopicYN="N">Bone Diseases, Metabolic</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">bone fragility</Keyword><Keyword MajorTopicYN="N">bone metabolism</Keyword><Keyword MajorTopicYN="N">gut peptides</Keyword><Keyword MajorTopicYN="N">neuropeptides</Keyword><Keyword MajorTopicYN="N">neurotensin</Keyword><Keyword MajorTopicYN="N">osteoporosis</Keyword></KeywordList><CoiStatement>The authors declare no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>10</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>12</Hour><Minute>28</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>12</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>55</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>10</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39655684</ArticleId><ArticleId IdType="pmc">PMC11629440</ArticleId><ArticleId IdType="doi">10.1002/dmrr.70018</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>
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This study aimed to investigate the relationship between the advanced lung cancer inflammation index (ALI) and OP in patients with T2DM.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">This cross-sectional analysis was conducted based on data from middle-aged and older adults aged 50 years and older with T2DM from the National Health and Nutrition Examination Survey (NHANES).Weighted multivariable logistic regression and linear regression were utilized to investigate the correlation between the ALI and OP with femur bone mineral density (BMD) in individuals with T2DM. Restricted cubic splines (RCS) were employed to assess potential nonlinear relationships, and receiver operating characteristic (ROC) curves were used to evaluate diagnostic accuracy.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 1596 patients with T2DM were included in this study, among whom 736 had OP. After adjusting for covariates, the multivariable logistic regression model showed that compared to participants in the fourth quartile of log2-transformed ALI, those in the first quartile had an increased prevalence of OP in T2DM (OR = 1.95, 95% CI=1.28-2.96, p < 0.01). The multivariable linear regression model indicated that a low log2-transformed ALI is associated with a low femur BMD.RCS demonstrated a linear dose-response relationship between the ALI index and OP in T2DM (p = 0.686), with the area under the ROC curve being 0.57 (95% CI: 0.54-0.60, p < 0.001), and the optimal cutoff value was 6.04.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Our findings indicate that low levels of ALI are independently associated with an increased prevalence of OP in middle-aged and older adults with T2DM in the United States. ALI may serve as a potential biomarker for assessing the prevalence of OP in middle-aged and older adults with T2DM.</AbstractText><CopyrightInformation>Copyright © 2024 Xu, Yan and Liu.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Yifeng</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>School of Clinical Medicine, Jiangxi University of Chinese Medicine, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Zhaoqi</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Liangji</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang, Jiangxi, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010024" MajorTopicYN="Y">Osteoporosis</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009749" MajorTopicYN="Y">Nutrition Surveys</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="Y">Inflammation</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015519" MajorTopicYN="Y">Bone Density</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015995" MajorTopicYN="N">Prevalence</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">NHANES</Keyword><Keyword MajorTopicYN="N">advanced lung cancer inflammation index</Keyword><Keyword MajorTopicYN="N">cross-sectional study</Keyword><Keyword MajorTopicYN="N">osteoporosis</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>4</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>4</Hour><Minute>40</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>1</Month><Day>1</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39655346</ArticleId><ArticleId IdType="pmc">PMC11625538</ArticleId><ArticleId IdType="doi">10.3389/fendo.2024.1421696</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Reid IR, Billington EO. 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Initially, we performed linkage disequilibrium score regression (LDSC) to explore the genetic correlation between T2DM and iRBD. Then the two-sample univariate MR (UVMR) analysis was conducted to examine the effects of T2DM and blood sugar metabolism-related factors on iRBD. Subsequently, we applied multivariable MR (MVMR) methods to further adjust for confounders. Lastly, we executed a network MR analysis, with cytokines and immune cell characteristics as potential mediators, aiming to investigate indirect effect of T2DM on iRBD.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Results from LDSC suggest a genetic correlation between T2DM and iRBD (rg=0.306, P=0.029). UVMR analysis indicates that both T2DM (Odds Ratio [95% Confidence Interval] = 1.19 [1.03, 1.37], P = 0.017) and high blood glucose levels (1.55 [1.04, 2.30], P = 0.032) are risk factors for iRBD. Even after adjusting for confounders in MVMR, the association between T2DM and iRBD remains robust. Finally, results from network MR analysis suggest that T2DM may indirectly promote the development of iRBD by reducing levels of Stromal Cell-Derived Factor 2 in circulation and by increasing BAFF-receptor expression in IgD- CD38- B cells.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">T2DM may promote the onset of iRBD by influencing immune-inflammatory responses. Our findings provide valuable insights and directions for understanding the pathogenesis of iRBD, identifying high-risk groups, and discovering new therapeutic targets.</AbstractText><CopyrightInformation>Copyright © 2024 Zhang, Li, Liu, Zhang, Zhao and Li.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Ru-Yu</ForeName><Initials>RY</Initials><AffiliationInfo><Affiliation>Department of Pulmonary and Critical Care Medicine, First People's Hospital of Zigong, Zigong, Sichuan, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jin-Yu</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yu-Ning</ForeName><Initials>YN</Initials><AffiliationInfo><Affiliation>Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Zi-Xuan</ForeName><Initials>ZX</Initials><AffiliationInfo><Affiliation>Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Fu-Jia</ForeName><Initials>FJ</Initials><AffiliationInfo><Affiliation>Department of Pulmonary and Critical Care Medicine, First People's Hospital of Zigong, Zigong, Sichuan, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Neurology, The Eighth Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057182" MajorTopicYN="Y">Mendelian Randomization Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020187" MajorTopicYN="Y">REM Sleep Behavior Disorder</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055106" MajorTopicYN="Y">Genome-Wide Association Study</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015810" MajorTopicYN="N">Linkage Disequilibrium</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Mendelian randomization</Keyword><Keyword MajorTopicYN="N">causal association</Keyword><Keyword MajorTopicYN="N">genetic correlation</Keyword><Keyword MajorTopicYN="N">isolated REM sleep behavior disorder</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of 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Complications such as foot ulcers can have a significant impact on patient care and healthcare resources. It is imperative to identify patients at risk of developing diabetic foot complications and empower them with diabetes self-management education and support from specialised foot clinics is crucial. However, the availability of such programmes and services in SSA is limited.</AbstractText><AbstractText Label="INCLUSION CRITERIA" NlmCategory="UNASSIGNED">Studies of nurse-led diabetic foot prevention services and/or educational programmes in low- or middle-income countries in SSA for adults with T2DM, written in English, between August 2013 and March 2024 were considered.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">Following the standard Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines for conducting and reporting scoping reviews, searches were conducted on four electronic databases (CINAHL, ProQuest, MEDLINE, and Scopus) and Google Scholar. The titles and abstracts were scrutinised. All eligible papers were retrieved and screened for full text.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">The review included ten studies (across 14 papers), all of which focused on nurse-led diabetes self-management education (DSME) programmes in SSA. There are no specific educational programmes or services led by nurses that focus exclusively on diabetic foot prevention. The analysis highlighted the components of successful nurse-led DSMEs that led to positive glycaemic control and self-care behaviors, including the focus on behavior change and the DSME should be co-produced with service users. The theoretical aspects of the DSME include evidence-based, structured, interactive, culturally and linguistically appropriate group-based activities. The DSME should be delivered over a period of several weeks, and sessions should last between 1.5 and 2 h. Barriers to delivery and participation include the rainy season, stockouts, time and resources needed, and a DSME that meets diverse levels of literacy and education.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">There is a heightened need for nurse-led, co-produced, culturally congruent, frugal, and sustainable education interventions or programmes. There is also a need for diabetic foot screening and foot ulcer prevention services that can operate sustainably alongside these educational interventions through task-shifted, simple, and frugal initiatives.</AbstractText><CopyrightInformation>Copyright © 2024 Sajith, Ackers, Ackers-Johnson, Parker and Stephens.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sajith</LastName><ForeName>Rincy</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>School of Health and Society, University of Salford, Salford, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ackers</LastName><ForeName>Louise</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>School of Health and Society, University of Salford, Salford, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ackers-Johnson</LastName><ForeName>Simona</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Wear Rivers Trust, Durham, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parker</LastName><ForeName>Daniel J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>School of Health and Society, University of Salford, Salford, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stephens</LastName><ForeName>Melanie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Health and Society, University of Salford, Salford, United Kingdom.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Public Health</MedlineTA><NlmUniqueID>101616579</NlmUniqueID><ISSNLinking>2296-2565</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017719" MajorTopicYN="Y">Diabetic Foot</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000451" MajorTopicYN="N">nursing</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017954" MajorTopicYN="N" Type="Geographic">Africa South of the Sahara</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000451" MajorTopicYN="N">nursing</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010353" MajorTopicYN="N">Patient Education as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057184" MajorTopicYN="N">Practice Patterns, Nurses'</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">LMIC</Keyword><Keyword MajorTopicYN="N">Sub-Saharan Africa</Keyword><Keyword MajorTopicYN="N">chronic disease management</Keyword><Keyword MajorTopicYN="N">diabetes self-management education (DSME)</Keyword><Keyword MajorTopicYN="N">foot prevention</Keyword><Keyword MajorTopicYN="N">nurse-led</Keyword><Keyword MajorTopicYN="N">public health</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>11</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>11</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>4</Hour><Minute>38</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39655252</ArticleId><ArticleId IdType="pmc">PMC11625785</ArticleId><ArticleId IdType="doi">10.3389/fpubh.2024.1465750</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>World Health Organisation (2023) Non-Communicable Diseases. 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(2017) 24:1–8.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39654602</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1177-8881</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Drug design, development and therapy</Title><ISOAbbreviation>Drug Des Devel Ther</ISOAbbreviation></Journal><ArticleTitle>Effects of Oltipraz on the Glycolipid Metabolism and the Nrf2/HO-1 Pathway in Type 2 Diabetic Mice.</ArticleTitle><Pagination><StartPage>5685</StartPage><EndPage>5700</EndPage><MedlinePgn>5685-5700</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2147/DDDT.S485729</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="UNASSIGNED">Oltipraz has various applications, including for treating cancer, liver fibrosis, and cirrhosis. However, its role in regulating metabolic processes, inflammation, oxidative stress, and insulin resistance in STZ-induced T2DM remains unclear. Hence, a comprehensive understanding of how oltipraz ameliorates diabetes, particularly inflammation and oxidative stress, is imperative.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">The negative control (NC), T2DM model (T2DM), and T2DM models treated with oltipraz (OLTI) and metformin (MET) were constructed. The RNA sequencing (RNA-Seq) was performed on the pancreatic tissues. H&E staining was conducted on the liver and pancreatic tissues. The intraperitoneal glucose tolerance test (IPGTT), blood glucose and lipids, inflammatory factors, and oxidative stress indexes were measured. qPCR and Western blotting examined the nuclear factor erythroid-derived 2-like 2 (Nrf2)<i>/</i> hemoglobin-1 (HO-1) signaling pathway, cell apoptosis-related genes, and Reg3g levels. Immunofluorescence (IF) analysis of the pancreas was performed to measure insulin secretion.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 256 DEGs were identified in OLTI_vs_T2DM, and they were mainly enriched in circadian rhythm, cAMP, AMPK, insulin, and MAPK signaling pathways. Moreover, Reg3g exhibits reduced expression in T2DM_vs_NC, and elevated expression in OLTI_vs_T2DM, yet remains unchanged in MET_vs_T2DM. OLTI reduced fasting blood glucose and alleviated T2DM-induced weight loss. It improved blood glucose and insulin resistance, decreased blood lipid metabolism, reduced inflammation and oxidative stress through the Nrf2/HO-1 signaling pathway, mitigated pancreatic and liver tissue injury, and enhanced pancreatic β-cell insulin secretion. OLTI exhibited anti-apoptosis effects in T2DM. Moreover, OLTI exhibits superior antioxidant activity than metformin.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">In summary, OLTI improves blood glucose and insulin resistance, decreases blood lipid metabolism, reduces inflammation and apoptosis, suppresses oxidative stress through the Nrf2/HO-1 signaling pathway, mitigates pancreatic and liver tissue injury, and enhances pancreatic β-cell insulin secretion, thereby mitigating T2DM symptoms. Moreover, Reg3g could be an important target for OLTI treatment of T2DM.</AbstractText><CopyrightInformation>© 2024 Luo et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Luo</LastName><ForeName>Yunfei</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Sun</LastName><ForeName>Shaohua</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Metabolism and Endocrinology, XinSteel Center Hospital, Xinyu, Jiangxi, 338000, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Zhang</LastName><ForeName>Yuying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Shuang</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zeng</LastName><ForeName>Haixia</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jin-E</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Jiadian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Lixuan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Shiqi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Peng</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jianping</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism of the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute for the Study of Endocrinology and Metabolism in Jiangxi Province, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Branch of National Clinical Research Center for Metabolic Diseases, Nanchang, Jiangxi, 330031, People's Republic of China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>New Zealand</Country><MedlineTA>Drug Des Devel 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Med Sci Monit. 2019;25:3880–3886. doi:10.12659/msm.913820</Citation><ArticleIdList><ArticleId IdType="doi">10.12659/msm.913820</ArticleId><ArticleId IdType="pmc">PMC6556067</ArticleId><ArticleId IdType="pubmed">31127077</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39654201</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>12</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1536-5964</ISSN><JournalIssue CitedMedium="Internet"><Volume>103</Volume><Issue>49</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>06</Day></PubDate></JournalIssue><Title>Medicine</Title><ISOAbbreviation>Medicine (Baltimore)</ISOAbbreviation></Journal><ArticleTitle>Determinants of developing cardiovascular disease risk with emphasis on type-2 diabetes and predictive modeling utilizing machine learning algorithms.</ArticleTitle><Pagination><StartPage>e40813</StartPage><MedlinePgn>e40813</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e40813</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1097/MD.0000000000040813</ELocationID><Abstract><AbstractText>This research aims to enhance our comprehensive understanding of the influence of type-2 diabetes on the development of cardiovascular diseases (CVD) risk, its underlying determinants, and to construct precise predictive models capable of accurately assessing CVD risk within the context of Bangladesh. This study combined data from the 2011 and 2017 to 2018 Bangladesh Demographic and Health Surveys, focusing on individuals with hypertension. CVD development followed World Health Organization (WHO) guidelines. Eight machine learning algorithms (Support Vector Machine, Logistic Regression, Decision Tree, Random Forest, Naïve Bayes, K-Nearest Neighbor, Light GBM, and XGBoost) were analyzed and compared using 6 evaluation metrics to assess model performance. The study reveals that individuals aged 35 to 54 years, 55 to 69 years, and ≥ 70 years face higher CVD risk with adjusted odds ratios (AOR) of 2.140, 3.015, and 3.963, respectively, compared to those aged 18 to 34 years. "Rich" respondents show increased CVD risk (AOR = 1.370, P < .01) compared to "poor" individuals. Also, "normal weight" (AOR = 1.489, P < .01) and "overweight/obese" (AOR = 1.871, P < .01) individuals exhibit higher CVD risk than "underweight" individuals. The predictive models achieve impressive performance, with 75.21% accuracy and an 80.79% AUC, with Random Forest (RF) excelling in specificity at 76.96%. This research holds practical implications for targeted interventions based on identified significant factors, utilizing ML models for early detection and risk assessment, enhancing awareness and education, addressing urbanization-related lifestyle changes, improving healthcare infrastructure in rural areas, and implementing workplace interventions to mitigate stress and promote physical activity.</AbstractText><CopyrightInformation>Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Das</LastName><ForeName>Shatabdi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Science Engineering and Technology School, Khulna University, Khulna, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rahman</LastName><ForeName>Riaz</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Science Engineering and Technology School, Khulna University, Khulna, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Talukder</LastName><ForeName>Ashis</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-2205-0696</Identifier><AffiliationInfo><Affiliation>Science Engineering and Technology School, Khulna University, Khulna, Bangladesh.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Centre for Epidemiology and Population Health, Australian National University, Canberra, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Medicine (Baltimore)</MedlineTA><NlmUniqueID>2985248R</NlmUniqueID><ISSNLinking>0025-7974</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069550" MajorTopicYN="Y">Machine Learning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001459" MajorTopicYN="N" Type="Geographic">Bangladesh</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000465" MajorTopicYN="N">Algorithms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012959" MajorTopicYN="N">Socioeconomic Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="N">Hypertension</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors have no funding and conflict of interest to discloser.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>1</Hour><Minute>2</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>6</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39654201</ArticleId><ArticleId IdType="pmc">PMC11630972</ArticleId><ArticleId IdType="doi">10.1097/MD.0000000000040813</ArticleId><ArticleId IdType="pii">00005792-202412060-00044</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Jin Z, Oresko J, Huang S, Cheng AC. 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Identifying specific phenotypic profiles within MASLD is essential for developing targeted therapeutic strategies. Here we investigated the heterogeneity of MASLD using partitioning around medoids clustering based on six simple clinical variables in a cohort of 1,389 individuals living with obesity. The identified clusters were applied across three independent MASLD cohorts with liver biopsy (totaling 1,099 participants), and in the UK Biobank to assess the incidence of chronic liver disease, cardiovascular disease and type 2 diabetes. Results unveiled two distinct types of MASLD associated with steatohepatitis on histology and liver imaging. The first cluster, liver-specific, was genetically linked and showed rapid progression of chronic liver disease but limited risk of cardiovascular disease. The second cluster, cardiometabolic, was primarily associated with dysglycemia and high levels of triglycerides, leading to a similar incidence of chronic liver disease but a higher risk of cardiovascular disease and type 2 diabetes. Analyses of samples from 831 individuals with available liver transcriptomics and 1,322 with available plasma metabolomics highlighted that these two types of MASLD exhibited distinct liver transcriptomic profiles and plasma metabolomic signatures, respectively. In conclusion, these data provide preliminary evidence of the existence of two distinct types of clinically relevant MASLD with similar liver phenotypes at baseline, but each with specific underlying biological profiles and different clinical trajectories, suggesting the need for tailored therapeutic strategies.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Raverdy</LastName><ForeName>Violeta</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0001-5754-2028</Identifier><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Tavaglione</LastName><ForeName>Federica</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0002-1720-4355</Identifier><AffiliationInfo><Affiliation>Operative Unit of Clinical Medicine and Hepatology, Fondazione Policlinico Universitario Campus Bio-Medico, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Unit of Clinical Medicine and Hepatology, Department of Medicine and Surgery, Università Campus Bio-Medico di Roma, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Chatelain</LastName><ForeName>Estelle</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>US 41 - UAR 2014 - PLBS Bilille, University of Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, F-59000, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Lassailly</LastName><ForeName>Guillaume</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Hepato-Gastroenterology CHU Lille, University of Lille, Inserm INFINITE-U1286, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>De Vincentis</LastName><ForeName>Antonio</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Operative Unit of Internal Medicine, Fondazione Policlinico Universitario Campus Bio-Medico, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Unit of Internal Medicine, Department of Medicine and Surgery, Università Campus Bio-Medico di Roma, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vespasiani-Gentilucci</LastName><ForeName>Umberto</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Operative Unit of Clinical Medicine and Hepatology, Fondazione Policlinico Universitario Campus Bio-Medico, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Unit of Clinical Medicine and Hepatology, Department of Medicine and Surgery, Università Campus Bio-Medico di Roma, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qadri</LastName><ForeName>Sami F</ForeName><Initials>SF</Initials><Identifier Source="ORCID">0000-0001-9313-9324</Identifier><AffiliationInfo><Affiliation>Department of Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Minerva Foundation Institute for Medical Research, Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caiazzo</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Verkindt</LastName><ForeName>Helene</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saponaro</LastName><ForeName>Chiara</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kerr-Conte</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baud</LastName><ForeName>Gregory</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marciniak</LastName><ForeName>Camille</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chetboun</LastName><ForeName>Mikael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oukhouya-Daoud</LastName><ForeName>Naima</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blanck</LastName><ForeName>Samuel</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>ULR 2694 METRICS: Évaluation des technologies de santé et des pratiques médicales, University of Lille, CHU Lille, F-59000, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vandel</LastName><ForeName>Jimmy</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0003-0189-0220</Identifier><AffiliationInfo><Affiliation>US 41 - UAR 2014 - PLBS Bilille, University of Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, F-59000, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olsson</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0001-9730-1915</Identifier><AffiliationInfo><Affiliation>Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, 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ValidYN="Y"><LastName>Yki-Järvinen</LastName><ForeName>Hannele</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Minerva Foundation Institute for Medical Research, Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Francque</LastName><ForeName>Sven</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-7527-4714</Identifier><AffiliationInfo><Affiliation>Department of Gastroenterology Hepatology, Antwerp University Hospital, Edegem, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>InflaMed Centre of Excellence, Laboratory for Experimental Medicine and Paediatrics, Translational Sciences in Inflammation and Immunology, Faculty of Medicine and Health Sciences, University of Antwerp, Wilrijk, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Staels</LastName><ForeName>Bart</ForeName><Initials>B</Initials><Identifier Source="ORCID">0000-0002-3784-1503</Identifier><AffiliationInfo><Affiliation>Nuclear Receptors, Metabolic and Cardiovascular Diseases - U1011, University of Lille, Inserm, CHU Lille, Institut Pasteur Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Le Roux</LastName><ForeName>Carel W</ForeName><Initials>CW</Initials><Identifier Source="ORCID">0000-0001-5521-5445</Identifier><AffiliationInfo><Affiliation>Diabetes Complications Research Centre, University College Dublin, Dublin, Ireland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tremaroli</LastName><ForeName>Valentina</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0002-9150-4233</Identifier><AffiliationInfo><Affiliation>Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mathurin</LastName><ForeName>Philippe</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Hepato-Gastroenterology CHU Lille, University of Lille, Inserm INFINITE-U1286, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marot</LastName><ForeName>Guillemette</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>ULR 2694 METRICS: Évaluation des technologies de santé et des pratiques médicales, University of Lille, CHU Lille, F-59000, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>MODAL: Models for Data Analysis and Learning, Inria, F-59000, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Romeo</LastName><ForeName>Stefano</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0001-9168-4898</Identifier><AffiliationInfo><Affiliation>Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden. stefano.romeo@wlab.gu.se.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Clinical Nutrition Unit, Department of Medical and Surgical Sciences, University Magna Graecia, Catanzaro, Italy. stefano.romeo@wlab.gu.se.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden. stefano.romeo@wlab.gu.se.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine Huddinge (H7), Karolinska Institutet and University Hospital, Stockholm, Sweden. stefano.romeo@wlab.gu.se.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Gothenburg, Sweden. stefano.romeo@wlab.gu.se.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pattou</LastName><ForeName>François</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0001-8388-3766</Identifier><AffiliationInfo><Affiliation>Translational Research for Diabetes UMR 1190, University of Lille, Inserm, Institut Pasteur Lille, CHU Lille, Lille, France. francois.pattou@univ-lille.fr.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of General and Endocrine Surgery, Centre Hospitalier et Universitaire de Lille, Lille, France. francois.pattou@univ-lille.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NNF23OC0082114</GrantID><Agency>Novo Nordisk Fonden (Novo Nordisk Foundation)</Agency><Country/></Grant><Grant><GrantID>NNF20OC0063883</GrantID><Agency>Novo Nordisk Fonden (Novo Nordisk Foundation)</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Nat Med</MedlineTA><NlmUniqueID>9502015</NlmUniqueID><ISSNLinking>1078-8956</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016000" MajorTopicYN="N">Cluster Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="Y">Liver</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000378" 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Yet, the mechanisms are elusive. Here, we investigate alterations in the fibrous repair processes in type 2 diabetes atherosclerotic plaque extracellular matrix by combining multi-omics from the human Carotid Plaque Imaging Project cohort and functional studies. Plaques from type 2 diabetes patients have less collagen. Interestingly, lower levels of transforming growth factor-ß distinguish type 2 diabetes plaques and, in these patients, lower levels of fibrous repair markers are associated with cardiovascular events. Transforming growth factor-ß2 originates mostly from contractile vascular smooth muscle cells that interact with synthetic vascular smooth muscle cells in the cap, leading to collagen formation and vascular smooth muscle cell differentiation. This is regulated by free transforming growth factor-ß2 which is affected by hyperglycemia. Our findings underscore the importance of transforming growth factor-ß2-driven fibrous repair in type 2 diabetes as an area for future therapeutic strategies.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Singh</LastName><ForeName>Pratibha</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Sun</LastName><ForeName>Jiangming</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-6814-1297</Identifier><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cavalera</LastName><ForeName>Michele</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Sharify</LastName><ForeName>Dania</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matthes</LastName><ForeName>Frank</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0002-5115-8831</Identifier><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barghouth</LastName><ForeName>Mohammad</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tengryd</LastName><ForeName>Christoffer</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dunér</LastName><ForeName>Pontus</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Persson</LastName><ForeName>Ana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sundius</LastName><ForeName>Lena</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nitulescu</LastName><ForeName>Mihaela</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bengtsson</LastName><ForeName>Eva</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biomedical Science, Malmö University, Malmö, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Biofilms-Research Center for Biointerfaces, Malmö University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rattik</LastName><ForeName>Sara</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Engelbertsen</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Orho-Melander</LastName><ForeName>Marju</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-3578-2503</Identifier><AffiliationInfo><Affiliation>Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nilsson</LastName><ForeName>Jan</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-9752-7479</Identifier><AffiliationInfo><Affiliation>Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Monaco</LastName><ForeName>Claudia</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0003-1985-4914</Identifier><AffiliationInfo><Affiliation>Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goncalves</LastName><ForeName>Isabel</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology, University Hospital of Skåne, Lund/Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Edsfeldt</LastName><ForeName>Andreas</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-2691-9192</Identifier><AffiliationInfo><Affiliation>Cardiovascular Research-Translational Studies, Lund University, Malmö, Sweden. Andreas.edsfeldt@med.lu.se.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology, University Hospital of Skåne, Lund/Malmö, Sweden. Andreas.edsfeldt@med.lu.se.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Wallenberg Centre for Molecular Medicine, Lund University, Lund, Sweden. Andreas.edsfeldt@med.lu.se.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CG-22-0254-H-02</GrantID><Agency>Svenska Sällskapet för Medicinsk Forskning (Swedish Society for Medical Research)</Agency><Country/></Grant><Grant><GrantID>2019-01907</GrantID><Agency>Vetenskapsrådet (Swedish Research Council)</Agency><Country/></Grant><Grant><GrantID>SLS-961085</GrantID><Agency>Svenska Läkaresällskapet (Swedish Society of Medicine)</Agency><Country/></Grant><Grant><GrantID>20220044 and 20220284; 20200403</GrantID><Agency>Hjärt-Lungfonden (Swedish Heart-Lung Foundation)</Agency><Country/></Grant><Grant><GrantID>20210796</GrantID><Agency>Crafoordska Stiftelsen (Crafoord Foundation)</Agency><Country/></Grant><Grant><GrantID>J.S, S-993166</GrantID><Agency>STROKE-Riksförbundet (Swedish Stroke Association)</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nat Commun</MedlineTA><NlmUniqueID>101528555</NlmUniqueID><ISSNLinking>2041-1723</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053781">Transforming Growth Factor beta2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.24.24</RegistryNumber><NameOfSubstance UI="D020778">Matrix Metalloproteinase 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.24.24</RegistryNumber><NameOfSubstance UI="C522361">MMP2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-34-5</RegistryNumber><NameOfSubstance UI="D003094">Collagen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C509041">TGFB2 protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053781" MajorTopicYN="Y">Transforming Growth Factor beta2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020778" MajorTopicYN="Y">Matrix Metalloproteinase 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058226" MajorTopicYN="Y">Plaque, Atherosclerotic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009131" MajorTopicYN="Y">Muscle, Smooth, Vascular</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032389" MajorTopicYN="Y">Myocytes, Smooth Muscle</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050197" MajorTopicYN="Y">Atherosclerosis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003094" MajorTopicYN="N">Collagen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005109" MajorTopicYN="N">Extracellular Matrix</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell 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General subjects</Title><ISOAbbreviation>Biochim Biophys Acta Gen Subj</ISOAbbreviation></Journal><ArticleTitle>Computational profiling and pharmacokinetic modelling of Febuxostat: Evaluating its potential as a therapeutic agent for diabetic wound healing.</ArticleTitle><Pagination><StartPage>130735</StartPage><MedlinePgn>130735</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbagen.2024.130735</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0304-4165(24)00178-8</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Diabetic wounds, a significant complication of Type 2 Diabetes Mellitus (T2DM), face delayed healing due to impaired inflammation, angiogenesis, and collagen synthesis. This study explores Febuxostat, a xanthine oxidase inhibitor for its therapeutic potential in wound healing. Combining computational approaches and in-vitro assays, the study evaluates its effects on key wound healing pathways, cell viability, migration.</AbstractText><AbstractText Label="METHODOLOGY" NlmCategory="METHODS">The potential of Febuxostat in diabetic wound healing was studied using in-silico tools for Molecular docking and ADMET profiling, alongside Molecular dynamics (MD) simulations. Toxicity was assessed with OSIRIS Explorer, and biological activity was predicted using the PASS tool. In-vitro MTT and scratch assays on L929 cells further validated cytotoxicity and wound healing efficacy.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Docking analysis revealed strong binding affinities to key wound healing targets, including VEGF (-9.11 kcal/mol) and NFKβ (-8.62 kcal/mol). Pharmacokinetic studies highlighted favorable skin permeability, supporting topical applications. Toxicity predictions indicated a safe profile. Molecular dynamics simulations demonstrated stable protein-ligand complexes, particularly with VEGF. Cytotoxicity studies on L929 cells revealed an IC<sub>50</sub> of 6.08 μM and the scratch assay demonstrated significant wound healing activity, highlighting its effectiveness in promoting cell migration and closure.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Febuxostat shows remarkable potential in enhancing diabetic wound healing by promoting cell migration, targeting wound-healing proteins, as demonstrated through in-silico and in-vitro studies. This drug is poised to effectively treat diabetic wounds, accelerating healing and reducing complications. Rigorous pre-clinical and clinical evaluations are essential to validate its safety, efficacy, and therapeutic potential.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nirenjen</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, Chengalpattu 603203, Tamil Nadu, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Narayanan</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, Chengalpattu 603203, Tamil Nadu, India. Electronic address: narayanj@srmist.edu.in.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta Gen Subj</MedlineTA><NlmUniqueID>101731726</NlmUniqueID><ISSNLinking>0304-4165</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>101V0R1N2E</RegistryNumber><NameOfSubstance UI="D000069465">Febuxostat</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000069465" MajorTopicYN="Y">Febuxostat</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014945" MajorTopicYN="Y">Wound Healing</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D062105" MajorTopicYN="Y">Molecular Docking Simulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056004" MajorTopicYN="Y">Molecular Dynamics Simulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetic wounds</Keyword><Keyword MajorTopicYN="N">Febuxostat</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">MRSA infections</Keyword><Keyword MajorTopicYN="N">Molecular docking</Keyword><Keyword MajorTopicYN="N">Molecular dynamics</Keyword><Keyword MajorTopicYN="N">Wound healing</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no competing financial interests or personal relationships that could have influenced the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>12</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>20</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>19</Hour><Minute>16</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39653251</ArticleId><ArticleId IdType="doi">10.1016/j.bbagen.2024.130735</ArticleId><ArticleId IdType="pii">S0304-4165(24)00178-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39653064</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>31</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>31</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1555</ISSN><JournalIssue CitedMedium="Internet"><Volume>328</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month><Day>01</Day></PubDate></JournalIssue><Title>American journal of physiology. Endocrinology and metabolism</Title><ISOAbbreviation>Am J Physiol Endocrinol Metab</ISOAbbreviation></Journal><ArticleTitle>Enhanced quantification of α-cell suppression by hyperglycemia using a high-sensitivity glucagon assay.</ArticleTitle><Pagination><StartPage>E62</StartPage><EndPage>E68</EndPage><MedlinePgn>E62-E68</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpendo.00301.2024</ELocationID><Abstract><AbstractText>Accurate measurement of glucagon concentrations in a variety of conditions is necessary for subsequent estimation of glucagon secretion. Glucagon arises in the α-cell as a product of proglucagon processing. Modern two-site immunoassays have overcome prior problems with glucagon measurement caused by cross-reactivity with other proglucagon-derived fragments. However, in response to hyperglycemia, glucagon concentrations can fall below the limit of quantification of commercial immunoassays. This has implications for the characterization of α-cell function in health, in prediabetes, and in type 2 diabetes. An increase in the sensitivity of glucagon measurement was achieved by ethanol precipitation and concentration of the sample before measurement. Concentrating the sample sixfold enabled a decrease in the level of quantitation from 1.7 to 0.3 pmol/L with acceptable precision. To establish whether this enhanced high-sensitivity glucagon assay enhances the characterization of α-cell function in health and disease, we then estimated glucagon secretion rate (GSR) in four subjects. We subsequently used the relationship of GSR to glucose concentrations to characterize the α-cell response to glucose and demonstrate improved characterization of α-cell dysfunction in vivo.<b>NEW & NOTEWORTHY</b> We describe a method that lowers the limit of quantification of a glucagon immunoassay thereby enhancing the ability to differentiate between normal and abnormal α-cell responsiveness to glucagon.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dyer</LastName><ForeName>Roy B</ForeName><Initials>RB</Initials><AffiliationInfo><Affiliation>Immunochemical Core Laboratory, Mayo Clinic College of Medicine, Rochester, Minnesota, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laurenti</LastName><ForeName>Marcello C</ForeName><Initials>MC</Initials><Identifier Source="ORCID">0000-0002-8697-6260</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Christie</LastName><ForeName>Hannah E</ForeName><Initials>HE</Initials><Identifier Source="ORCID">0000-0002-0606-6778</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohan</LastName><ForeName>Sneha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Egan</LastName><ForeName>Aoife M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dalla Man</LastName><ForeName>Chiara</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-4908-0596</Identifier><AffiliationInfo><Affiliation>Department of Information Engineering, University of Padova, Padova, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vella</LastName><ForeName>Adrian</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0001-6493-7837</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>DK134767</GrantID><Agency>HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM)</Agency><Country/></Grant><Grant><GrantID>DK78646</GrantID><Agency>HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM)</Agency><Country/></Grant><Grant><GrantID>DK116231</GrantID><Agency>HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM)</Agency><Country/></Grant><Grant><GrantID>DK126206</GrantID><Agency>HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM)</Agency><Country/></Grant><Grant><GrantID>DK TR000135</GrantID><Agency>HHS | NIH | NIH Office of the Director (OD)</Agency><Country/></Grant><Grant><GrantID>Departments of Excellence (Law 232/2016)</GrantID><Agency>Ministero dell'Istruzione, dell'Università e della Ricerca (MIUR)</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Endocrinol Metab</MedlineTA><NlmUniqueID>100901226</NlmUniqueID><ISSNLinking>0193-1849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9007-92-5</RegistryNumber><NameOfSubstance UI="D005934">Glucagon</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005934" MajorTopicYN="Y">Glucagon</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050416" MajorTopicYN="Y">Glucagon-Secreting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006943" MajorTopicYN="Y">Hyperglycemia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007118" MajorTopicYN="N">Immunoassay</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">glucagon secretion</Keyword><Keyword MajorTopicYN="N">glucagon suppression</Keyword><Keyword MajorTopicYN="N">α-cell function</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>1</Day><Hour>12</Hour><Minute>41</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>10</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>19</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39653064</ArticleId><ArticleId IdType="doi">10.1152/ajpendo.00301.2024</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39652177</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>08</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2731-7013</ISSN><JournalIssue CitedMedium="Internet"><Volume>76</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Dermatologie (Heidelberg, Germany)</Title><ISOAbbreviation>Dermatologie (Heidelb)</ISOAbbreviation></Journal><ArticleTitle>[Atopic dermatitis and diabetes mellitus-is there a link?].</ArticleTitle><Pagination><StartPage>21</StartPage><EndPage>26</EndPage><MedlinePgn>21-26</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00105-024-05440-6</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Atopic dermatitis and diabetes mellitus are chronic, immune-mediated, inflammatory diseases that significantly affect patients' quality of life and also represent a considerable socioeconomic burden. Despite intensive research in recent decades, the possible link between these two medical conditions remains a controversial topic due to sparse and sometimes contradictory data. Nevertheless, the potential link between them is based on some recognized common pathophysiological features.</AbstractText><AbstractText Label="AIM" NlmCategory="OBJECTIVE">To summarize and evaluate a possible association between atopic dermatitis and diabetes mellitus.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">A literature review on the potential association between atopic dermatitis and diabetes mellitus was conducted.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Several studies have reported a correlation between atopic dermatitis and type 1 or type 2 diabetes mellitus. However, other studies have shown no association between these two conditions or even suggested that atopic dermatitis could reduce the risk of developing diabetes mellitus in certain patients. In addition, these two chronic diseases also have certain clinical features that suggest a possible correlation. However, there is currently no clear scientific evidence of a significant positive association between atopic dermatitis and diabetes mellitus, mainly due to the lack of large and diverse demographic studies.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Clinicians should be aware of this potential correlation in both adult and pediatric patients and consider the importance of an interdisciplinary approach for the management of atopic dermatitis. Further research is needed to determine possible associations between atopic dermatitis and diabetes mellitus in specific populations.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sendrea</LastName><ForeName>Adelina-Maria</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Carol Davila Universität für Medizin und Pharmacie, 8 Eroilor Sanitari Boulevard, 050474, Bukarest, Rumänien. adelinalopotaru@yahoo.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Abteilung Pädiatrische Dermatologie, Colentina Klinik, Bukarest, Rumänien. adelinalopotaru@yahoo.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Dermatologische Forschungsabteilung, Colentina Klinik, Bukarest, Rumänien. adelinalopotaru@yahoo.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Salavastru</LastName><ForeName>Carmen Maria</ForeName><Initials>CM</Initials><AffiliationInfo><Affiliation>Carol Davila Universität für Medizin und Pharmacie, 8 Eroilor Sanitari Boulevard, 050474, Bukarest, Rumänien.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Abteilung Pädiatrische Dermatologie, Colentina Klinik, Bukarest, Rumänien.</Affiliation></AffiliationInfo></Author></AuthorList><Language>ger</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Atopische Dermatitis und Diabetes mellitus – Gibt es Zusammenhänge?</VernacularTitle><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Dermatologie (Heidelb)</MedlineTA><NlmUniqueID>9918384885206676</NlmUniqueID><ISSNLinking>2731-7005</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003876" MajorTopicYN="Y">Dermatitis, Atopic</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="N">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="N">Diabetes Mellitus</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="ger"><AbstractText Label="ZUSAMMENFASSUNG" NlmCategory="UNASSIGNED">HINTERGRUND: Atopische Dermatitis und Diabetes mellitus sind chronische, immunvermittelte, entzündliche Erkrankungen, die die Lebensqualität der Patienten erheblich beeinträchtigen und zudem eine beträchtliche sozioökonomische Belastung darstellen. Trotz intensiver Forschung in den letzten Jahrzehnten bleibt der mögliche Zusammenhang zwischen diesen beiden medizinischen Zuständen aufgrund spärlicher und manchmal widersprüchlicher Daten ein umstrittenes Thema. Dennoch beruht die potenzielle Verbindung zwischen ihnen auf einigen anerkannten gemeinsamen pathophysiologischen Merkmalen.</AbstractText><AbstractText Label="ZIELE" NlmCategory="UNASSIGNED">Ein möglicher Zusammenhang zwischen atopischer Dermatitis und Diabetes mellitus soll dargestellt und bewertet werden.</AbstractText><AbstractText Label="MATERIAL UND METHODEN" NlmCategory="METHODS">Wir führten eine Literaturrecherche zum potenziellen Zusammenhang zwischen atopischer Dermatitis und Diabetes mellitus durch.</AbstractText><AbstractText Label="ERGEBNISSE" NlmCategory="UNASSIGNED">Mehrere Studien haben eine Korrelation zwischen atopischer Dermatitis und Diabetes mellitus Typ 1 oder Typ 2 festgestellt. Andere Studien zeigten jedoch keinen Zusammenhang zwischen diesen beiden Erkrankungen oder deuteten sogar darauf hin, dass atopische Dermatitis das Risiko für die Entwicklung von Diabetes mellitus bei bestimmten Patienten verringern könnte. Darüber hinaus weisen diese beiden chronischen Erkrankungen auch bestimmte klinische Merkmale auf, die auf eine mögliche Korrelation hindeuten. Derzeit gibt es jedoch keinen eindeutigen wissenschaftlichen Beweis für einen signifikant positiven Zusammenhang zwischen atopischer Dermatitis und Diabetes mellitus, was v. a. auf das Fehlen umfangreicher und vielfältiger demografischer Studien zurückzuführen ist.</AbstractText><AbstractText Label="SCHLUSSFOLGERUNGEN" NlmCategory="UNASSIGNED">Ärzte sollten sich dieser potenziellen Korrelation sowohl bei Erwachsenen als auch bei pädiatrischen Patienten bewusst sein und die Bedeutung eines multidisziplinären Ansatzes für das Management der atopischen Dermatitis berücksichtigen. Weitere Untersuchungen sind erforderlich, um mögliche Zusammenhänge zwischen atopischer Dermatitis und Diabetes mellitus in spezifischen Bevölkerungsgruppen zu bestimmen.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adiponectin</Keyword><Keyword MajorTopicYN="N">Correlations</Keyword><Keyword MajorTopicYN="N">Leptin</Keyword><Keyword MajorTopicYN="N">Multidisciplinary approach</Keyword><Keyword MajorTopicYN="N">Th1/Th2 paradigm</Keyword></KeywordList><CoiStatement>Einhaltung ethischer Richtlinien. Interessenkonflikt: A.-M. Sendrea und C.M. Salavastru geben an, dass kein Interessenkonflikt besteht. Für diesen Beitrag wurden von den Autorinnen keine Studien an Menschen oder Tieren durchgeführt. 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Br J Dermatol 177:1043–1051</Citation><ArticleIdList><ArticleId IdType="pubmed">28617976</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39651976</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1935-5548</ISSN><JournalIssue CitedMedium="Internet"><Volume>48</Volume><Issue>Supplement_1</Issue><PubDate><Year>2025</Year><Month>Jan</Month><Day>01</Day></PubDate></JournalIssue><Title>Diabetes care</Title><ISOAbbreviation>Diabetes Care</ISOAbbreviation></Journal><ArticleTitle>8. Obesity and Weight Management for the Prevention and Treatment of Type 2 Diabetes: Standards of Care in Diabetes-2025.</ArticleTitle><Pagination><StartPage>S167</StartPage><EndPage>S180</EndPage><MedlinePgn>S167-S180</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2337/dc25-S008</ELocationID><Abstract><AbstractText>The American Diabetes Association (ADA) "Standards of Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, an interprofessional expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations and a full list of Professional Practice Committee members, please refer to Introduction and Methodology. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.</AbstractText><CopyrightInformation>© 2024 by the American Diabetes Association.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><CollectiveName>American Diabetes Association Professional Practice Committee
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Available from https://healthdata.gov/dataset/NADAC-National-Average-Drug-Acquisition-Cost-2024/3tha-57c6/about_data</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39651921</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">0975-4466</ISSN><JournalIssue CitedMedium="Internet"><Volume>44</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Season>Nov-Dec</Season></PubDate></JournalIssue><Title>Annals of Saudi medicine</Title><ISOAbbreviation>Ann Saudi Med</ISOAbbreviation></Journal><ArticleTitle>Efficacy and safety of semaglutide: real-world tertiary care experience from Saudi Arabia.</ArticleTitle><Pagination><StartPage>361</StartPage><EndPage>368</EndPage><MedlinePgn>361-368</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.5144/0256-4947.2024.361</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">Semaglutide, a glucagon-like peptide-1, is an effective antidiabetic drug promoting weight loss and providing cardiovascular protection. The original trials did not include participants from Saudi Arabia; hence, the study's findings are expected to be useful.</AbstractText><AbstractText Label="OBJECTIVES" NlmCategory="UNASSIGNED">Explore the efficacy, safety, and favorable effects of once-weekly subcutaneous semaglutide (1 mg) in patients with type 2 diabetes and those who received it as an off-license prescription without having diabetes.</AbstractText><AbstractText Label="DESIGN" NlmCategory="UNASSIGNED">Retrospective review of medical records.</AbstractText><AbstractText Label="SETTING" NlmCategory="UNASSIGNED">Department of medicine at our institution.</AbstractText><AbstractText Label="PATIENTS AND METHODS" NlmCategory="UNASSIGNED">This retrospective observational study evaluated patients receiving the glucagon-like peptide-1 analog semaglutide, with the trade name Ozempic. The weight, height, body mass index, blood pressure, and laboratory data, including serum creatinine and hemoglobin A1c (HbA1c) levels and urine albumin/creatinine ratio, were recorded. Moreover, any history of medical comorbidities, such as cardiovascular diseases, cerebrovascular diseases, and heart failure, was documented before and after drug administration.</AbstractText><AbstractText Label="MAIN OUTCOME MEASURES" NlmCategory="UNASSIGNED">Glycemic and weight loss efficacy.</AbstractText><AbstractText Label="SAMPLE SIZE" NlmCategory="UNASSIGNED">1007 patients.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">The median age of the patients was 57.0 years, comprising 60.28% females. Among them, 955 and 442 patients received the medication for at least 3 and 6 months, respectively. Our results show a 4.4% weight loss and 0.4% improvement in HBA1c in patients with diabetes. Similar results were observed in the patients without diabetes in terms of weight along with a significant decrease in diastolic blood pressure. Our results also show stability in the serum creatinine and urine albumin creatinine ratio. The drug was equally effective in males and females.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Treatment with once-weekly subcutaneous semaglutide (1 mg) led to clinically significant weight loss and improved HbA1c level and cardiometabolic risk factors such as blood pressure.</AbstractText><AbstractText Label="LIMITATIONS" NlmCategory="UNASSIGNED">Retrospective design.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Butt</LastName><ForeName>Muhammad Imran</ForeName><Initials>MI</Initials><Identifier Source="ORCID">0000-0002-2143-7303</Identifier><AffiliationInfo><Affiliation>From the Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alkhalifah</LastName><ForeName>Khalid Mania</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riazuddin</LastName><ForeName>Muhammad</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Almuammar</LastName><ForeName>Saud Mohammed</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Almuammar</LastName><ForeName>Salman Mohammed</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alhifthi</LastName><ForeName>Ghayda Abdulkader</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>Fahad Wali</ForeName><Initials>FW</Initials><AffiliationInfo><Affiliation>From the Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al Hashim</LastName><ForeName>Samia Mohamed</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>From the Department of Biostatistics, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Waheed</LastName><ForeName>Najeeb</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>From the Department of Endocrinology, Imperial College London Diabetes Centre, Al Ain, Abu Dhabi, United Arab Emirates.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>Saudi Arabia</Country><MedlineTA>Ann Saudi Med</MedlineTA><NlmUniqueID>8507355</NlmUniqueID><ISSNLinking>0256-4947</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>62340-29-8</RegistryNumber><NameOfSubstance UI="D004763">Glucagon-Like Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>53AXN4NNHX</RegistryNumber><NameOfSubstance UI="C000591245">semaglutide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C517652">hemoglobin A1c protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004763" MajorTopicYN="Y">Glucagon-Like Peptides</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012529" MajorTopicYN="N" Type="Geographic">Saudi Arabia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015431" MajorTopicYN="Y">Weight Loss</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D063128" MajorTopicYN="N">Tertiary Healthcare</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001794" MajorTopicYN="N">Blood Pressure</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007279" MajorTopicYN="N">Injections, Subcutaneous</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>None.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>17</Hour><Minute>34</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>17</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>9</Hour><Minute>14</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>11</Month><Day>1</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39651921</ArticleId><ArticleId 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J Family Community Med 2003;10:49–53.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3425767</ArticleId><ArticleId IdType="pubmed">23011992</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39650851</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1177-8881</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Drug design, development and therapy</Title><ISOAbbreviation>Drug Des Devel Ther</ISOAbbreviation></Journal><ArticleTitle>The Clinical Efficacy of Gegen Qinlian Decoction in Treating Type 2 Diabetes is Positively Correlated with the Dose of <i>Coptidis rhizoma</i>: Three Randomized, Doubleblind, Dose-Parallel Controlled Clinical Trials.</ArticleTitle><Pagination><StartPage>5573</StartPage><EndPage>5582</EndPage><MedlinePgn>5573-5582</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2147/DDDT.S487315</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">The results of Study 1 we have published proved that medium and high doses of Gegen Qinlian Decoction (GQD) were effective in treating type 2 diabetes (T2D) with damp-heat syndrome. However, whether the main drug of GQD in treating T2D was <i>Puerariae Lobatae Radix</i> or <i>Coptidis Rhizoma</i> has always been a hot topic of debate among many doctors. Therefore, we conducted Study 2 and Study 3 to determine the main drug of GQD for treating T2D.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">Both Study 2 and Study 3 were randomized, double-blind, dose-parallel controlled, multicenter trials. In Study 2, <i>Puerariae Lobatae Radix</i> was used as the main drug, and in Study 3, <i>Coptidis Rhizoma</i> was used as the main drug. About 120 patients with newly diagnosed T2D were enrolled in each study and randomized 1:1:1 to three treatment groups. The three treatment groups were named HD, MD, and LD groups according to the high, medium, and low doses of the main drug. The course of treatment was 12 weeks. The primary outcomes were the changes in HbA1c.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">In Study 2, the HbA1c decreased by 0.58 (0.87), 0.28 (1.17), and 0.55 (0.85) in the HD, MD, and LD groups, respectively, with no significant difference between treatment groups according to covariance analysis (F=0.66, P=0.5206). In Study 3, the HbA1c decreased by 0.75 (0.82), 0.34 (0.71), and 0.26 (0.79) in the HD, MD, and LD groups respectively. By analysis of covariance, the change values of HbA1c were significantly different among the three groups (F=3.11, P=0.0492).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">The changes in HbA1c were positively correlated with the dose of <i>Coptidis Rhizoma</i>, but not significantly with the dose of <i>Puerariae Lobatae Radix</i>. It demonstrated that the main drug of GQD in treating T2D patients is <i>Coptidis Rhizoma</i>.</AbstractText><CopyrightInformation>© 2024 Kang et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Kang</LastName><ForeName>Xiaomin</ForeName><Initials>X</Initials><Identifier Source="ORCID">0000-0002-3002-3786</Identifier><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Beijing University of Chinese Medicine, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Jin</LastName><ForeName>De</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Ji</LastName><ForeName>Hangyu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>An</LastName><ForeName>Xuedong</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yuehong</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0000-0001-8024-9751</Identifier><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duan</LastName><ForeName>Liyun</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Cunqing</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Rongrong</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duan</LastName><ForeName>Yingying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Beijing University of Chinese Medicine, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yuqing</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Yuting</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Linlin</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Beijing University of Chinese Medicine, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lian</LastName><ForeName>Fengmei</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tong</LastName><ForeName>Xiaolin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>New Zealand</Country><MedlineTA>Drug Des Devel Ther</MedlineTA><NlmUniqueID>101475745</NlmUniqueID><ISSNLinking>1177-8881</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>CXS4LJR7EL</RegistryNumber><NameOfSubstance UI="C107393">Coptidis rhizoma extract</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004365">Drugs, Chinese Herbal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C542794">gegenqinlian</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000089042" MajorTopicYN="N">Coptis chinensis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="Y">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004311" MajorTopicYN="N">Double-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004365" MajorTopicYN="Y">Drugs, Chinese Herbal</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Coptidis rhizoma</Keyword><Keyword MajorTopicYN="N">Gegen Qinlian Decoction</Keyword><Keyword MajorTopicYN="N">Huanglian</Keyword><Keyword MajorTopicYN="N">clinical trial</Keyword><Keyword MajorTopicYN="N">dose-parallel controlled</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>The authors report no conflicts of interest in this work.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate 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-<PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39650653</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1664-3224</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in immunology</Title><ISOAbbreviation>Front Immunol</ISOAbbreviation></Journal><ArticleTitle>Global and regional genetic association analysis of ulcerative colitis and type 2 diabetes mellitus and causal validation analysis of two-sample two-way Mendelian randomization.</ArticleTitle><Pagination><StartPage>1375915</StartPage><MedlinePgn>1375915</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1375915</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fimmu.2024.1375915</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">Clinical co-occurrence of UC (Ulcerative Colitis) and T2DM (Type 2 Diabetes Mellitus) is observed. The aim of this study is to investigate the potential causal relationship between Ulcerative Colitis (UC) and Type 2 Diabetes Mellitus (T2DM) using LDSC and LAVA analysis, followed by genetic verification through TSMR, providing insights for clinical prevention and treatment.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">Genetic loci closely related to T2DM were extracted as instrumental variables from the GWAS database, with UC as the outcome variable, involving European populations. The UC data included 27,432 samples and 8,050,003 SNPs, while the T2DM data comprised 406,831 samples and 11,914,699 SNPs. LDSC and LAVA were used for quantifying genetic correlation at both global (genome-wide) and local (genomic regions) levels. MR analysis was conducted using IVW, MR-Egger regression, Weighted median, and Weighted mode, assessing the causal relationship between UC and diabetes with OR values and 95% CI. Heterogeneity and pleiotropy were tested using Egger-intercept, MR-PRESSO, and sensitivity analysis through the "leave-one-out" method and Cochran Q test. Subsequently, a reverse MR operation was conducted using UC as the exposure data and T2DM as the outcome data for validation.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Univariable and bivariable LDSC calculated the genetic correlation and potential sample overlap between T2DM and UC, resulting in rg = -0.0518, se = 0.0562, <i>P</i> = 0.3569 with no significant genetic association found for paired traits. LAVA analysis identified 9 regions with local genetic correlation, with 6negative and 3 positive associations, indicating a negative correlation between T2DM and UC. MR analysis, with T2DM as the exposure and UC as the outcome, involved 34 SNPs as instrumental variables. The OR values and 95% CI from IVW, MR-Egger, Weighted median, and Weighted mode were 0.917 (0.848~0.992), 0.949 (0.800~1.125), 0.881 (0.779~0.996), 0.834(0.723~0.962) respectively, with IVW <i>P</i>-value < 0.05, suggesting a negative causal relationship between T2DM and UC. MR-Egger regression showed an intercept of -0.004 with a standard error of 0.009, <i>P</i> = 0.666, and MR-PRESSO Global Test <i>P</i>-value > 0.05, indicating no pleiotropy and no outliers detected. Heterogeneity tests showed no heterogeneity, and the "leave-one-out" sensitivity analysis results were stable. With UC as the exposure and T2DM as the outcome, 32 SNPs were detected, but no clear causal association was found.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">There is a causal relationship between T2DM and UC, where T2DM reduces the risk of UC, while no significant causal relationship was observed from UC to T2DM.</AbstractText><CopyrightInformation>Copyright © 2024 Hu, Chen, Zhou, Zhao, Wang, Huang, Li and Zeng.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Yan-Zhi</ForeName><Initials>YZ</Initials><AffiliationInfo><Affiliation>The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Zhe</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Thoracic Surgery, The Second Xiangya Hospital, Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Ming-Han</ForeName><Initials>MH</Initials><AffiliationInfo><Affiliation>The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Zhen-Yu</ForeName><Initials>ZY</Initials><AffiliationInfo><Affiliation>College of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xiao-Yan</ForeName><Initials>XY</Initials><AffiliationInfo><Affiliation>The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xin-Tian</ForeName><Initials>XT</Initials><AffiliationInfo><Affiliation>The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zeng</LastName><ForeName>Juan-Ni</ForeName><Initials>JN</Initials><AffiliationInfo><Affiliation>The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, Changsha, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Immunol</MedlineTA><NlmUniqueID>101560960</NlmUniqueID><ISSNLinking>1664-3224</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003093" MajorTopicYN="Y">Colitis, Ulcerative</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="Y">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="Y">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055106" MajorTopicYN="Y">Genome-Wide Association Study</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057182" MajorTopicYN="Y">Mendelian Randomization Analysis</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">LAVA analysis</Keyword><Keyword MajorTopicYN="N">LDSC analysis</Keyword><Keyword MajorTopicYN="N">Mendelian randomization</Keyword><Keyword MajorTopicYN="N">T2DM</Keyword><Keyword MajorTopicYN="N">UC</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate 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(2019) 30:1300–0. doi: 10.4103/1319-2442.275474</Citation><ArticleIdList><ArticleId IdType="doi">10.4103/1319-2442.275474</ArticleId><ArticleId IdType="pubmed">31929277</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39649227</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>10</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>A scoping review of type 2 diabetes mellitus in Pakistan investigating the status of glycemic control, awareness, treatment adherence, complications and cost.</ArticleTitle><Pagination><StartPage>1441591</StartPage><MedlinePgn>1441591</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1441591</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1441591</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">The high prevalence of Type 2 diabetes mellitus(T2DM) in Pakistan is a challenge to the existing healthcare system. This is the first comprehensive review of the status of glycemic control, diabetes knowledge, treatment adherence, complications and financial burden faced by the diabetic patient population of the country.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">We searched PubMed, Web of Science and Scopus for studies on diabetes control, knowledge, treatment adherence, prevalence of complications and cost in Pakistan published in English from 2000 to 2024. We hand-searched Google Scholar for additional papers and included a total of 45 studies in our review.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">The review shows that poor glycemic control prevails among diabetic patients ranging from 44.7% to 86.4% along with half of the patients have poor diabetes knowledge (46.0% -70.0%). Treatment adherence level in diabetic patients varies widely in different studies, frequently reported complications are retinopathy (14.5%-43.0%), nephropathy (14.0%-31.0%) and neuropathy (10.8%-59.6%); and the disease poses a great deal of economic burden.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Most of the studies were observational. Glycemic control and knowledge among individuals with T2DM in Pakistan are inadequate, leading to a high prevalence of complications that impose significant health and economic burdens. Further longitudinal studies generating evidence of lifestyle modifications as primary and secondary prevention strategies against diabetes in the Pakistani population can form a strong foundation for awareness campaigns and policy revisions.</AbstractText><CopyrightInformation>Copyright © 2024 Taimur, Ahmad, Khan, Shirayama, Okamoto, Aung, Shabbir and Yuasa.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Taimur</LastName><ForeName>Hira</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Global Health Research, Graduate School of Medicine, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahmad</LastName><ForeName>Ishtiaq</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Global Health Research, Graduate School of Medicine, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khan</LastName><ForeName>Hamza</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Global Health Research, Graduate School of Medicine, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shirayama</LastName><ForeName>Yoshihisa</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Global Health Research, Graduate School of Medicine, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Okamoto</LastName><ForeName>Miyoko</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Global Health Research, Graduate School of Medicine, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aung</LastName><ForeName>Myo Nyein</ForeName><Initials>MN</Initials><AffiliationInfo><Affiliation>Department of Global Health Research, Graduate School of Medicine, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Advanced Research Institute for Health Sciences, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of International Liberal Arts, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shabbir</LastName><ForeName>Sameera</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Central Campus, International Higher School of Medicine, Bishkek, Kyrgyzstan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuasa</LastName><ForeName>Motoyuki</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Global Health Research, Graduate School of Medicine, Juntendo University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010154" MajorTopicYN="N" Type="Geographic">Pakistan</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000085002" MajorTopicYN="Y">Glycemic Control</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007722" MajorTopicYN="N">Health Knowledge, Attitudes, Practice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D048909" MajorTopicYN="N">Diabetes Complications</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000074822" MajorTopicYN="N">Treatment Adherence and Compliance</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017048" MajorTopicYN="N">Health Care Costs</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Pakistan</Keyword><Keyword MajorTopicYN="N">T2DM</Keyword><Keyword MajorTopicYN="N">awareness</Keyword><Keyword MajorTopicYN="N">complications</Keyword><Keyword MajorTopicYN="N">cost</Keyword><Keyword MajorTopicYN="N">glycemic control</Keyword><Keyword MajorTopicYN="N">medication adherence</Keyword></KeywordList><CoiStatement>The 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(2011) 61:210–5.</Citation><ArticleIdList><ArticleId IdType="pubmed">21465929</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39649224</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>10</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>The harmful effect of ankylosing spondylitis on diabetes mellitus: new evidence from the Mendelian randomization analysis.</ArticleTitle><Pagination><StartPage>1369466</StartPage><MedlinePgn>1369466</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1369466</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1369466</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">While observational research has highlighted a possible link between ankylosing spondylitis (AS) and type 2 diabetes (T2DM), the quality of evidence remains limited, and the causal relationship is yet to be established. This study aims to explore the causal link between AS and T2DM, as well as its impact on traits related to glucose metabolism.</AbstractText><AbstractText Label="METHOD" NlmCategory="UNASSIGNED">To infer a causal relationship between AS and various diabetes-related traits, including type 1 diabetes (T1DM), T2DM, blood glucose levels, fasting glucose, glycated hemoglobin, and fasting insulin, we employed Mendelian randomization (MR) analysis. We sourced GWAS summary data for both exposure and outcome variables from the IEU OpenGWAS database, GWAS Catalog, and FinnGen database. To synthesize the results of the MR analyses, we applied meta-analysis techniques using either a fixed or random effects model. For identifying and excluding instrumental variants (IVs) that exhibit horizontal pleiotropy with the outcomes, we utilized the MR-PRESSO method. Sensitivity analyses were conducted using the MR-Egger method, along with Q and I^2 tests, to ensure the robustness of our findings.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Our analysis revealed a significant association between AS and an increased risk of T1DM with an odds ratio (OR) of 1.5754 (95% CI: 1.2935 to 1.9187) and T2DM with an OR of 1.0519 (95% CI: 1.0059 to 1.1001). Additionally, AS was associated with elevated levels of fasting glucose (beta coefficient = 0.0165, 95% CI: 0.0029 to 0.0301) and blood glucose (beta coefficient = 0.0280, 95% CI: 0.0086 to 0.0474), alongside a decrease in fasting insulin levels (beta coefficient = -0.0190, 95% CI: -0.0330 to -0.0050).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Our findings collectively underscore the detrimental impact of AS on the development of diabetes, highlighting the critical influence of autoimmune disorders in diabetes onset. This provides profound insights into the pathogenesis of diabetes from an immunological standpoint.</AbstractText><CopyrightInformation>Copyright © 2024 Ren, He, Wang, Shu, Li and Ma.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Ren</LastName><ForeName>Zheng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Xinjiang Institute of Spinal Surgery, Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>He</LastName><ForeName>Liang</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute of General Surgery, Wulumuqi General Hospital of People's Liberation Army (PLA), Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Wang</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Xinjiang Institute of Spinal Surgery, Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shu</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Xinjiang Institute of Spinal Surgery, Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chenyang</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Micro Operation of the Third People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Yuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Xinjiang Institute of Spinal Surgery, Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="N">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055106" MajorTopicYN="Y">Genome-Wide Association Study</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057182" MajorTopicYN="N">Mendelian Randomization Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013167" MajorTopicYN="Y">Spondylitis, Ankylosing</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Mendelian randomization</Keyword><Keyword MajorTopicYN="N">ankylosing spondylitis</Keyword><Keyword MajorTopicYN="N">glucose metabolism</Keyword><Keyword MajorTopicYN="N">meta-analysis</Keyword><Keyword MajorTopicYN="N">type 1 and 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>2</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>17</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>11</Hour><Minute>28</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>5</Hour><Minute>58</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>1</Month><Day>1</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39649224</ArticleId><ArticleId IdType="pmc">PMC11624504</ArticleId><ArticleId 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This study evaluated the 18-month effects of the Automated Personalized Self-Care (APSC) program on self-care self-efficacy, diabetes self-care, and complication risk indices in T2DM patients through a randomized controlled trial. Participants aged 40-69 years were assigned to either an intervention group using the APSC mobile app, which provided personalized goals, automated feedback, and monthly support, or a comparison group. The final analysis included 43 engaged participants from the intervention group and 78 from the comparison group. Data were collected at baseline, 6, 12, and 18 months using structured questionnaires and medical record reviews and analyzed using generalized estimating equations. Significant effects were observed for self-care self-efficacy, diabetes self-care activities, vegetable intake, HbA1c, and total cholesterol levels. The APSC program showed potential to improve long-term self-care and reduce complication risk in T2DM patients. Further research with a larger samples and strategies to promote long-term engagement is needed for its integration into routine diabetes care. Trial Registration: Clinical Research Information Service: KCT0007672.</AbstractText><CopyrightInformation>© 2024 John Wiley & Sons Australia, Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Haejung</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0003-0291-9945</Identifier><AffiliationInfo><Affiliation>College of Nursing, Pusan National University, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Institute of Nursing Science, Pusan National University, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Gaeun</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0003-0923-4340</Identifier><AffiliationInfo><Affiliation>Research Institute of Nursing Science, Pusan National University, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>DaeEun</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-3136-2739</Identifier><AffiliationInfo><Affiliation>College of Nursing, Pusan National University, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khang</LastName><ForeName>Ah Reum</ForeName><Initials>AR</Initials><Identifier Source="ORCID">0000-0002-9154-6468</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Min Jin</ForeName><Initials>MJ</Initials><Identifier Source="ORCID">0000-0002-4351-789X</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NRF-2019R1I1A3A01062513</GrantID><Agency>National Research Foundation of Korea</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Australia</Country><MedlineTA>Nurs Health Sci</MedlineTA><NlmUniqueID>100891857</NlmUniqueID><ISSNLinking>1441-0745</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012648" MajorTopicYN="Y">Self Care</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011795" MajorTopicYN="N">Surveys and Questionnaires</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020377" MajorTopicYN="N">Self Efficacy</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">evidence‐based practice</Keyword><Keyword MajorTopicYN="N">mobile applications</Keyword><Keyword MajorTopicYN="N">randomized controlled trial</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>18</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>17</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>1</Hour><Minute>43</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39648515</ArticleId><ArticleId IdType="doi">10.1111/nhs.70008</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>Al Mahrouqi, A. 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Tao, Y. Ma, et al. 2024. “Improving the Management of Type 2 Diabetes in China Using a Multifaceted Digital Health Intervention in Primary Health Care: The SMARTDiabetes Cluster Randomised Controlled Trial.” Lancet Regional Health–Western Pacific 49: 101130. https://doi.org/10.1016/j.lanwpc.2024.101130.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39648376</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1681-7168</ISSN><JournalIssue CitedMedium="Internet"><Volume>34</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Journal of the College of Physicians and Surgeons--Pakistan : JCPSP</Title><ISOAbbreviation>J Coll Physicians Surg Pak</ISOAbbreviation></Journal><ArticleTitle>Relationship of HbA1c with Mean Platelet Volume and Leucocyte Count in Patients with Type 2 Diabetes Mellitus.</ArticleTitle><Pagination><StartPage>1436</StartPage><EndPage>1440</EndPage><MedlinePgn>1436-1440</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.29271/jcpsp.2024.12.1436</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To determine the relationship between mean platelet volume (MPV), leucocyte count, and HbA1c levels in patients with type 2 diabetes mellitus (DM).</AbstractText><AbstractText Label="STUDY DESIGN" NlmCategory="METHODS">Observational study. Place and Duration of the Study: Bahcesehir Family Healthcare Centre (FHC), Adana, Turkiye, from January 2023 to 2024.</AbstractText><AbstractText Label="METHODOLOGY" NlmCategory="METHODS">This study included 101 controls and 106 patients with Type 2 diabetes mellitus (DM). Age, gender, body mass index (BMI), duration of diabetes, smoking, type of diabetic medication, and presence of chronic diseases were all assessed in relation to the patients. Analysis of leucocyte count, MPV, and HbA1c was conducted retrospectively. IBM SPSS version 25.0 was utilised for the statistical analysis, with p <0.05 being considered as the significance threshold.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The DM group exhibited significantly higher levels of HbA1c (7.8 ± 1.5%), MPV (9.2 ± 1.3 fL), and leucocyte count (7.1 ± 1.8 x10^3/µL) in comparison to the control group (p <0.001). There was a positive and statistically significant association found between the leucocyte count, MPV, and HbA1c. In the control group, there was no significant link onserved.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">In patients with Type 2 DM, a favourable connection between HbA1c, MPV, and leucocyte count was observed. These results point to a higher risk of thrombosis and inflammation in DM patients. Patients with HbA1c values above 7 showed increased leucocyte counts and MPV, which indicated that these patients were at a higher risk of vascular problems. Leucocyte counts and MPV may serve as useful biomarkers to gauge the likelihood of vascular problems in DM.</AbstractText><AbstractText Label="KEY WORDS" NlmCategory="BACKGROUND">Type 2 diabetes mellitus, HbA1c, Mean platelet volume, Leucocyte count, Inflammation, Vascular complications.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kiziltas</LastName><ForeName>Ozlem</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Seyhan Health Directorate, Adana, Turkiye.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Family Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkiye.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fidanci</LastName><ForeName>Izzet</ForeName><Initials>I</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Pakistan</Country><MedlineTA>J Coll Physicians Surg Pak</MedlineTA><NlmUniqueID>9606447</NlmUniqueID><ISSNLinking>1022-386X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C517652">hemoglobin A1c protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D063847" MajorTopicYN="Y">Mean Platelet Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007958" MajorTopicYN="N">Leukocyte Count</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>18</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>17</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>48</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39648376</ArticleId><ArticleId IdType="doi">10.29271/jcpsp.2024.12.1436</ArticleId><ArticleId IdType="pii">040579197</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39648027</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>08</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0412-4081</ISSN><JournalIssue CitedMedium="Print"><Volume>60</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>11</Day></PubDate></JournalIssue><Title>[Zhonghua yan ke za zhi] Chinese journal of ophthalmology</Title><ISOAbbreviation>Zhonghua Yan Ke Za Zhi</ISOAbbreviation></Journal><ArticleTitle>[Association between type 2 diabetes mellitus and the risk of developing cataracts: based on the research of two-sample Mendelian randomization].</ArticleTitle><Pagination><StartPage>991</StartPage><EndPage>997</EndPage><MedlinePgn>991-997</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3760/cma.j.cn112142-20240107-00005</ELocationID><Abstract><AbstractText><b>Objective:</b> To determine the causal relationship between cataracts and type 2 diabetes mellitus (T2D) by the Mendelian randomization (MR) analysis using the genome-wide association study (GWAS) data. <b>Methods:</b> Data on T2D and cataracts in the European population were obtained from the OpenGWAS database. The single nucleotide polymorphisms (SNPs) that met the genome-wide significance criteria (<i>P</i><5×10⁻⁸) of T2D (48 286 cases, 250 671 controls) and cataracts (5 045 cases, 356 096 controls) were selected. The main method was random effects inverse variance weighting (IVW), and four other two-sample MR methods were also used, including MR Egger, Simple median, Weighted median, and Weighted mode, to assess the causal relationship using odds ratios (<i>OR</i>). Sensitivity analyses were conducted using the leave-one-out approach to evaluate the robustness of the results. <b>Results:</b> The MR Egger analysis showed a significant risk association between T2D and cataracts (<i>OR=</i>1.003, 95%<i>CI</i>=1.001-1.006; <i>P</i>=0.013). Using the methods of Weighted median (<i>OR</i>=1.002, 95%<i>CI</i>=1.000-1.004; <i>P</i>=0.029) and Weighted mode (<i>OR</i>=1.002, 95%<i>CI</i>=1.000-1.005; <i>P</i>=0.046), similar results were obtained. However, the IVW test failed to confirm the causality (<i>P</i>=0.149). The sensitivity analyses using the MR Egger and IVW tests did not show significant heterogeneity between T2D and cataracts (all <i>P</i>>0.05). With the leave-one-out analysis, the SNPs with significant effects were not identified, indicating the robustness of the MR results in this study. The MR Egger interception of the SNPs showed significant directional pleiotropy (<i>P</i>=0.038), suggesting a directional pleiotropy between T2D and cataracts. <b>Conclusions:</b> The results of the MR analysis suggest there is a causal relationship between T2D and cataracts, and T2D increases the risk of cataracts.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>X H</ForeName><Initials>XH</Initials><AffiliationInfo><Affiliation>Eye Hospital of Wenzhou Medical University, National Clinical Research Center for Ocular Diseases, Wenzhou325027, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Eye Hospital of Wenzhou Medical University, National Clinical Research Center for Ocular Diseases, Wenzhou325027, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>W F</ForeName><Initials>WF</Initials><AffiliationInfo><Affiliation>Eye Hospital of Wenzhou Medical University, National Clinical Research Center for Ocular Diseases, Wenzhou325027, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Y E</ForeName><Initials>YE</Initials><AffiliationInfo><Affiliation>Eye Hospital of Wenzhou Medical University, National Clinical Research Center for Ocular Diseases, Wenzhou325027, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><GrantList CompleteYN="Y"><Grant><GrantID>2022C03070</GrantID><Agency>Key S&T Project of Zhejiang Provincial Department of Science and Technology</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Yan Ke Za Zhi</MedlineTA><NlmUniqueID>16210540R</NlmUniqueID><ISSNLinking>0412-4081</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002386" MajorTopicYN="Y">Cataract</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057182" MajorTopicYN="Y">Mendelian Randomization Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055106" MajorTopicYN="Y">Genome-Wide Association Study</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="Y">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016017" MajorTopicYN="N">Odds Ratio</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><AbstractText><b>目的：</b> 探讨白内障与2型糖尿病的因果关系。 <b>方法：</b> 孟德尔随机化（MR）研究。于 全基因组关联研究（GWAS）的OpenGWAS 数据库获取欧洲人种的 2型糖尿病（病例数 48 286，对照数 250 671）和白内障（病例数 5 045，对照数 356 096）的数据。选取符合全基因组显著性标准（<i>P</i><5×10⁻⁸）的2型糖尿病和白内障的单核多态性（SNP）。主要采用随机效应逆方差加权（IVW）模型，同时运用了其他4种双样本MR模型，包括MR Egger、中位数、加权中位数（WM）和加权模式，用比值比（<i>OR）</i>及其95%置信区间（<i>CI</i>）来评估两者的因果关系；使用逐个剔除检验评估结果的稳健性。 <b>结果：</b> MR Egger 分析结果表明，2型糖尿病与白内障之间存在显著的风险关联（<i>OR</i>=1.003，95%<i>CI</i>=1.001~1.006，<i>P</i>=0.013）；其他模型中WM（<i>OR</i>=1.002，95%<i>CI</i>=1.000~1.004，<i>P</i>=0.029）和加权模式（<i>OR</i>=1.002，95%<i>CI</i>=1.000~1.005，<i>P</i>=0.046）也得到类似的结果。但IVW检验结果显示无明显因果关系（<i>P</i>=0.149）。通过 MR Egger 和 IVW 检验开展敏感性分析，均未显示2型糖尿病与白内障之间存在显著的异质性（均<i>P</i>>0.05）。应用逐个剔除检验，未确定有显著影响的 SNP，表明该MR分析结果具有稳健性。SNP 的 MR Egger 截距（-0.0002）显示出显著的定向多效性（<i>P</i>=0.038），这些结果提示2型糖尿病与白内障之间存在方向性多效性作用。 <b>结论：</b> 基于欧洲人MR分析结果显示，2型糖尿病与白内障之间存在因果关系，2型糖尿病增加了白内障的风险。.</AbstractText></OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>21</Hour><Minute>14</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39648027</ArticleId><ArticleId IdType="doi">10.3760/cma.j.cn112142-20240107-00005</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39647851</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>09</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1475-2727</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>09</Day></PubDate></JournalIssue><Title>Public health nutrition</Title><ISOAbbreviation>Public Health Nutr</ISOAbbreviation></Journal><ArticleTitle>Dietary fat quality indices and risk of pre-diabetes and type 2 diabetes mellitus: Tehran Lipid and Glucose Study.</ArticleTitle><Pagination><StartPage>e8</StartPage><MedlinePgn>e8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1368980024001216</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To assess associations between dietary fat quality indices and risk of pre-diabetes and type 2 diabetes mellitus (T2DM) among Iranian adults.</AbstractText><AbstractText Label="DESIGN" NlmCategory="METHODS">Daily intakes of fatty acids were estimated using a validated FFQ with 168 food items. Adjusted hazard ratios (HR) and 95 % CI for pre-diabetes and T2DM were calculated across tertile categories of dietary fat quality indices including the atherogenic index, thrombogenic index, health-promoting index, ratio of PUFA to SFA (PUFA:SFA) and ratio of hypo- and hypercholesterolaemia (h:H).</AbstractText><AbstractText Label="SETTING" NlmCategory="METHODS">Tehran Lipid and Glucose Study.</AbstractText><AbstractText Label="PARTICIPANTS" NlmCategory="METHODS">Iranian men and women.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The mean (sd) age of the 2042 pre-diabetes-free participants in pre-diabetes analysis was 38·84 (12·97), and 55·2 % were women. In T2DM analysis, the mean (sd) age of the 2295 T2DM-free participants was 40·06 (13·42), and 54·6 % of them were women. In the crude model, the PUFA:SFA ratio was positively associated with T2DM incidence (HR = 1·43; 95 % CI 1·04, 1·98). However, after adjustment for confounding variables, there were no significant associations between dietary fat quality indices and risk of pre-diabetes and T2DM.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">We found no significant association between fat quality indices and risk of pre-diabetes and T2DM. Further prospective and clinical trial studies are needed to clarify the issue.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gaeini</LastName><ForeName>Zahra</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alvirdizadeh</LastName><ForeName>Sevda</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hosseinpour-Niazi</LastName><ForeName>Somayeh</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mirmiran</LastName><ForeName>Parvin</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Azizi</LastName><ForeName>Fereidoun</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Public Health Nutr</MedlineTA><NlmUniqueID>9808463</NlmUniqueID><ISSNLinking>1368-9800</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004041">Dietary Fats</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005227">Fatty Acids</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007492" MajorTopicYN="N" Type="Geographic">Iran</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004041" MajorTopicYN="Y">Dietary Fats</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011236" MajorTopicYN="Y">Prediabetic State</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005227" MajorTopicYN="N">Fatty Acids</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004032" MajorTopicYN="N">Diet</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Fat quality indices</Keyword><Keyword MajorTopicYN="N">Pre-diabetes</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>9</Day><Hour>6</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>20</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39647851</ArticleId><ArticleId IdType="doi">10.1017/S1368980024001216</ArticleId><ArticleId IdType="pii">S1368980024001216</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39647763</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0003</ISSN><JournalIssue CitedMedium="Internet"><Volume>286</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>International journal of biological macromolecules</Title><ISOAbbreviation>Int J Biol Macromol</ISOAbbreviation></Journal><ArticleTitle>Low-dose IL-2 restores metabolic dysfunction and immune dysregulation in mice with type 2 diabetes induced by a high-fat, high-sugar diet and streptozotocin.</ArticleTitle><Pagination><StartPage>138468</StartPage><MedlinePgn>138468</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ijbiomac.2024.138468</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0141-8130(24)09279-1</ELocationID><Abstract><AbstractText>Interleukin-2 (IL-2) is pivotal in immune regulation, particularly in the promotion of regulatory T (Treg) cells and the maintenance of immune tolerance. While its efficacy in autoimmune diseases is well established, its role in type 2 diabetes (T2D) remains largely unexplored. This study investigates the effects of low-dose IL-2 in a KM mouse model of T2D induced by streptozotocin (STZ) and a high-fat, high-sugar (HFHS) diet. We found that low-dose IL-2 administration significantly improved fasting plasma glucose (FPG), glycosylated hemoglobin (HbA1c) levels, and glucose tolerance, indicating better glycemic control. Additionally, IL-2 treatment improved insulin sensitivity, enhanced insulin secretion, and ameliorated lipid metabolism, as evidenced by reduced cholesterol and triglyceride levels. These metabolic improvements were associated with a modulation of inflammation, including a reduction in pro-inflammatory cytokines (TNF-α, IL-1β) and an increase in anti-inflammatory cytokines (IL-10). Importantly, IL-2 also altered the gut microbiome, reducing intestinal inflammation and endotoxin levels, which suggests a broader impact on metabolic health beyond immune regulation. These findings support the potential of low-dose IL-2 as an immunotherapeutic approach for improving metabolic dysfunction and inflammation in T2D.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huo</LastName><ForeName>Lijing</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>College of Life Science, Hebei Normal University, No. 20 Road East of 2nd Ring South, Shijiazhuang City, Hebei Province 050024, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Hairui</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>College of Life Science, Hebei Normal University, No. 20 Road East of 2nd Ring South, Shijiazhuang City, Hebei Province 050024, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hou</LastName><ForeName>Shiyu</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>College of Life Science, Hebei Normal University, No. 20 Road East of 2nd Ring South, Shijiazhuang City, Hebei Province 050024, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Wenting</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>College of Life Science, Hebei Normal University, No. 20 Road East of 2nd Ring South, Shijiazhuang City, Hebei Province 050024, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meng</LastName><ForeName>Qingwen</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>College of Life Science, Hebei Normal University, No. 20 Road East of 2nd Ring South, Shijiazhuang City, Hebei Province 050024, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chenhui</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Hebei Fitness Biotechnology Co., Ltd., Shijiazhuang High-tech Industrial Park, Shijiazhuang City, Hebei Province, People's Republic of China; Hebei Key Laboratory of Autoimmune Disease Medicine Research, Shijiazhuang City, Hebei Province 050035, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Xiaohan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Hebei Fitness Biotechnology Co., Ltd., Shijiazhuang High-tech Industrial Park, Shijiazhuang City, Hebei Province, People's Republic of China; Hebei Key Laboratory of Autoimmune Disease Medicine Research, Shijiazhuang City, Hebei Province 050035, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Lijing</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Hebei Fitness Biotechnology Co., Ltd., Shijiazhuang High-tech Industrial Park, Shijiazhuang City, Hebei Province, People's Republic of China; Hebei Key Laboratory of Autoimmune Disease Medicine Research, Shijiazhuang City, Hebei Province 050035, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Jintian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Life Science, Hebei Normal University, No. 20 Road East of 2nd Ring South, Shijiazhuang City, Hebei Province 050024, People's Republic of China. Electronic address: 576477418@qq.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Baohua</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>College of Life Science, Hebei Normal University, No. 20 Road East of 2nd Ring South, Shijiazhuang City, Hebei Province 050024, People's Republic of China. Electronic address: zhaobaohua@mail.hebtu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Biol Macromol</MedlineTA><NlmUniqueID>7909578</NlmUniqueID><ISSNLinking>0141-8130</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007376">Interleukin-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>5W494URQ81</RegistryNumber><NameOfSubstance UI="D013311">Streptozocin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="Y">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007376" MajorTopicYN="Y">Interleukin-2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013311" MajorTopicYN="Y">Streptozocin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069196" MajorTopicYN="N">Gastrointestinal Microbiome</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050356" MajorTopicYN="N">Lipid Metabolism</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Gut microbiota</Keyword><Keyword MajorTopicYN="N">IL-2</Keyword><Keyword MajorTopicYN="N">Immunotherapy</Keyword><Keyword MajorTopicYN="N">Macrophage polarization</Keyword><Keyword MajorTopicYN="N">Regulatory T cells</Keyword><Keyword MajorTopicYN="N">Th17 T cells</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors have no financial or non-financial interests that may be relevant to the submitted work.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>11</Day><Hour>14</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>19</Hour><Minute>17</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39647763</ArticleId><ArticleId IdType="doi">10.1016/j.ijbiomac.2024.138468</ArticleId><ArticleId IdType="pii">S0141-8130(24)09279-1</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39647665</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8227</ISSN><JournalIssue CitedMedium="Internet"><Volume>219</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Diabetes research and clinical practice</Title><ISOAbbreviation>Diabetes Res Clin Pract</ISOAbbreviation></Journal><ArticleTitle>Diabetes specialist nurse support, training and 'virtual' advice reduces district nurse visits and improves outcomes for people with diabetes requiring visits for insulin administration.</ArticleTitle><Pagination><StartPage>111948</StartPage><MedlinePgn>111948</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.diabres.2024.111948</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0168-8227(24)00858-1</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">We evaluated the effectiveness of a community diabetes specialist nurse (cDSN) working with district nurses (DNs) to optimise insulin therapy on DN workload and patient outcomes.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">This was an observational clinical improvement study of outcomes pre- and post-introduction of an intervention within a community diabetes service in an areas of England. Patients were followed up for 6 months. The intervention was a cDSN providing advice and support to DNs in safe diabetes management, with a particular focus on insulin use.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">in total, 148 of 224 patients were reviewed; 130 (87.8 %) were available for follow up 6 months after their first review. Comparing pre- to post-intervention outcomes, number of patients with a hypoglycaemic event reduced from 21/129 to 1/128 (X<sup>2</sup> = 19.71, p < 0.001) as did the number with a hyperglycaemic event; 53/129 to 23/128 (X<sup>2</sup> = 16.48, p < 0.001). Number of DN visits and use of acute hospital services also improved significantly. Estimated cost savings through reduced DN visits, insulin usage, and hospital service use totalled £1.9 million.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Significant financial savings and reduced patient harms were identified following our intervention in this cohort. Roll-out to other sites in England is a next step.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gilligan</LastName><ForeName>Laura</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>The Diabetes Centre, Ipswich Hospital, East Suffolk and North East Essex NHS Trust, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Page</LastName><ForeName>Emma</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>The Diabetes Centre, Ipswich Hospital, East Suffolk and North East Essex NHS Trust, UK; Getting It Right First Time Programme, NHS England, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hall</LastName><ForeName>Jo</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Diabetes Centre, Ipswich Hospital, East Suffolk and North East Essex NHS Trust, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ward</LastName><ForeName>Kelly</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>The Diabetes Centre, Ipswich Hospital, East Suffolk and North East Essex NHS Trust, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gray</LastName><ForeName>William K</ForeName><Initials>WK</Initials><AffiliationInfo><Affiliation>Getting It Right First Time Programme, NHS England, London, UK. Electronic address: William.gray5@nhs.net.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Briggs</LastName><ForeName>Tim W R</ForeName><Initials>TWR</Initials><AffiliationInfo><Affiliation>Getting It Right First Time Programme, NHS England, London, UK; Royal National Orthopaedic Hospital NHS Trust, Stanmore, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rayman</LastName><ForeName>Gerry</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>The Diabetes Centre, Ipswich Hospital, East Suffolk and North East Essex NHS Trust, UK; Getting It Right First Time Programme, NHS England, London, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Diabetes Res Clin Pract</MedlineTA><NlmUniqueID>8508335</NlmUniqueID><ISSNLinking>0168-8227</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="Y">Insulin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004739" MajorTopicYN="N" Type="Geographic">England</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="N">Diabetes Mellitus</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000451" MajorTopicYN="N">nursing</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000451" MajorTopicYN="N">nursing</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000072184" MajorTopicYN="N">Nurse Specialists</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes</Keyword><Keyword MajorTopicYN="N">Diabetes specialist nurse</Keyword><Keyword MajorTopicYN="N">District nurse</Keyword><Keyword MajorTopicYN="N">Insulin</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>12</Day><Hour>15</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>19</Hour><Minute>15</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39647665</ArticleId><ArticleId IdType="doi">10.1016/j.diabres.2024.111948</ArticleId><ArticleId IdType="pii">S0168-8227(24)00858-1</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39647587</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>13</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-2517</ISSN><JournalIssue CitedMedium="Internet"><Volume>372</Volume><PubDate><Year>2025</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of affective disorders</Title><ISOAbbreviation>J Affect Disord</ISOAbbreviation></Journal><ArticleTitle>A randomised controlled feasibility trial of Behavioural activation as a treatment for people with diabetes and depression: (DiaDeM feasibility trial).</ArticleTitle><Pagination><StartPage>333</StartPage><EndPage>346</EndPage><MedlinePgn>333-346</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jad.2024.11.079</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0165-0327(24)01970-0</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">There is a lack of evidence on effective treatments for depression in people with T2DM, particularly in Low and Middle-Income Countries (LMICs). This study aims to test the feasibility and acceptability of a culturally adapted Behavioural Activation (BA) intervention (DiaDeM) for people with depression and T2DM in two South Asian LMICs.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A multicountry, individually randomised-controlled feasibility trial was conducted from March 2022 to November 2022. We recruited adults from diabetes healthcare facilities in Bangladesh and Pakistan with a diagnosis of depression and T2DM. Consenting individuals were randomised to either optimised usual care or the DiaDeM intervention, which comprised six BA sessions delivered by non-mental health facilitators over six to twelve weeks. Participants were followed up at three and six months post-randomisation. The feasibility and acceptability of recruitment and retention, intervention delivery, and data collection were assessed. A mixed-methods process evaluation was also performed to inform the main trial.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The DiaDeM feasibility trial successfully recruited 128 participants, with 85 % retention at six months follow-up. The majority of participants engaged with the intervention, demonstrating good adherence to the Behavioural Activation (BA) sessions. Data completeness for key outcomes, including depression severity and HbA1c levels, was high across all time points (>90 %). The process evaluation showed high acceptability of the intervention, with participants reporting increased motivation and improved management of both T2DM and depression.</AbstractText><AbstractText Label="DISCUSSION" NlmCategory="CONCLUSIONS">Good recruitment and retention rates, completeness of data collection, and high acceptability of the intervention showed that it would be feasible to undertake a full-scale trial.</AbstractText><CopyrightInformation>Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>Naveed</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Centre for Health Research and Implementation, Diabetic Association of Bangladesh, Bangladesh; BIRDEM General Hospital, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zavala</LastName><ForeName>Gerardo A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, University of York, United Kingdom. Electronic address: g.zavala@york.ac.uk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Siddiqui</LastName><ForeName>Faraz</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, University of York, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aslam</LastName><ForeName>Faiza</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Institute of Psychiatry, Rawalpindi Medical University, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Keding</LastName><ForeName>Ada</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, York, Trials Unit, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Halmkan</LastName><ForeName>Shannon</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, York, Trials Unit, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Afaq</LastName><ForeName>Saima</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, University of York, United Kingdom; Institute of Public Health and Social Sciences, Khyber Medical University, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jennings</LastName><ForeName>Hannah Maria</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, University of York, United Kingdom; Hull York Medical School, York, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anas</LastName><ForeName>Ashraful</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre for Health Research and Implementation, Diabetic Association of Bangladesh, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shaha</LastName><ForeName>Sanjit K</ForeName><Initials>SK</Initials><AffiliationInfo><Affiliation>Centre for Health Research and Implementation, Diabetic Association of Bangladesh, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jahan</LastName><ForeName>Kazi Moriom</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>Centre for Health Research and Implementation, Diabetic Association of Bangladesh, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kuddus</LastName><ForeName>Abdul</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre for Health Research and Implementation, Diabetic Association of Bangladesh, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nisar</LastName><ForeName>Zara</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Institute of Public Health and Social Sciences, Khyber Medical University, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Walker</LastName><ForeName>Simon M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Centre for Health Economics, University of York, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Naz</LastName><ForeName>Anum</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute of Psychiatry, Rawalpindi Medical University, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shakoor</LastName><ForeName>Hira</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Institute of Public Health and Social Sciences, Khyber Medical University, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Niazi</LastName><ForeName>Asima K</ForeName><Initials>AK</Initials><AffiliationInfo><Affiliation>Baqai Institute of Diabetes and Endocrinology(BIDE), Karachi, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jacobs</LastName><ForeName>Rowena</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Centre for Health Economics, University of York, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Coales</LastName><ForeName>Karen</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, University of York, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Azad</LastName><ForeName>Kishwar</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Centre for Health Research and Implementation, Diabetic Association of Bangladesh, Bangladesh.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fottrell</LastName><ForeName>Edward</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institute for Global Health, University College London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Haq</LastName><ForeName>Zia Ul</ForeName><Initials>ZU</Initials><AffiliationInfo><Affiliation>Institute of Public Health and Social Sciences, Khyber Medical University, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ekers</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, University of York, United Kingdom; Tees Esk and Wear Valleys NHS Foundation Trust, York, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Siddiqi</LastName><ForeName>Najma</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, University of York, United Kingdom; Hull York Medical School, York, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hewitt</LastName><ForeName>Catherine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Health Sciences, York, Trials Unit, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>DiaDeM Global Health Research Group</CollectiveName></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>J Affect Disord</MedlineTA><NlmUniqueID>7906073</NlmUniqueID><ISSNLinking>0165-0327</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005240" MajorTopicYN="Y">Feasibility Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003863" MajorTopicYN="N">Depression</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001459" MajorTopicYN="N" Type="Geographic">Bangladesh</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010154" MajorTopicYN="N" Type="Geographic">Pakistan</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001521" MajorTopicYN="N">Behavior Therapy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010342" MajorTopicYN="N">Patient Acceptance of Health Care</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>14</Day><Hour>0</Hour><Minute>20</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>19</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39647587</ArticleId><ArticleId IdType="doi">10.1016/j.jad.2024.11.079</ArticleId><ArticleId IdType="pii">S0165-0327(24)01970-0</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39647240</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-1983</ISSN><JournalIssue CitedMedium="Internet"><Volume>44</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Clinical nutrition (Edinburgh, Scotland)</Title><ISOAbbreviation>Clin Nutr</ISOAbbreviation></Journal><ArticleTitle>Beyond fat: Does semaglutide affect lean mass?</ArticleTitle><Pagination><StartPage>104</StartPage><EndPage>108</EndPage><MedlinePgn>104-108</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.clnu.2024.12.004</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0261-5614(24)00445-X</ELocationID><Abstract><AbstractText>This opinion paper aims to discuss the influence of semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), on lean mass beyond its impact on weight loss. Although significant weight loss is achieved with semaglutide, the impact of this drug on lean mass remains controversial. Several investigations have demonstrated that semaglutide-induced weight loss is linked to decreases in lean mass as well as fat mass; on the other hand, the ratio of lean mass to total body mass rises. Nevertheless, larger clinical trials have reported converse findings and significant reductions in lean mass following treatment with semaglutide. This disparity in research findings emphasizes the necessity for additional studies on this subject because semaglutide use is rising quickly.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jamialahmadi</LastName><ForeName>Tannaz</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eid</LastName><ForeName>Ali H</ForeName><Initials>AH</Initials><AffiliationInfo><Affiliation>Department of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gadde</LastName><ForeName>Kishore M</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>Department of Surgery, University of California Irvine Medical Center, Orange, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Almahmeed</LastName><ForeName>Wael</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Heart and Vascular Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kroh</LastName><ForeName>Matthew</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, OH, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al Zein</LastName><ForeName>Mohammad</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Faculty of Medical Sciences, Lebanese University, Hadath, Beirut, Lebanon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sahebkar</LastName><ForeName>Amirhossein</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Center for Global Health Research, Saveetha Medical College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: amir_saheb2000@yahoo.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Clin Nutr</MedlineTA><NlmUniqueID>8309603</NlmUniqueID><ISSNLinking>0261-5614</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>53AXN4NNHX</RegistryNumber><NameOfSubstance UI="C000591245">semaglutide</NameOfSubstance></Chemical><Chemical><RegistryNumber>62340-29-8</RegistryNumber><NameOfSubstance UI="D004763">Glucagon-Like Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000067757">Glucagon-Like Peptide-1 Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D004763" MajorTopicYN="Y">Glucagon-Like Peptides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015431" MajorTopicYN="Y">Weight Loss</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000067757" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001823" MajorTopicYN="Y">Body Composition</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000273" MajorTopicYN="N">Adipose Tissue</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Body composition</Keyword><Keyword MajorTopicYN="N">Glucagon-like peptide-1 receptor agonist</Keyword><Keyword MajorTopicYN="N">Lean mass</Keyword><Keyword MajorTopicYN="N">Semaglutide</Keyword></KeywordList><CoiStatement>Conflict of interest The authors have no competing interests to disclose.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>7</Day><Hour>0</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>9</Day><Hour>0</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>18</Hour><Minute>2</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39647240</ArticleId><ArticleId IdType="doi">10.1016/j.clnu.2024.12.004</ArticleId><ArticleId IdType="pii">S0261-5614(24)00445-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39645620</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>08</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1788-6120</ISSN><JournalIssue CitedMedium="Internet"><Volume>165</Volume><Issue>49</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>08</Day></PubDate></JournalIssue><Title>Orvosi hetilap</Title><ISOAbbreviation>Orv Hetil</ISOAbbreviation></Journal><ArticleTitle>[Drug repositioning and its aspects in clinical diabetology].</ArticleTitle><Pagination><StartPage>1919</StartPage><EndPage>1926</EndPage><MedlinePgn>1919-1926</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1556/650.2024.33177</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pokoly</LastName><ForeName>Bence</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>1 Országos Mozgásszervi Intézet - Országos Reumatológiai és Fizioterápiás Intézet Budapest, Frankel Leó út 25-29., 1023 Magyarország.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>2 Szent Margit Kórház Budapest Magyarország.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Somogyi</LastName><ForeName>Anikó</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>3 Semmelweis Egyetem, Általános Orvostudományi Kar, Belgyógyászati és Hematológiai Klinika Budapest Magyarország.</Affiliation></AffiliationInfo></Author></AuthorList><Language>hun</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>A gyógyszer-repozicionálás és klinikai diabetológiai vonatkozásai.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>Hungary</Country><MedlineTA>Orv Hetil</MedlineTA><NlmUniqueID>0376412</NlmUniqueID><ISSNLinking>0030-6002</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058492" MajorTopicYN="Y">Drug Repositioning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="N">Diabetes Mellitus</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="hun"><AbstractText>A gyógyszer-repozicionálás a gyógyszerfejlesztés különleges, mind gyakrabban alkalmazott útja. Az eljárás eredményeként bizonyos betegségek kezelésére már forgalomba került, illetve a fejlesztés különböző fázisaiban található gyógyszereket, hatóanyagokat új, az eredetitől néha teljesen eltérő indikációval kezdenek sikerrel használni. A közlemény első felében e folyamatról adunk rövid áttekintést, vázoljuk előnyeit és lehetséges buktatóit. Az általános bevezető részt követően számba vesszük a korábban antidiabetikumként forgalomba került gyógyszerek újabb sikeres alkalmazási területeit, majd megemlítünk néhány olyan készítményt, amely mára a diabetes mellitus kezelésében is felhasználhatóvá vált, időközben felismert számottevőbb vércukorszint-csökkentő tulajdonságai révén. Orv Hetil. 2024; 165(49): 1919–1926.</AbstractText></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">diabetes mellitus</Keyword><Keyword MajorTopicYN="N">drug repositioning</Keyword><Keyword MajorTopicYN="N">gyógyszer-repozicionálás</Keyword><Keyword MajorTopicYN="N">terápia</Keyword><Keyword MajorTopicYN="N">treatment</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>9</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>12</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>12</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>11</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39645620</ArticleId><ArticleId IdType="doi">10.1556/650.2024.33177</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39645259</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>23</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>10</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1468-3296</ISSN><JournalIssue CitedMedium="Internet"><Volume>80</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>23</Day></PubDate></JournalIssue><Title>Thorax</Title><ISOAbbreviation>Thorax</ISOAbbreviation></Journal><ArticleTitle>Comparative estimate of glucose-lowering therapies on risk of incident pneumonia and severe sepsis: an analysis of real-world cohort data.</ArticleTitle><Pagination><StartPage>32</StartPage><EndPage>41</EndPage><MedlinePgn>32-41</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e221906</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/thorax-2024-221906</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are treatments for type 2 diabetes (T2D). Beyond glucose-lowering and cardiorenal protection, these drugs may protect against pneumonia and sepsis.</AbstractText><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">This study assesses the impact of SGLT2i and GLP-1 RAs on the risk of incident pneumonia and severe sepsis.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A retrospective cohort study was conducted using anonymised electronic medical records from TriNetX, a global federated database. Two intention-to-treat analyses were performed, each with two cohorts of adult T2D patients. The first analysis compared individuals prescribed SGLT2i, and the second individuals prescribed GLP-1 RAs, with those prescribed dipeptidyl peptidase-4 inhibitors (DPP-4i). An active comparator new user design was used, with outcomes defined as time-to-incident pneumonia and severe sepsis. Propensity score matching (1:1) was applied to control for potential confounders, and patients were followed for 12 months. Secondary analyses compared SGLT2i and GLP-1 RAs against other glucose-lowering therapies.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">After propensity score matching, 352 687 patients were included in the SGLT2i versus DPP-4i comparison. SGLT2i treatment was associated with a risk reduction in incident pneumonia (HR 0.75 (95% CI 0.73, 0.78)) and severe sepsis (0.75 (0.73, 0.77)). In the GLP-1 RA versus DPP-4i comparison, 331 863 patients were included. GLP-1 RA treatment was associated with a risk reduction in incident pneumonia (0.60 (0.58, 0.62)) and severe sepsis (0.61 (0.59, 0.63)).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">SGLT2i and GLP-1 RAs are associated with a reduced risk of incident pneumonia and severe sepsis in patients with T2D. Further research and focused randomised controlled trials are warranted to explore the broader clinical implications of these treatments.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2025. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ Group.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Henney</LastName><ForeName>Alex E</ForeName><Initials>AE</Initials><Identifier Source="ORCID">0000-0002-8066-9470</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riley</LastName><ForeName>David R</ForeName><Initials>DR</Initials><Identifier Source="ORCID">0000-0002-0905-6524</Identifier><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hydes</LastName><ForeName>Theresa J</ForeName><Initials>TJ</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anson</LastName><ForeName>Matthew</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ibarburu</LastName><ForeName>Gema H</ForeName><Initials>GH</Initials><AffiliationInfo><Affiliation>TriNetX LLC, Cambridge, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frost</LastName><ForeName>Frederick</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Liverpool Heart and Chest Hospital NHS Foundation Trust, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alam</LastName><ForeName>Uazman</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, University of Liverpool, Liverpool, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cuthbertson</LastName><ForeName>Daniel J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Metabolic Medicine, University of Liverpool, Liverpool, UK dan.cuthbertson@liverpool.ac.uk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Thorax</MedlineTA><NlmUniqueID>0417353</NlmUniqueID><ISSNLinking>0040-6376</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>doi: 10.1136/thorax-2024-222540</RefSource></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018805" MajorTopicYN="Y">Sepsis</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011014" MajorTopicYN="Y">Pneumonia</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054873" MajorTopicYN="Y">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Bacterial Infection</Keyword><Keyword MajorTopicYN="N">Clinical Epidemiology</Keyword><Keyword MajorTopicYN="N">Infection Control</Keyword><Keyword MajorTopicYN="N">Pneumonia</Keyword><Keyword MajorTopicYN="N">Respiratory Infection</Keyword></KeywordList><CoiStatement>Competing interests: MA receives a fellowship from the Novo Nordisk UK research foundation and JDRF. DJJC has received investigator-initiated grants from Astra Zeneca and Novo Nordisk, support for education from Perspectum with any financial remuneration from pharmaceutical company consultation made to the University of Liverpool. GHI is an employee of TriNetX LLC. UA has received honoraria from Procter & Gamble, Viatris, Grunenthal and Sanofi for educational meetings and funding for attendance at an educational meeting from Diiachi Sankyo. UA has also received investigator-led funding from Procter & Gamble and is a council member of the Royal Society of Medicine’s Vascular, Lipid & Metabolic Medicine Section. All other authors declare that there are no financial relationships or activities that might bias, or be perceived to bias, their contribution to this manuscript.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>5</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>24</Day><Hour>0</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>11</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>20</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>27</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39645259</ArticleId><ArticleId IdType="pmc">PMC11671942</ArticleId><ArticleId IdType="doi">10.1136/thorax-2024-221906</ArticleId><ArticleId IdType="pii">thorax-2024-221906</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Anderson R, Feldman C. 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This study will be conducted as part of the Diabetes Alliance Program Plus (DAP+), a large-scale integrated health service intervention in a large health district in Australia. The ecofit program has previously demonstrated efficacy and effectiveness in insufficiently active people with (or at risk of) T2D and community dwelling-adults, respectively. The aim of this study is to assess the reach (primary outcome), adoption, appropriateness, feasibility and fidelity of the implementation of ecofit and the overall effectiveness of the intervention.</AbstractText><AbstractText Label="RESEARCH DESIGN AND METHODS" NlmCategory="METHODS">Prospective participants are adults diagnosed with T2D, who attend primary care settings enrolled in DAP+, and are identified and referred to ecofit by a primary care clinician. To support the implementation of ecofit a host of strategies will be utilised, which includes the education and upskilling of primary care clinicians enrolled in DAP+ using brief training sessions, the supply of an information package and access to professional development. The co-primary outcomes of reach will be defined as the number of participant registrations on the ecofit platform and the number of primary care clinicians who have been introduced to ecofit.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">This study will evaluate the implementation of ecofit among adults with T2D within the primary care setting. The results may help improve T2D lifestyle interventions in primary care settings across Australia.</AbstractText><CopyrightInformation>Copyright © 2024. Published by Elsevier Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jansson</LastName><ForeName>Anna K</ForeName><Initials>AK</Initials><AffiliationInfo><Affiliation>Centre for Active Living and Learning, School of Education, University of Newcastle, Callaghan, NSW, Australia; Active Living and Learning Research Program, Hunter Medical Research Institute, New Lambton Heights, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Beacroft</LastName><ForeName>Sam</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Centre for Active Living and Learning, School of Education, University of Newcastle, Callaghan, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duncan</LastName><ForeName>Mitch J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Centre for Active Living and Learning, School of Education, University of Newcastle, Callaghan, NSW, Australia; Active Living and Learning Research Program, Hunter Medical Research Institute, New Lambton Heights, NSW, Australia; School of Medicine and Public Health, University of Newcastle, Callaghan, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cox</LastName><ForeName>Emily R</ForeName><Initials>ER</Initials><AffiliationInfo><Affiliation>Centre for Active Living and Learning, School of Education, University of Newcastle, Callaghan, NSW, Australia; Active Living and Learning Research Program, Hunter Medical Research Institute, New Lambton Heights, NSW, Australia; School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robards</LastName><ForeName>Sara L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Centre for Active Living and Learning, School of Education, University of Newcastle, Callaghan, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferris</LastName><ForeName>Wendy</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Centre for Active Living and Learning, School of Education, University of Newcastle, Callaghan, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hure</LastName><ForeName>Alexis</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>School of Medicine and Public Health, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute, Kookaburra Circuit, New Lambton Heights, Newcastle, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Acharya</LastName><ForeName>Shamasunder</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>School of Medicine and Public Health, University of Newcastle, Callaghan, NSW, Australia; Hunter New England Local Health District, John Hunter Hospital, New Lambton Heights, Newcastle, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Plotnikoff</LastName><ForeName>Ronald C</ForeName><Initials>RC</Initials><AffiliationInfo><Affiliation>Centre for Active Living and Learning, School of Education, University of Newcastle, Callaghan, NSW, Australia; Active Living and Learning Research Program, Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. Electronic address: ron.plotnikoff@newcastle.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D000078325">Clinical Trial Protocol</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Contemp Clin Trials</MedlineTA><NlmUniqueID>101242342</NlmUniqueID><ISSNLinking>1551-7144</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001315" MajorTopicYN="N" Type="Geographic">Australia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="Y">Exercise</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006293" MajorTopicYN="N">Health Promotion</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011320" MajorTopicYN="Y">Primary Health Care</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012017" MajorTopicYN="N">Referral and Consultation</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012424" MajorTopicYN="N">Rural Population</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017216" MajorTopicYN="Y">Telemedicine</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000068456" MajorTopicYN="N">Clinical Studies as Topic</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Physical activity</Keyword><Keyword MajorTopicYN="N">Primary care</Keyword><Keyword MajorTopicYN="N">Resistance training</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword><Keyword MajorTopicYN="N">mHealth</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>7</Day><Hour>0</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>11</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>19</Hour><Minute>15</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39645032</ArticleId><ArticleId IdType="doi">10.1016/j.cct.2024.107774</ArticleId><ArticleId IdType="pii">S1551-7144(24)00357-4</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39644731</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>26</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-0334</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><Issue>11-12</Issue><PubDate><Year>2024</Year><Season>Nov-Dec</Season></PubDate></JournalIssue><Title>Diabetes & metabolic syndrome</Title><ISOAbbreviation>Diabetes Metab Syndr</ISOAbbreviation></Journal><ArticleTitle>The mediating role of the food environment, greenspace, and walkability in the association between socioeconomic position and type 2 diabetes - The Maastricht Study.</ArticleTitle><Pagination><StartPage>103155</StartPage><MedlinePgn>103155</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.dsx.2024.103155</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1871-4021(24)00216-9</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">This study investigates the interplay between socioeconomic position (SEP), the residential food environment, walkability, greenspace, and type 2 diabetes (T2D), particularly whether the environmental factors mediate the association between SEP and T2D.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">SEP, T2D status, residential Food Environment Healthiness Index (FEHI), number of fast-food outlets (FF), walkability index (WI), and proportion of greenspace (GS) were ascertained in 9188 participants. The associations between SEP, the environment and T2D were modeled with logistic regression and survival analysis. The proportion of mediation of the association between SEP and T2D was estimated with causal mediation analysis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Lower SEP was associated with higher risk of T2D. Hazard ratios (HR) were 2.03 (95 % CI 1.60-2.58), 1.79 (1.40-2.30) and 1.77 (1.21-2.58) for an interquartile range decrease (IQR) of education, income, and occupation, respectively. HRs for IQR changes of the environmental factors were: FEHI 1.20 (1.00-1.43), FF 0.87 (0.76-0.99), WI 1.23 (0.95-1.58) and GS 1.16 (0.96-1.43). Regression on prevalent T2D yielded similar results. Lower socioeconomic position was associated with a less healthy environment (e.g., FEHI -0.10 (-0.12--0.07) for education). Environmental exposures mediated between 0.1 % (-0.7-0.9) and 2.6 % (0.4-5.2) of the cross-sectional associations and 0.3 % (-8.6-8.6) and 8.5 % (2.3-27.4) of the longitudinal associations.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">People with lower SEP had higher risk and prevalence of T2D and lived in a slightly less healthy residential environment. The association between SEP and T2D is not strongly mediated by FEHI, FF, WI, or GS.</AbstractText><CopyrightInformation>Copyright © 2024 Research Trust of DiabetesIndia (DiabetesIndia) and National Diabetes Obesity and Cholesterol Foundation (N-DOC). Published by Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Albers</LastName><ForeName>Jeroen D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Department of Social Medicine, Maastricht University, Maastricht, the Netherlands; Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands. Electronic address: j.albers@maastrichtuniversity.nl.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koster</LastName><ForeName>Annemarie</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Social Medicine, Maastricht University, Maastricht, the Netherlands; Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sezer</LastName><ForeName>Bengisu</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Social Medicine, Maastricht University, Maastricht, the Netherlands; Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meisters</LastName><ForeName>Rachelle</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Social Medicine, Maastricht University, Maastricht, the Netherlands; Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schram</LastName><ForeName>Miranda T</ForeName><Initials>MT</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; MHeNS School for Mental Health and Neuroscience, Maastricht University and Heart and Vascular Center, Maastricht University Medical Center+, Maastricht, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eussen</LastName><ForeName>Simone J P M</ForeName><Initials>SJPM</Initials><AffiliationInfo><Affiliation>Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; Department of Epidemiology, Maastricht University, Maastricht, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dukers</LastName><ForeName>Nicole H T M</ForeName><Initials>NHTM</Initials><AffiliationInfo><Affiliation>Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands; Department of Health Promotion, Maastricht University, Maastricht, the Netherlands and Sexual Health, Infectious Diseases and Environmental Health, Public Health Service South Limburg, Heerlen, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jansen</LastName><ForeName>Maria W J</ForeName><Initials>MWJ</Initials><AffiliationInfo><Affiliation>Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands; Living Lab Public Health Limburg, Public Health Service South Limburg, Heerlen, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stehouwer</LastName><ForeName>Coen D A</ForeName><Initials>CDA</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lakerveld</LastName><ForeName>Jeroen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Epidemiology and Data Science, Amsterdam University Medical Centers,Vrije Universiteit Amsterdam and Amsterdam Public Health, Health Behaviours and Chronic Diseases, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bosma</LastName><ForeName>Hans</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Social Medicine, Maastricht University, Maastricht, the Netherlands; Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Diabetes Metab Syndr</MedlineTA><NlmUniqueID>101462250</NlmUniqueID><ISSNLinking>1871-4021</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016138" MajorTopicYN="Y">Walking</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012111" MajorTopicYN="N">Residence Characteristics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012959" MajorTopicYN="N">Socioeconomic Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012923" MajorTopicYN="N">Social Class</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000091542" MajorTopicYN="N">Neighborhood Characteristics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Food environment</Keyword><Keyword MajorTopicYN="N">Greenspace</Keyword><Keyword MajorTopicYN="N">Socioeconomic position</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword><Keyword MajorTopicYN="N">Walkability</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>2</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>27</Day><Hour>0</Hour><Minute>20</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>11</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>18</Hour><Minute>6</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39644731</ArticleId><ArticleId IdType="doi">10.1016/j.dsx.2024.103155</ArticleId><ArticleId IdType="pii">S1871-4021(24)00216-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39644730</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>26</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-0334</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><Issue>11-12</Issue><PubDate><Year>2024</Year><Season>Nov-Dec</Season></PubDate></JournalIssue><Title>Diabetes & metabolic syndrome</Title><ISOAbbreviation>Diabetes Metab Syndr</ISOAbbreviation></Journal><ArticleTitle>Machine learning algorithms mimicking specialists decision making on initial treatment for people with type 2 diabetes mellitus in Japan diabetes data management study (JDDM76).</ArticleTitle><Pagination><StartPage>103168</StartPage><MedlinePgn>103168</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.dsx.2024.103168</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1871-4021(24)00229-7</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To evaluate whether typical machine learning models that mimic specialists' care can successfully reproduce information, not only on whether to prescribe medications but also which hypoglycemic agents to prescribe as initial treatment for type 2 diabetes.</AbstractText><AbstractText Label="RESEARCH DESIGN AND METHODS" NlmCategory="METHODS">A medical records database containing prescriptions for medications for 16,005 patients who visited a diabetologist's office for the first time was utilized to train five typical machine learning models as well-as a model used for logistic analysis. Prescribed were no medications (diet and exercise therapy), insulin, biguanides (BG), sulfonylureas (SU), dipeptidyl peptidase-4 inhibitors (DPP-4I), alpha-glucosidase inhibitors (α-GI) or glinides. Models were compared based on the F1 score and ROC/AUC scores.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">XGBoost, which splits decision-making into three sections, was the top performing model (42 % accuracy) among five models and conventional logistic regression (35 % accuracy). The second highest scoring model was Support Vector Machines, which had an accuracy of 40 %. When using XGBoost to compare decisions on no medication needed vs. needing medication the AUC was 0.96. Insulin vs. oral medications had an AUC of 0.78. With all remaining oral medications removed, the AUC was 0.76.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Among the five models investigated, XGBoost outperformed the other machine learning models examined as well as the traditional logistic model, suggesting that its accuracy had the potential to assist non-specialists in decision-making regarding treatment of patients with type 2 diabetes in the future.</AbstractText><CopyrightInformation>Copyright © 2024 Research Trust of DiabetesIndia (DiabetesIndia) and National Diabetes Obesity and Cholesterol Foundation (N-DOC). Published by Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Price</LastName><ForeName>Jenny Elizabeth</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Graduate School of Science and Technology, Niigata University, Niigata, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fujihara</LastName><ForeName>Kazuya</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Hematology, Endocrinology and Metabolism, University Faculty of Medicine, Niigata, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kodama</LastName><ForeName>Satoru</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Hematology, Endocrinology and Metabolism, University Faculty of Medicine, Niigata, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamazaki</LastName><ForeName>Katsuya</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Kawai Clinic, Tsukuba, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maegawa</LastName><ForeName>Hiroshi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Medicine, Shiga University of Medical Science, Shiga, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamazaki</LastName><ForeName>Tatsuya</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Faculty of Engineering, Niigata University, Niigata, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sone</LastName><ForeName>Hirohito</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Hematology, Endocrinology and Metabolism, University Faculty of Medicine, Niigata, Japan. Electronic address: sone@med.niigata-u.ac.jp.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>Japan Diabetes Clinical Data Management Study Group (JDDM study group)</CollectiveName></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Diabetes Metab Syndr</MedlineTA><NlmUniqueID>101462250</NlmUniqueID><ISSNLinking>1871-4021</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069550" MajorTopicYN="Y">Machine Learning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007564" MajorTopicYN="N" Type="Geographic">Japan</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000465" MajorTopicYN="N">Algorithms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003657" MajorTopicYN="N">Decision Making</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013038" MajorTopicYN="N">Specialization</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes specialists</Keyword><Keyword MajorTopicYN="N">Initial therapy</Keyword><Keyword MajorTopicYN="N">Machine learning</Keyword><Keyword MajorTopicYN="N">Patterns of usage</Keyword><Keyword MajorTopicYN="N">XGBoost</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that there is no duality of interest associated with this manuscript.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>1</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>27</Day><Hour>0</Hour><Minute>20</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>10</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>18</Hour><Minute>6</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39644730</ArticleId><ArticleId IdType="doi">10.1016/j.dsx.2024.103168</ArticleId><ArticleId IdType="pii">S1871-4021(24)00229-7</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39644661</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>08</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-7072</ISSN><JournalIssue CitedMedium="Internet"><Volume>467</Volume><PubDate><Year>2025</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>Food chemistry</Title><ISOAbbreviation>Food Chem</ISOAbbreviation></Journal><ArticleTitle>Chemical characterization and DPP IV inhibitory capacity of purified adzuki bean β-vignin digest in comparison to soybean β-conglycinin and in vitro effect of β-vignin on diabetic-related outcomes.</ArticleTitle><Pagination><StartPage>142285</StartPage><MedlinePgn>142285</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.foodchem.2024.142285</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0308-8146(24)03935-9</ELocationID><Abstract><AbstractText>Adzuki bean (AB) is a legume with a low glycemic index and is traditionally used in Asian cultures to modulate type 2 diabetes (T2D). Our objectives were to characterize the functional peptides from purified AB β-vignin after simulated gastrointestinal digestion in comparison to soybean β-conglycinin, to evaluate their DPP IV inhibitory capacity, and to determine in vitro the effect of digested AB β-vignin on diabetic-related outcomes using HepG2 cells in healthy and insulin-resistant states. Five peptides (215-742 Da) from AB β-vignin and five peptides (215-447 Da) from β-conglycinin were identified to exhibit bioactivity as DPP IV inhibitors. Molecular docking demonstrated peptides could bind to DPP IV at the same binding site as a diabetic medication, linagliptin. Digested AB β-vignin significantly increased (p < 0.05) hepatic glucose uptake (> 290 %) via DPP IV inhibition (> 40 %) in healthy and insulin-resistant states. IRS-1, Akt-1, and Glut 2 increased after treating cells with digested AB β-vignin in healthy and insulin-resistant states.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kwan</LastName><ForeName>Shu Hang</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Champaign, IL 61801, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Esteves</LastName><ForeName>Frida</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Champaign, IL 61801, USA; Tecnologico de Monterrey, Monterrey, Mexico.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Davis</LastName><ForeName>Emily</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, Champaign, IL 61801, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gonzalez de Mejia</LastName><ForeName>Elvira</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Champaign, IL 61801, USA; Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, Champaign, IL 61801, USA. Electronic address: edemejia@illinois.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Food Chem</MedlineTA><NlmUniqueID>7702639</NlmUniqueID><ISSNLinking>0308-8146</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005916">Globulins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C013894">beta-conglycinin protein, Glycine max</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D055314">Seed Storage Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D030262">Soybean Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber><NameOfSubstance UI="D018819">Dipeptidyl Peptidase 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D052179">Antigens, Plant</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005916" MajorTopicYN="Y">Globulins</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055314" MajorTopicYN="Y">Seed Storage Proteins</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D030262" MajorTopicYN="Y">Soybean Proteins</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018819" MajorTopicYN="Y">Dipeptidyl Peptidase 4</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056945" MajorTopicYN="N">Hep G2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054873" MajorTopicYN="Y">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052179" MajorTopicYN="Y">Antigens, Plant</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D062105" MajorTopicYN="N">Molecular Docking Simulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004063" MajorTopicYN="N">Digestion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000070658" MajorTopicYN="N">Vigna</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013025" MajorTopicYN="N">Glycine max</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adzuki bean β-vignin</Keyword><Keyword MajorTopicYN="N">Antidiabetic potential</Keyword><Keyword MajorTopicYN="N">Dipeptidyl peptidase IV inhibition</Keyword><Keyword MajorTopicYN="N">Glucose uptake</Keyword><Keyword MajorTopicYN="N">Insulin resistance</Keyword><Keyword MajorTopicYN="N">Vigna angularis</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>8</Day><Hour>6</Hour><Minute>20</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>11</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>18</Hour><Minute>4</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39644661</ArticleId><ArticleId IdType="doi">10.1016/j.foodchem.2024.142285</ArticleId><ArticleId IdType="pii">S0308-8146(24)03935-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39644538</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-460X</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of diabetes and its complications</Title><ISOAbbreviation>J Diabetes Complications</ISOAbbreviation></Journal><ArticleTitle>Hepatic effects of GLP-1 mimetics in diabetic milieu: A mechanistic review of involved pathways.</ArticleTitle><Pagination><StartPage>108928</StartPage><MedlinePgn>108928</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jdiacomp.2024.108928</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1056-8727(24)00254-X</ELocationID><Abstract><AbstractText>Patients with diabetic are at a higher risk of developing hepatic disorders compared to non-diabetic individuals. This increased risk can be attributed to the diabetic environment, which triggers and exacerbates harmful pathways involved in both diabetic complications and hepatic disorders. Therefore, it is important to consider the use of antidiabetic agents that offer benefits beyond glycemic control and have positive effects on liver tissues. Glucagon-like peptide-1 (GLP-1) mimetics are a novel class of antidiabetic medications known for their potent blood sugar-lowering effects. Emerging evidence suggests that these drugs also have favorable effects on the liver. However, the precise effects and underlying mechanisms are not yet fully understood. In this review, we aim to provide a mechanistic perspective on the liver benefits of GLP-1 mimetics and outline the mediating mechanisms involved.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yaribeygi</LastName><ForeName>Habib</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran. Electronic address: habib.yari@yahoo.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kashian</LastName><ForeName>Kiana</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Student Research Committee, Semnan University of Medical Sciences, Semnan, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moghaddam</LastName><ForeName>Kimia Imani</ForeName><Initials>KI</Initials><AffiliationInfo><Affiliation>Student Research Committee, Semnan University of Medical Sciences, Semnan, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karim</LastName><ForeName>Sheida Rashmeh</ForeName><Initials>SR</Initials><AffiliationInfo><Affiliation>Student Research Committee, Semnan University of Medical Sciences, Semnan, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bagheri</LastName><ForeName>Narges</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Student Research Committee, Semnan University of Medical Sciences, Semnan, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karav</LastName><ForeName>Sercan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Molecular Biology and Genetics, Canakkale Onsekiz Mart University, Canakkale 17100, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jamialahmadi</LastName><ForeName>Tannaz</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rizzo</LastName><ForeName>Manfredi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Medicine, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (Promise), University of Palermo, Italy; Department of Biochemistry, Mohamed Bin Rashid University, Dubai, United Arab Emirates.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sahebkar</LastName><ForeName>Amirhossein</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Center for Global Health Research, Saveetha Medical College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: amir_Saheb2000@yahoo.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Diabetes Complications</MedlineTA><NlmUniqueID>9204583</NlmUniqueID><ISSNLinking>1056-8727</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>89750-14-1</RegistryNumber><NameOfSubstance UI="D052216">Glucagon-Like Peptide 1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052216" MajorTopicYN="Y">Glucagon-Like Peptide 1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="Y">Liver</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008107" MajorTopicYN="N">Liver Diseases</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048909" MajorTopicYN="N">Diabetes Complications</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes mellitus</Keyword><Keyword MajorTopicYN="N">GLP-1</Keyword><Keyword MajorTopicYN="N">Hepatic disorder</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Liver</Keyword><Keyword MajorTopicYN="N">NAFLD</Keyword><Keyword MajorTopicYN="N">Oxidative stress</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that have no conflict of interest in this study.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>11</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>18</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39644538</ArticleId><ArticleId IdType="doi">10.1016/j.jdiacomp.2024.108928</ArticleId><ArticleId IdType="pii">S1056-8727(24)00254-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39644537</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-460X</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of diabetes and its complications</Title><ISOAbbreviation>J Diabetes Complications</ISOAbbreviation></Journal><ArticleTitle>Glucagon-like Peptide-1 receptor agonists versus dipeptidyl-peptidase 4 inhibitors in advanced chronic kidney disease and end stage kidney disease: Real world effectiveness and persistence of therapy.</ArticleTitle><Pagination><StartPage>108925</StartPage><MedlinePgn>108925</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jdiacomp.2024.108925</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1056-8727(24)00251-4</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Atherosclerotic cardiovascular disease is the leading cause of death in people with type 2 diabetes (T2D) and chronic kidney disease (CKD) or end-stage kidney disease (ESKD). Glucagon-Like Peptide-1 receptor agonists (GLP-1RA) reduce cardiovascular events, improve glycemic control, promote weight loss, and slow progression of nephropathy. Despite these benefits and professional society treatment guidelines recommendations, GLP-1RAs remain under-utilized in people with advanced CKD and ESKD due to tolerability and safety concerns.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We conducted a retrospective cohort study comparing clinical outcomes and medication use details after initiating GLP-1RA or dipeptidyl-peptidase 4 inhibitor (DPP-4i) in people with T2D and advanced CKD or ESKD. Eligible patients were identified via electronic health record query with extraction of baseline demographics, vital signs, and laboratory values. A manual chart review was undertaken to confirm eligibility, medication use, and extract a detailed account of all side effects.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">A total of 236 eligible patients (149 in the GLP-1RA group and 87 in the DPP-4i group) were identified. The average duration of treatment was 1036 (±909.9) and 1109 (±1090.9) days for GLP-1RA and DPP-4i, respectively. The average percentage weight loss from baseline to 36 months of treatment in the GLP-1RA group was -9.6 % (95 % CI, -11.3 to -7.8) versus -2.4 % (95 % CI, -5.4 to 0.5) in the DPP-4i group (estimated treatment difference (ETD) -7.1 (95 % CI, -10.6 to -3.7) percentage-points, p < 0.001). The change in HbA1c from baseline to 36 months of treatment was significantly greater in the GLP-1RA (-1.0 %) compared with the DPP-4i group (0.2 %) (ETD -1.2 (95 % CI, -2.1 to -0.3) percentage-points, p = 0.04).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">In patients with T2D and advanced CKD or ESKD, treatment with GLP-1RAs in a real-world setting had long treatment persistence, and compared to DPP-4is, was associated with greater weight loss and glycemic improvement.</AbstractText><CopyrightInformation>Published by Elsevier Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sidra</LastName><ForeName>F N U</ForeName><Initials>FNU</Initials><AffiliationInfo><Affiliation>Division of Endocrinology, Dept of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Agarwal</LastName><ForeName>Shubham</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Endocrinology, Dept of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA. Electronic address: shubhamagarwaldr@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lockhart Pastor</LastName><ForeName>Paola</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Division of Endocrinology, Dept of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Donglu</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xilong</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Peter O'Donnell Jr. School of Public Health, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lingvay</LastName><ForeName>Ildiko</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Division of Endocrinology, Dept of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA; Peter O'Donnell Jr. School of Public Health, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Diabetes Complications</MedlineTA><NlmUniqueID>9204583</NlmUniqueID><ISSNLinking>1056-8727</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054873" MajorTopicYN="Y">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007676" MajorTopicYN="Y">Kidney Failure, Chronic</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="Y">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003928" MajorTopicYN="Y">Diabetic Nephropathies</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000099059" MajorTopicYN="N">Assessment of Medication Adherence</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Advanced CKD</Keyword><Keyword MajorTopicYN="N">DPP-4i</Keyword><Keyword MajorTopicYN="N">Dialysis</Keyword><Keyword MajorTopicYN="N">ESKD</Keyword><Keyword MajorTopicYN="N">GLP-1RA</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Donglu Xie reports financial support was provided by National Center for Advancing Translational Sciences. Ildiko Lingvay reports a relationship with Novo Nordisk that includes: consulting or advisory and funding grants. Ildiko Lingvay reports a relationship with Sanofi that includes: consulting or advisory and funding grants. Ildiko Lingvay reports a relationship with Merck that includes: consulting or advisory and funding grants. Ildiko Lingvay reports a relationship with Pfizer that includes: consulting or advisory and funding grants. Ildiko Lingvay reports a relationship with Mylan that includes: consulting or advisory and funding grants. Ildiko Lingvay reports a relationship with Boehringer Ingelheim that includes: consulting or advisory and funding grants. Ildiko Lingvay reports a relationship with Eli Lilly that includes: consulting or advisory. Ildiko Lingvay reports a relationship with AstraZeneca that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Janssen that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Intercept that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Intarcia that includes: consulting or advisory. Ildiko Lingvay reports a relationship with TargetPharma that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Novartis that includes: consulting or advisory. Ildiko Lingvay reports a relationship with GI Dynamics that includes: consulting or advisory. Ildiko Lingvay reports a relationship with MannKind that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Valeritas that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Carmot that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Zealand Pharma that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Shionogi that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Mediflix that includes: consulting or advisory. Ildiko Lingvay reports a relationship with Bayer that includes: consulting or advisory. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>11</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>18</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39644537</ArticleId><ArticleId IdType="doi">10.1016/j.jdiacomp.2024.108925</ArticleId><ArticleId IdType="pii">S1056-8727(24)00251-4</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39644303</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>07</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0869-866X</ISSN><JournalIssue CitedMedium="Print"><Volume>32</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Problemy sotsial'noi gigieny, zdravookhraneniia i istorii meditsiny</Title><ISOAbbreviation>Probl Sotsialnoi Gig Zdravookhranenniiai Istor Med</ISOAbbreviation></Journal><ArticleTitle>[The inadequate physical activity as risk factor of non-communicable diseases].</ArticleTitle><Pagination><StartPage>1267</StartPage><EndPage>1272</EndPage><MedlinePgn>1267-1272</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.32687/0869-866X-2024-32-6-1267-1272</ELocationID><Abstract><AbstractText>The article presents brief review of impact of inadequate physical activity on development of non-communicable diseases. The low physical activity is among top five most significant factors of premature death and is the cause of more than 20% of cases of diabetes mellitus II and chronic cardiovascular diseases. The article considers mode of assessing intensity of physical activity based on using metabolic equivalent. The effect of hypodynamia on development of obesity, diseases of musculoskeletal system, diabetes mellitus II, cardio-vascular and oncological diseases is considered. The relationship between inadequate physical activity and population mental health is considered too.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Amlaev</LastName><ForeName>K R</ForeName><Initials>KR</Initials><AffiliationInfo><Affiliation>The Federal State Budget Educational Institution of Higher Education "The Stavropol State Medical University" of the Minzdrav of Russia, 355017, Stavropol, Russia, kum672002@mail.ru.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dahkilgova</LastName><ForeName>Kh T</ForeName><Initials>KT</Initials><AffiliationInfo><Affiliation>The Federal State Budget Educational Institution of Higher Education "The Stavropol State Medical University" of the Minzdrav of Russia, 355017, Stavropol, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blinkova</LastName><ForeName>L N</ForeName><Initials>LN</Initials><AffiliationInfo><Affiliation>The Federal State Budget Educational Institution of Higher Education "The Stavropol State Medical University" of the Minzdrav of Russia, 355017, Stavropol, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mazharov</LastName><ForeName>V N</ForeName><Initials>VN</Initials><AffiliationInfo><Affiliation>The Federal State Budget Educational Institution of Higher Education "The Stavropol State Medical University" of the Minzdrav of Russia, 355017, Stavropol, Russia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>rus</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D004740">English Abstract</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Russia (Federation)</Country><MedlineTA>Probl Sotsialnoi Gig Zdravookhranenniiai Istor Med</MedlineTA><NlmUniqueID>101270373</NlmUniqueID><ISSNLinking>0869-866X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073296" MajorTopicYN="Y">Noncommunicable Diseases</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="Y">Exercise</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">exercise</Keyword><Keyword MajorTopicYN="N">hypodynamia</Keyword><Keyword MajorTopicYN="N">physical activity</Keyword><Keyword MajorTopicYN="N">risk factor</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>5</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>9</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>10</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>8</Day><Hour>1</Hour><Minute>9</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>10</Hour><Minute>33</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39644303</ArticleId><ArticleId IdType="doi">10.32687/0869-866X-2024-32-6-1267-1272</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39643900</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1475-2840</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>06</Day></PubDate></JournalIssue><Title>Cardiovascular diabetology</Title><ISOAbbreviation>Cardiovasc Diabetol</ISOAbbreviation></Journal><ArticleTitle>Diabetes does not increase in-hospital or short-term mortality in patients undergoing surgical repair for type A aortic dissection: insight from the national readmission database.</ArticleTitle><Pagination><StartPage>436</StartPage><MedlinePgn>436</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">436</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12933-024-02524-4</ELocationID><Abstract><AbstractText Label="BACKGROUND">Previous studies have reported a protective effect of type 2 diabetes on the incidence and progression of aortic aneurysms. We investigated whether this protective effect extends to aortic dissections.</AbstractText><AbstractText Label="METHODS">Data from the US Nationwide Readmission Database (2016-2019) were analyzed. Patients admitted for open surgery repair of acute type A aortic dissection (TAAD) were initially analyzed (index group). Those discharged alive were followed for up to 30 days (readmission group). The co-primary outcomes were in-hospital and 30-day mortality.</AbstractText><AbstractText Label="RESULTS">Between 2016 and 2019, 7,324 patients were admitted for open surgical repair of acute TAAD, of whom 965 (13.2%) had diabetes. Patients with diabetes were older and had a higher prevalence of obesity, hypertension, smoking, dyslipidemia, and chronic kidney disease (CKD). 15.2% of patients with diabetes and 14.6% without diabetes died; hence, diabetes did not have a significant impact on in-hospital mortality (adjusted odd ratio [aOR] = 1.02 [0.84-1.24]). Similarly, diabetes was not associated with a higher adjusted risk of atrial fibrillation (aOR = 1.03 [0.89-1.20]), stroke (aOR = 0.83 [0.55-1.26]), cardiogenic shock (aOR = 1.18 [0.98-1.42]), but increased the risk of acute renal failure (aOR = 1.20 [1.04-1.39]). Within 30 days of discharge, 154 (15.9%) patients with diabetes and 952 (15%) from the non-diabetes group were readmitted. Readmitted patients with diabetes were older and had a higher prevalence of cardiovascular comorbidities. We didn't observe any significant difference in the adjusted risk of 30-day mortality between the diabetes and non-diabetes groups (adjusted hazard ratio [aHR] = 0.81 [0.41-1.60]). However, diabetes was associated with a lower risk of readmission (aHR = 0.81 [0.68-0.97]). Age was the most significant predictor of all outcomes. CKD was the most significant predictor of 30-day mortality, with the risk increasing five-fold in patients with diabetes (HR = 5.58 [2.58-6.62]. Cardiovascular-related conditions were the most common causes of readmission in both groups. However, respiratory-related conditions were more prevalent in the diabetes group compared to the non-diabetes group (19.5% vs. 13%, respectively, p = 0.032).</AbstractText><AbstractText Label="CONCLUSIONS">Diabetes does not increase in-hospital or short-term mortality in patients undergoing surgical repair for Type A aortic dissection.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chaudhry</LastName><ForeName>Hamza</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Research Department, Weill Cornell Medicine-Qatar, Doha, Qatar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dargham</LastName><ForeName>Soha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Medical Education, Weill Cornell Medicine- Qatar, Doha, Qatar.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Biostatistics Core, Weill Cornell Medicine- Qatar, Doha, Qatar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jayyousi</LastName><ForeName>Amin</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Hamad Medical Corporation, Doha, Qatar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al Suwaidi</LastName><ForeName>Jassim</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Heart hospital, Hamad Medical Corporation, Doha, Qatar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abi Khalil</LastName><ForeName>Charbel</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-1428-6324</Identifier><AffiliationInfo><Affiliation>Research Department, Weill Cornell Medicine-Qatar, Doha, Qatar. cha2022@med.cornell.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Heart hospital, Hamad Medical Corporation, Doha, Qatar. cha2022@med.cornell.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Sanford and I. Weill Department of Medicine, Weill Cornell Medicine, New York, USA. cha2022@med.cornell.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cardiovasc Diabetol</MedlineTA><NlmUniqueID>101147637</NlmUniqueID><ISSNLinking>1475-2840</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000784" MajorTopicYN="Y">Aortic Dissection</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016208" MajorTopicYN="Y">Databases, Factual</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017052" MajorTopicYN="Y">Hospital Mortality</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014481" MajorTopicYN="N" Type="Geographic">United States</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010359" MajorTopicYN="Y">Patient Readmission</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001014" MajorTopicYN="Y">Aortic Aneurysm</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D065840" MajorTopicYN="N">Protective Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015995" MajorTopicYN="N">Prevalence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014656" MajorTopicYN="N">Vascular Surgical Procedures</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Aortic dissection</Keyword><Keyword MajorTopicYN="N">Cardiology</Keyword><Keyword MajorTopicYN="N">Diabetes</Keyword><Keyword MajorTopicYN="N">Type A aortic dissection</Keyword><Keyword MajorTopicYN="N">Vascular medicine</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: This study was approved by WCM-Q’s institutional review board (record number 21−0002). Consent for publication: Not applicable. 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JAMA Netw Open. 2021;4(3):e210469.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7930924</ArticleId><ArticleId IdType="pubmed">33656527</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39643008</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8227</ISSN><JournalIssue CitedMedium="Internet"><Volume>219</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Diabetes research and clinical practice</Title><ISOAbbreviation>Diabetes Res Clin Pract</ISOAbbreviation></Journal><ArticleTitle>Responses to lifestyle interventions among individuals with distinct pre-diabetes phenotypes: A systematic review and Meta-Analysis.</ArticleTitle><Pagination><StartPage>111939</StartPage><MedlinePgn>111939</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.diabres.2024.111939</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0168-8227(24)00849-0</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">To assess responses to lifestyle interventions (LIs) among individuals with distinct pre-diabetes phenotypes (isolated impaired fasting glucose [i-IFG], isolated impaired glucose tolerance [i-IGT], and combined IFG + IGT) for reducing diabetes incidence, reversing pre-diabetes, and improving glycemic control and insulin sensitivity.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">PubMed, Embase, Cochrane Library, and Web of Science were searched until December 6th, 2023. We included randomized controlled trials examining responses to LIs (including diet and/or physical activity) among adults with i-IFG, i-IGT, and IFG + IGT. Outcomes included diabetes incidence, normoglycemia incidence, fasting plasma glucose (FPG), 2-hour plasma glucose (2 h-PG), hemoglobin A1c, fasting insulin (FI), and homeostasis model assessment-insulin resistance (HOMA-IR). Random-effects meta-analyses were performed to estimate risk ratios (RRs) and mean differences.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Twenty-seven studies were included. Meta-analysis of 10 studies that performed stratified analyses by pre-diabetes phenotype found that LIs significantly reduced diabetes incidence in i-IGT (RR = 0.69 [0.56; 0.85], I<sup>2</sup> = 14 %) and IFG + IGT (RR = 0.56 [0.48; 0.66], I<sup>2</sup> = 0 %) but not in i-IFG (RR = 0.85 [0.66; 1.11], I<sup>2</sup> = 0 %; p<sub>subgroup</sub> = 0.02). Meta-analysis of 20 studies using IGT for participant recruitment showed that LIs significantly decreased diabetes incidence, increased normoglycemia incidence, and improved FPG, 2 h-PG, FI and HOMA-IR.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">LIs are effective for IGT (with or without IFG), but tailored LIs are needed for i-IFG to prevent diabetes.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rong</LastName><ForeName>Jincheng</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>School of Nursing, LKS Faculty of Medicine, the University of Hong Kong, Hong Kong, SAR, China. Electronic address: u3010481@connect.hku.hk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Mandy</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Nursing, LKS Faculty of Medicine, the University of Hong Kong, Hong Kong, SAR, China. Electronic address: mandyho1@hku.hk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Disheng</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>School of Nursing, LKS Faculty of Medicine, the University of Hong Kong, Hong Kong, SAR, China. Electronic address: zdison@connect.hku.hk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chau</LastName><ForeName>Pui Hing</ForeName><Initials>PH</Initials><AffiliationInfo><Affiliation>School of Nursing, LKS Faculty of Medicine, the University of Hong Kong, Hong Kong, SAR, China. Electronic address: phchau@graduate.hku.hk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D000078182">Systematic Review</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Diabetes Res Clin Pract</MedlineTA><NlmUniqueID>8508335</NlmUniqueID><ISSNLinking>0168-8227</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011236" MajorTopicYN="Y">Prediabetic State</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="Y">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008019" MajorTopicYN="Y">Life Style</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="N">Exercise</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018149" MajorTopicYN="N">Glucose Intolerance</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes prevention</Keyword><Keyword MajorTopicYN="N">Impaired fasting glucose</Keyword><Keyword MajorTopicYN="N">Impaired glucose tolerance</Keyword><Keyword MajorTopicYN="N">Lifestyle intervention</Keyword><Keyword MajorTopicYN="N">Pre-diabetes</Keyword><Keyword MajorTopicYN="N">Systematic review</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>10</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>12</Day><Hour>15</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>14</Hour><Minute>46</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>20</Hour><Minute>38</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39643008</ArticleId><ArticleId IdType="doi">10.1016/j.diabres.2024.111939</ArticleId><ArticleId IdType="pii">S0168-8227(24)00849-0</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39643007</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8227</ISSN><JournalIssue CitedMedium="Internet"><Volume>219</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Diabetes research and clinical practice</Title><ISOAbbreviation>Diabetes Res Clin Pract</ISOAbbreviation></Journal><ArticleTitle>Efficacy of flash glucose monitoring on HbA1c in type 2 diabetes: An individual patient data meta-analysis of real-world evidence.</ArticleTitle><Pagination><StartPage>111950</StartPage><MedlinePgn>111950</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.diabres.2024.111950</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0168-8227(24)00860-X</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">There is a growing body of evidence demonstrating the benefit of flash glucose monitoring in type 2 diabetes mellitus (T2DM). This individual patient data meta-analysis aimed to investigate the impact of commencing flash glucose monitoring on HbA1c in people living with T2DM treated with insulin in a real-world setting.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A meta-analysis of eight observational studies which assessed change in HbA1c at 3-6 months following initiating flash glucose monitoring for which Abbott Diabetes Care could provide individual patient data was performed. Studies included adults with T2DM managed with insulin and baseline HbA1c between 8.0 %-12.0 % (64-108 mmol/mol). A one-stage model was created to explore heterogeneity.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">A total of 803 patients were included in the analysis (mean(SD) age: 62.8(11.4) years, BMI: 32.2(6.8) kg/m<sup>2</sup>, baseline HbA1c 9.0(0.9) % [75 (10) mmol/mol]). Commencement of flash glucose monitoring was associated with an HbA1c reduction of 0.89 % (95 % CI 0.71 to 1.08) (9.8 mmol/mol (95 % CI 7.8 to 11.8)) at 3-6 months. In the one stage model, age, BMI and baseline HbA1c accounted for the substantial heterogeneity observed between studies.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Commencement of flash glucose monitoring was associated with a significant reduction in HbA1c at 3-6 months in a real-world setting in T2DM managed with insulin.</AbstractText><CopyrightInformation>Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Heer</LastName><ForeName>Randeep S</ForeName><Initials>RS</Initials><AffiliationInfo><Affiliation>Abbott Diabetes Care, Witney, UK. Electronic address: randeep.heer@abbott.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lovegrove</LastName><ForeName>Joshua</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Abbott Diabetes Care, Witney, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Welsh</LastName><ForeName>Zoë</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Abbott Diabetes Care, Witney, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Diabetes Res Clin Pract</MedlineTA><NlmUniqueID>8508335</NlmUniqueID><ISSNLinking>0168-8227</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C517652">hemoglobin A1c protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015190" MajorTopicYN="Y">Blood Glucose Self-Monitoring</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Continuous glucose monitoring</Keyword><Keyword MajorTopicYN="N">Flash glucose monitoring</Keyword><Keyword MajorTopicYN="N">Meta-analysis</Keyword><Keyword MajorTopicYN="N">Real-world</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest RSH, JL and ZW are employees of Abbott Diabetes Care, Witney, UK.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>12</Day><Hour>15</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>14</Hour><Minute>46</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>20</Hour><Minute>38</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39643007</ArticleId><ArticleId IdType="doi">10.1016/j.diabres.2024.111950</ArticleId><ArticleId IdType="pii">S0168-8227(24)00860-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39642712</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>19</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>742</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>1,25(OH)2D3 promotes insulin secretion through the classical pyroptosis pathway in vitro and vivo.</ArticleTitle><Pagination><StartPage>151058</StartPage><MedlinePgn>151058</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2024.151058</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(24)01594-8</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Diabetes is a chronic metabolic disorder characterized by persistently elevated levels of blood glucose. Research has demonstrated a close relationship between inflammation and the development of diabetes. Vitamin D has been shown to be significantly associated with type 2 diabetes; however, the mechanisms by which it regulates inflammation during the onset of the disease remain incompletely understood. In this study, we investigated the effect of pyroptosis on pancreatic β-cell function in diabetes and explored the role of 1,25(OH)2D3 in type 2 diabetes through the pyroptosis signaling pathway.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">In both in vivo and in vitro settings, we established a diabetes model combined with 1,25(OH)₂D₃ intervention to investigate its impact on insulin secretion levels, the release of inflammatory factors, and the expression levels of pyroptosis-related proteins.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">In both in vivo and in vitro experiments, we have observed that 1,25(OH)₂D₃ exhibits anti-inflammatory properties by downregulating the expression levels of pyroptosis-related proteins. Furthermore, it provides protection against pancreatic β-cell damage caused by type 2 diabetes mellitus (T2DM) and enhances insulin secretion. Inhibition of gasdermin D (GSDMD) expression impedes the progression of cell pyroptosis, reduces the amplification of the inflammatory response, and protects pancreatic cells from injury.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">We hypothesize that the induction of pancreatic cells through pyroptosis occurs via the classical pathway in T2DM, and propose that 1,25(OH)2D3 may have a beneficial effect on this process. Consequently, 1,25(OH)2D3 could potentially serve as an adjuvant to inhibit the pyroptosis of pancreatic β cells by targeting the classical signaling pathway, thereby reducing the inflammatory response and alleviating symptoms associated with diabetes.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>Yuxuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Laboratory Animal Center of Suzhou Medical College, Soochow University, Suzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Zhihao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Laboratory Animal Center of Suzhou Medical College, Soochow University, Suzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>Xun</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Center of Laboratory Animal, Shanghai Jiao Tong University, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Lewen</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratory Animal Center of Suzhou Medical College, Soochow University, Suzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Yudie</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Laboratory Animal Center of Suzhou Medical College, Soochow University, Suzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Zhengyu</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Laboratory Animal Center of Suzhou Medical College, Soochow University, Suzhou, China. Electronic address: zacharyzhou@suda.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>FXC9231JVH</RegistryNumber><NameOfSubstance UI="D002117">Calcitriol</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D028044">Phosphate-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C498368">Gsdmd protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000094524">Gasdermins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000069292" MajorTopicYN="Y">Pyroptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002117" MajorTopicYN="Y">Calcitriol</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000078790" MajorTopicYN="Y">Insulin Secretion</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050417" MajorTopicYN="Y">Insulin-Secreting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="Y">Insulin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D028044" MajorTopicYN="N">Phosphate-Binding Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000094524" MajorTopicYN="N">Gasdermins</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">1,25(OH)2D3</Keyword><Keyword MajorTopicYN="N">Diabetes</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Pyroptosis</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>20</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>14</Hour><Minute>45</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>18</Hour><Minute>8</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39642712</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2024.151058</ArticleId><ArticleId IdType="pii">S0006-291X(24)01594-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39642665</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>19</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0306-4565</ISSN><JournalIssue CitedMedium="Internet"><Volume>126</Volume><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Journal of thermal biology</Title><ISOAbbreviation>J Therm Biol</ISOAbbreviation></Journal><ArticleTitle>The effect of repeated hot water immersion on vascular function, blood pressure and central haemodynamics in individuals with type 2 diabetes mellitus.</ArticleTitle><Pagination><StartPage>104017</StartPage><MedlinePgn>104017</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jtherbio.2024.104017</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0306-4565(24)00235-3</ELocationID><Abstract><AbstractText>Type 2 diabetes mellitus (T2DM) is characterised by endothelial dysfunction, leading to increased risk of cardiovascular disease. Emerging evidence suggest that HWI may favourably improve vascular function but data are limited in individual with T2DM. The aim was to investigate whether repeated hot water immersion (HWI) improved macrovascular, microvascular and central haemodynamic function in individuals with T2DM. Fourteen individuals completed a pre-post experimental study where participants were assessed pre- and post-8-10 × 1 h HWI sessions (40 °C water) undertaken within a 14-day period. During HWIs, body position was adjusted to clamp rectal temperature at 38.5-39.0 °C for the duration of the immersion. Stroke volume index (SVi), cardiac index (Q˙ i), resting heart rate (HR), systolic blood pressure (SBP), diastolic BP (DBP), brachial flow-mediated dilation (FMD) and cutaneous microvascular endothelial function (via transdermal iontophoresis) and plasma [nitrate] and [nitrite] (NOX; via ozone chemiluminescence) were assessed pre- and post HWI. Neither brachial FMD measures of macrovascular endothelial function (p = 0.43) or forearm microvascular function (ACh max, p = 0.63; ACh area under curve (AUC), p = 0.63; insulin max, p = 0.51; insulin AUC, p = 0.86) or NOX (p = 0.38) were changed. Q˙ i (p < 0.01), SVi (p < 0.02) and resting HR (p < 0.01) were all significantly reduced following the 10-days HWI intervention. SBP was reduced (p = 0.03), whereas DBP was unchanged (p = 0.56). HWI may represent an appropriate intervention to improve Q˙ I, SVi and BP in individuals with T2DM, but not macrovascular endothelial or cutaneous microvascular function.</AbstractText><CopyrightInformation>Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>James</LastName><ForeName>Thomas J</ForeName><Initials>TJ</Initials><AffiliationInfo><Affiliation>School of Sport and Exercise Sciences, Faculty of Science, Liverpool John Moores University, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Corbett</LastName><ForeName>Jo</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cummings</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Diabetes and Endocrinology Department, Portsmouth Hospitals University NHS Trust, Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Allard</LastName><ForeName>Sharon</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Diabetes and Endocrinology Department, Portsmouth Hospitals University NHS Trust, Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bailey</LastName><ForeName>Stephen J</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eglin</LastName><ForeName>Clare</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Belcher</LastName><ForeName>Harvey</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piccolo</LastName><ForeName>Daniel D</ForeName><Initials>DD</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tipton</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perissiou</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saynor</LastName><ForeName>Zoe L</ForeName><Initials>ZL</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK; School of Health Sciences, Faculty of Environmental and Life Sciences, University of Southampton, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shepherd</LastName><ForeName>Anthony I</ForeName><Initials>AI</Initials><AffiliationInfo><Affiliation>School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK; Diabetes and Endocrinology Department, Portsmouth Hospitals University NHS Trust, Portsmouth, UK. Electronic address: ant.shepherd@port.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Therm Biol</MedlineTA><NlmUniqueID>7600115</NlmUniqueID><ISSNLinking>0306-4565</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001794" MajorTopicYN="Y">Blood Pressure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006439" MajorTopicYN="Y">Hemodynamics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007101" MajorTopicYN="Y">Immersion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006358" MajorTopicYN="N">Hot Temperature</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004730" MajorTopicYN="N">Endothelium, Vascular</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="N">Heart Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014664" MajorTopicYN="N">Vasodilation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Blood pressure</Keyword><Keyword MajorTopicYN="N">Cardiac output</Keyword><Keyword MajorTopicYN="N">Endothelial function</Keyword><Keyword MajorTopicYN="N">Hot water immersion</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>Declaration of competing interest All authors report no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>20</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>7</Day><Hour>14</Hour><Minute>46</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>18</Hour><Minute>7</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39642665</ArticleId><ArticleId IdType="doi">10.1016/j.jtherbio.2024.104017</ArticleId><ArticleId IdType="pii">S0306-4565(24)00235-3</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39642136</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>08</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>12</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Exploring the link between dietary thiamine and type 2 diabetes mellitus risk in US adults aged 45 years and older: Insights from a cross-sectional investigation.</ArticleTitle><Pagination><StartPage>e0313114</StartPage><MedlinePgn>e0313114</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e0313114</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0313114</ELocationID><Abstract><AbstractText>The correlation between dietary thiamine intake and the incidence of type 2 diabetes mellitus (T2DM) remains a subject of controversy within the academic community. While numerous studies have attempted to elucidate this relationship, conclusive evidence remains elusive. A survey of U.S. adults aged 45 years and older examined the supposed association between dietary thiamine intake and the risk of developing T2DM with the aim of clarifying the potential link. In this cross-sectional investigation, we evaluated dietary thiamine intake data sourced from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2020. Using weighted multivariate logistic regression analysis, we assessed the potential risk of T2DM associated with varying levels of thiamine intake. The observation of nonlinear relationships was accomplished by fitting smoothed curves. This study ultimately included 15,231 participants aged 45 years and older. Dietary thiamine intake (after log transformation) was inversely related to T2DM after accounting for potential confounders (OR = 0.86, 95% CI: 0.78, 0.95). An increase in dietary thiamine intake by one unit is associated with a 14% reduction in the risk of T2DM. Furthermore, our analysis revealed that the associations between dietary thiamine intake and T2DM risk, such as age, gender, race, smoking status, alcohol use, hypertension, body mass index (BMI), and cardiovascular disease (CVD), remained consistent across multiple stratified subgroups (p values >0.05). According to this study, dietary thiamine intake may be associated with the incidence of T2DM among US residents aged 45 years and older. Appropriate increases in dietary thiamine intake are expected to offer substantial preventive potential for T2DM and significant clinical implications.</AbstractText><CopyrightInformation>Copyright: © 2024 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Hong</ForeName><Initials>H</Initials><Identifier Source="ORCID">0009-0002-0505-0368</Identifier><AffiliationInfo><Affiliation>Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Zhengwei</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ni</LastName><ForeName>Hengfan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Haoran</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qin</LastName><ForeName>Bo</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, Sichuan Provincial Maternity and Child Health Care Hospital, Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Zhiyao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Zhaohui</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>X66NSO3N35</RegistryNumber><NameOfSubstance UI="D013831">Thiamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013831" MajorTopicYN="Y">Thiamine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014481" MajorTopicYN="N" Type="Geographic">United States</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009749" MajorTopicYN="N">Nutrition Surveys</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004032" MajorTopicYN="N">Diet</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>18</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>18</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>13</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>6</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId 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Nutr Diabetes. 2022;12(1):32. doi: 10.1038/s41387-022-00211-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/s41387-022-00211-5</ArticleId><ArticleId IdType="pmc">PMC9209469</ArticleId><ArticleId IdType="pubmed">35725834</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39642126</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>12</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Effects of probiotic supplementation on the anthropometric nutritional status of patients with type 2 Diabetes mellitus: A systematic review and meta-analysis protocol.</ArticleTitle><Pagination><StartPage>e0314971</StartPage><MedlinePgn>e0314971</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e0314971</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0314971</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Diabetes mellitus (DM) is characterized by hyperglycemia due to insufficient insulin production or utilization. Previous studies have shown a relationship between the gut microbiota and DM, driving interest in probiotic supplementation to modulate the microbiota and glucose metabolism in patients with DM, although the exact mechanisms remain unclear. Probiotics can influence metabolic factors and improve the composition of the microbiota, possibly helping to reduce weight in patients with DM.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">The objective of this review is to compile and analyze the most relevant evidence on the effects of probiotic supplementation on the nutritional anthropometric status of patients with type 2 Diabetes mellitus (T2DM).</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Methodological guidelines will be followed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement and the study has been registered in the International Prospective Register of Systematic Reviews under reference number CRD42023480243. Studies will be selected through an active search of the PubMed, Science Direct, and SCOPUS databases using the following search descriptors: gut microbiota, body weight, and metabolic diseases, according to medical subject headings. The assessment of the methodological quality of the studies will be carried out using the Cochrane Collaboration instrument. The risk of bias will be analyzed using the Revised Cochrane tool for risk of bias in randomized controlled trials (RoB 2). A meta-analysis will be performed if heterogeneity is acceptable and justifiable; otherwise, the results will be presented in a qualitative narrative synthesis.</AbstractText><AbstractText Label="EXPECTED RESULTS" NlmCategory="RESULTS">The results of probiotic supplementation are expected to demonstrate improvements in anthropometric parameters such as body weight, BMI and abdominal and waist circumference in patients with T2DM, thus providing valuable evidence for clinical application.</AbstractText><CopyrightInformation>Copyright: © 2024 Ribeiro et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ribeiro</LastName><ForeName>Dálete Assíria de Souza</ForeName><Initials>DAS</Initials><AffiliationInfo><Affiliation>Nutrition Postgraduate Program, Center for Health Sciences, Federal University of Rio Grande Do Norte, Natal, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Araújo</LastName><ForeName>Anny Cristine</ForeName><Initials>AC</Initials><AffiliationInfo><Affiliation>Health Sciences Postgraduate Program, Center for Health Sciences, Federal University of Rio Grande do Norte, Natal, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>do Nascimento</LastName><ForeName>Priscila Kelly da Silva Bezerra</ForeName><Initials>PKDSB</Initials><AffiliationInfo><Affiliation>Nutrition Postgraduate Program, Center for Health Sciences, Federal University of Rio Grande Do Norte, Natal, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>da Rocha</LastName><ForeName>Ilanna Marques Gomes</ForeName><Initials>IMG</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Faculty of Medicine, Hospital das Clinicas HCFMUSP, University of São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rezende</LastName><ForeName>Adriana Augusto de</ForeName><Initials>AA</Initials><Identifier Source="ORCID">0000-0003-2452-4047</Identifier><AffiliationInfo><Affiliation>Nutrition Postgraduate Program, Center for Health Sciences, Federal University of Rio Grande Do Norte, Natal, Brazil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Health Sciences Postgraduate Program, Center for Health Sciences, Federal University of Rio Grande do Norte, Natal, Brazil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical and Toxicological Analyses, Federal University of Rio Grande do Norte, Natal, Brazil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000886" MajorTopicYN="N">Anthropometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000178" MajorTopicYN="N">diet therapy</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019587" MajorTopicYN="Y">Dietary Supplements</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069196" MajorTopicYN="N">Gastrointestinal Microbiome</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015201" MajorTopicYN="N">Meta-Analysis as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009752" MajorTopicYN="Y">Nutritional Status</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019936" MajorTopicYN="Y">Probiotics</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000078202" MajorTopicYN="N">Systematic Reviews as Topic</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>18</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>18</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>13</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate 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Sci Rep 10, 11787 (2020). doi: 10.1038/s41598-020-68440-1</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/s41598-020-68440-1</ArticleId><ArticleId IdType="pmc">PMC7366719</ArticleId><ArticleId IdType="pubmed">32678128</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39641545</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>01</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1369-1619</ISSN><JournalIssue CitedMedium="Internet"><Volume>35</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>International journal of environmental health research</Title><ISOAbbreviation>Int J Environ Health Res</ISOAbbreviation></Journal><ArticleTitle>The effect of eating motivation on adherence to the Mediterranean diet, glycemia and lipid profile in individuals with type 2 diabetes.</ArticleTitle><Pagination><StartPage>257</StartPage><EndPage>268</EndPage><MedlinePgn>257-268</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/09603123.2024.2438122</ELocationID><Abstract><AbstractText>The aim of this study was to investigate the effect of eating motivation on Mediterranean diet adherence, glycemia and lipid profile in individuals with type 2 diabetes. A questionnaire consisting of general information, eating motivation scale and Mediterranean diet adherence scale was applied to 400 individuals with diabetes. Height, weight, plasma glucose, total cholesterol, triglycerides, low density lipoprotein and high density lipoprotein values were measured. Environmental and political, health, commercial and marketing, economic and affordability motivations are effective in individuals with diabetes. Emotional motivation and social motivation were positively correlated with body mass index, HbA1C, total cholesterol, triglyceride and low density lipoprotein levels. Health motivation increased the likelihood of having glucose levels below 130 mg/dl. Individuals with diabetes were influenced by eating motivations and these motivations were associated with adherence to the Mediterranean diet and glycemia. Eating motivation may be effective in the management of type 2 diabetes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Öztürk Özkan</LastName><ForeName>Gülin</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Faculty of Health Sciences, Department of Nutrition and Dietetics, İstanbul Medeniyet University, İstanbul, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Çeteoğlu</LastName><ForeName>Büşra</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Faculty of Health Sciences, Department of Nutrition and Dietetics, İstanbul Medeniyet University, İstanbul, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Temiz</LastName><ForeName>Beyza</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Faculty of Health Sciences, Department of Nutrition and Dietetics, İstanbul Medeniyet University, İstanbul, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dursun</LastName><ForeName>Hüsna</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Faculty of Health Sciences, Department of Nutrition and Dietetics, İstanbul Medeniyet University, İstanbul, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karaçam</LastName><ForeName>Melike</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Faculty of Health Sciences, Department of Nutrition and Dietetics, İstanbul Medeniyet University, İstanbul, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sarğın</LastName><ForeName>Mehmet</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>İstanbul Göztepe Prof. Dr. Süleyman Yalçın City Hospital, Famıly Medıcıne, İstanbul, Turkey.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Int J Environ Health Res</MedlineTA><NlmUniqueID>9106628</NlmUniqueID><ISSNLinking>0960-3123</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008055">Lipids</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D038441" MajorTopicYN="Y">Diet, Mediterranean</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009042" MajorTopicYN="Y">Motivation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008055" MajorTopicYN="Y">Lipids</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010349" MajorTopicYN="N">Patient Compliance</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011795" MajorTopicYN="N">Surveys and Questionnaires</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">EATMOT</Keyword><Keyword MajorTopicYN="N">M editerranean diet</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword><Keyword MajorTopicYN="N">eating motivation</Keyword><Keyword MajorTopicYN="N">glycemia</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>2</Day><Hour>0</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>12</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>9</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39641545</ArticleId><ArticleId IdType="doi">10.1080/09603123.2024.2438122</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39641406</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>06</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1118-4841</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>10s</Issue><PubDate><Year>2024</Year><Month>Oct</Month><Day>31</Day></PubDate></JournalIssue><Title>African journal of reproductive health</Title><ISOAbbreviation>Afr J Reprod Health</ISOAbbreviation></Journal><ArticleTitle>Patients' experiences in receiving family support for type-2 diabetes mellitus: A scoping review.</ArticleTitle><Pagination><StartPage>411</StartPage><EndPage>420</EndPage><MedlinePgn>411-420</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.29063/ajrh2024/v28i10s.43</ELocationID><Abstract><AbstractText>The aim of the study was to determine how patients' experiences in receiving family support for type-2 diabetes mellitus. We conducted scoping review using the Joanna briggs institute guidelines and Levac, Colquhoun and O'Brien. Five electronic databases including PubMed, Scopus, ScienceDirect, ProQuest and Sage Pub were systematically searched by keywords for literature published between 2013 to 2023. Ten articles were used to final review. Analysis revealed that family support is an important factor to improve diabetes self-management behaviour for patients with type-2 diabetes mellitus. The availability of family support primarily comes from their spouses and children. Some obstacles, such as the emotional distance between patients and their families, can be overcome by improving shared knowledge and skills in self-management. Family support also has a positive impact on behavioural control and health outcomes for patients with type 2 diabetes mellitus.</AbstractText><CopyrightInformation>African Journal of Reproductive Health © 2024.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Suhamdani</LastName><ForeName>Haris</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Doctorate Degree Program in Public Health, Faculty of Public Health Universitas Airlangga, Surabaya, 60115, Indonesia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yusuf</LastName><ForeName>Ah</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Nursing, Faculty of Nursing Universitas Airlangga, Surabaya, 60115, Indonesia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ernawaty</LastName><ForeName>Ernawaty</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Health Policy and Administration, Faculty of Public Health Universitas Airlangga, Surabaya, 60115, Indonesia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Airlangga Centre for Health Policy Research Group, Surabaya, 60115, Indonesia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sulistyo</LastName><ForeName>Angger A H</ForeName><Initials>AAH</Initials><AffiliationInfo><Affiliation>Doctorate Degree Program in Public Health, Faculty of Public Health Universitas Airlangga, Surabaya, 60115, Indonesia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Nigeria</Country><MedlineTA>Afr J Reprod Health</MedlineTA><NlmUniqueID>9712263</NlmUniqueID><ISSNLinking>1118-4841</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012944" MajorTopicYN="Y">Social Support</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005190" MajorTopicYN="Y">Family</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012648" MajorTopicYN="N">Self Care</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000073278" MajorTopicYN="N">Self-Management</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000092802" MajorTopicYN="N">Family Support</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="fre"><AbstractText>L'objectif de cette étude était de déterminer comment les expériences des patients en matière de soutien familial pour le diabète sucré de type 2. Nous avons procédé à un examen de la portée de l'étude en utilisant les lignes directrices de l'institut Joanna Briggs et Levac, Colquhoun et O'Brien. Cinq bases de données électroniques, dont PubMed, Scopus, ScienceDirect, ProQuest et Sage Pub, ont fait l'objet d'une recherche systématique par mots-clés de la littérature publiée entre 2013 et 2023. Dix articles ont été retenus pour l'examen final. L'analyse a révélé que le soutien familial est un facteur important pour améliorer le comportement d'autogestion du diabète chez les patients atteints de diabète sucré de type 2. Le soutien familial provient principalement des conjoints et des enfants. Certains obstacles, comme la distance émotionnelle entre les patients et leur famille, peuvent être surmontés en améliorant le partage des connaissances et des compétences en matière d'autogestion. Le soutien familial a également un impact positif sur le contrôle du comportement et les résultats pour la santé des patients atteints de diabète de type 2.</AbstractText><CopyrightInformation>African Journal of Reproductive Health © 2024.</CopyrightInformation></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">T2DM</Keyword><Keyword MajorTopicYN="N">family support</Keyword><Keyword MajorTopicYN="N">patient experiences</Keyword><Keyword MajorTopicYN="N">review</Keyword></KeywordList><CoiStatement>The Authors declared no conflict of interest</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>12</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>12</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>7</Hour><Minute>29</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39641406</ArticleId><ArticleId IdType="doi">10.29063/ajrh2024/v28i10s.43</ArticleId><ArticleId IdType="pii">Afr J Reprod Health 2024; 28 [10s]: 411-420</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39641242</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1753-9455</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><PubDate><Year>2024</Year><Season>Jan-Dec</Season></PubDate></JournalIssue><Title>Therapeutic advances in cardiovascular disease</Title><ISOAbbreviation>Ther Adv Cardiovasc Dis</ISOAbbreviation></Journal><ArticleTitle>Angiotensin receptor neprilysin inhibitor in chronic heart failure and comorbidity management: Indian consensus statement.</ArticleTitle><Pagination><StartPage>17539447241301959</StartPage><MedlinePgn>17539447241301959</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">17539447241301959</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1177/17539447241301959</ELocationID><Abstract><AbstractText>Heart failure (HF) is a significant public health concern characterized by notable rates of morbidity and mortality. Multimorbidity, ranging from 43% to 98% among HF patients, significantly impacts prognosis and treatment response. HF management requires a holistic approach, including guideline-directed medical therapy. Sacubitril/valsartan (angiotensin receptor neprilysin inhibitor [ARNI]) is a cornerstone of HF treatment, supported by robust evidence from large-scale clinical trials across different levels of left ventricular ejection fraction. The recommendations presented in this paper have been developed by a group of cardiologists in India who convened in expert opinion meetings to discuss the utilization of ARNI in chronic HF patients with five different comorbid conditions like type 2 diabetes mellitus (T2DM), chronic kidney disease, myocardial infarction (MI), obesity, and hypertension. Key focus areas include initiation, dose titration, and management across different HF phenotypes and comorbidities. Emphasis is placed on the efficacy of ARNI irrespective of glycemic status in the T2DM population, its role in HF patients with obesity, and addressing challenges related to renal function decline and hyperkalemia. Additionally, the document highlights ARNI's potential benefits in hypertensive and post-MI HF patients, alongside observations on the obesity paradox in HF prognosis. Overall, these recommendations aim to optimize ARNI therapy in HF patient populations with different comorbidities, addressing specific challenges and considerations to improve outcomes and quality of life.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mittal</LastName><ForeName>Sanjay</ForeName><Initials>S</Initials><Identifier Source="ORCID">0009-0002-9179-5840</Identifier><AffiliationInfo><Affiliation>Clinical and Preventive Cardiology, Cardiac Care, Medanta-The Medicity Hospital, Sector 38, Gurugram, Haryana 122001, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harikrishnan</LastName><ForeName>Sivadasanpillai</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gupta</LastName><ForeName>Anoop</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Epic Multispeciality Hospital, Ahmedabad, Gujarat, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bansal</LastName><ForeName>Sandeep</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koshy</LastName><ForeName>George A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Cosmopolitan Hospital, Trivandrum, Kerala, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohanan</LastName><ForeName>Padhinhare P</ForeName><Initials>PP</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Westfort Hi-Tech Hospital, Thrissur, Kerala, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bhattacharya</LastName><ForeName>Debdatta</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Narayana Hrudayalaya Hospital, Rabindranath Tagore International Institute of Cardiac Sciences, Kolkata, West Bengal, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kerkar</LastName><ForeName>Prafulla</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Asian Heart Institute, Mumbai, Maharashtra, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Swamy</LastName><ForeName>Ajay</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>KIMS Hospital, Hyderabad, Telangana, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aggarwal</LastName><ForeName>Vinayak</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Non-Invasive and Clinical Cardiology, Fortis Memorial Research Institute, Fortis Hospital, Gurgaon, Haryana, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srivastava</LastName><ForeName>Sameer</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Max Hospital, New Delhi, Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mahajan</LastName><ForeName>Ajay</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiology, King Edward Memorial Hospital and Seth Gordhandas Sunderdas Medical College, Mumbai, Maharashtra, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mehta</LastName><ForeName>Ashwani</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Sir Gangaram Hospital, New Delhi, Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Kamal</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0001-5866-2566</Identifier><AffiliationInfo><Affiliation>Sal Hospital, Ahmedabad, Gujarat, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shetty</LastName><ForeName>Sadanand</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Sadanand Healthy Living Center, Mumbai, Maharashtra, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D017065">Practice Guideline</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Ther Adv Cardiovasc Dis</MedlineTA><NlmUniqueID>101316343</NlmUniqueID><ISSNLinking>1753-9447</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D057911">Angiotensin Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000613">Aminobutyrates</NameOfSubstance></Chemical><Chemical><RegistryNumber>WB8FT61183</RegistryNumber><NameOfSubstance UI="C549068">sacubitril and valsartan sodium hydrate drug combination</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.24.11</RegistryNumber><NameOfSubstance UI="D015260">Neprilysin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001713">Biphenyl Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004338">Drug Combinations</NameOfSubstance></Chemical><Chemical><RegistryNumber>80M03YXJ7I</RegistryNumber><NameOfSubstance UI="D000068756">Valsartan</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057911" MajorTopicYN="Y">Angiotensin Receptor Antagonists</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000613" MajorTopicYN="Y">Aminobutyrates</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="Y">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015260" MajorTopicYN="Y">Neprilysin</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001713" MajorTopicYN="Y">Biphenyl Compounds</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004338" MajorTopicYN="Y">Drug Combinations</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032921" MajorTopicYN="Y">Consensus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007194" MajorTopicYN="N" Type="Geographic">India</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000068756" MajorTopicYN="Y">Valsartan</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="N">Hypertension</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="N">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="plain-language-summary" Language="eng"><AbstractText><b>Angiotensin receptor neprilysin inhibitor (ARNI) in chronic heart failure and comorbidity management: Indian consensus statement</b>Heart failure (HF) is a significant public health concern characterized by notable rates of morbidity and mortality. Multimorbidity, ranging from 43% to 98% among HF patients, significantly impacts prognosis and treatment response. HF management requires a holistic approach, including guideline-directed medical therapy (GDMT). Sacubitril/valsartan (ARNI) is a cornerstone of HF treatment, supported by robust evidence from large-scale clinical trials across different levels of left ventricular ejection fraction (LVEF). The recommendations presented in this paper have been developed by a group of cardiologists in India who convened in seven advisory board meetings to discuss the utilization of ARNI in chronic HF (CHF) patients with different comorbid conditions like Type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), myocardial infarction (MI), obesity, and hypertension. Key focus areas include initiation, dose titration, and management across different HF phenotypes and comorbidities. Emphasis is placed on the efficacy of ARNI irrespective of glycemic status in the T2DM population, its role in HF patients with obesity, and addressing challenges related to renal function decline and hyperkalemia. Additionally, the document highlights ARNI’s potential benefits in hypertensive and post-MI HF patients, alongside observations on the “obesity paradox” in HF prognosis. The paper underscores the importance of accurate biomarkers and imaging in HF diagnosis and monitoring. Overall, these recommendations aim to optimize ARNI therapy in HF patient populations with different comorbidities, addressing specific challenges and considerations to improve outcomes and quality of life.</AbstractText></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ARNI</Keyword><Keyword MajorTopicYN="N">chronic heart failure</Keyword><Keyword MajorTopicYN="N">chronic kidney disease</Keyword><Keyword MajorTopicYN="N">sacubitril/valsartan</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>12</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>5</Hour><Minute>43</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>6</Day></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39641242</ArticleId><ArticleId IdType="pmc">PMC11622297</ArticleId><ArticleId IdType="doi">10.1177/17539447241301959</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Harikrishnan S, Sanjay G, Anees T, et al.. 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Front Cardiovasc Med 2022; 9: 988117..</Citation><ArticleIdList><ArticleId IdType="pmc">PMC9448932</ArticleId><ArticleId IdType="pubmed">36093128</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39640885</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>Study on the characteristics of carotid wall shear stress in type 2 diabetes patients based on ultrasound vector flow imaging.</ArticleTitle><Pagination><StartPage>1409082</StartPage><MedlinePgn>1409082</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1409082</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1409082</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="UNASSIGNED">We aimed to quantitatively analyze wall shear stress (WSS) of the common carotid artery (CCA) and elucidate the relationship between WSS and cardiovascular disease (CVD) in patients with type 2 diabetes mellitus (T2DM) using ultrasound vector flow (V-Flow) imaging.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">A total of 109 T2DM patients were selected as the DM group, while 49 healthy volunteers served as the control group. V-Flow examination of the bilateral CCA was conducted. The maximum wall shear stress (WSS<sub>max</sub>) and mean wall shear stress (WSS<sub>mean</sub>) at the bifurcation, proximal bifurcation and middle segment of the bilateral CCA were obtained.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">The DM group showed decreased WSS<sub>mean</sub> in the middle region and proximal bifurcation of the CCA compared with the control group (p < 0.05). The WSS<sub>mean</sub> was further decreased in T2DM patients with CVD compared to those without CVD (middle region: 0.71 ± 0.17 Pa <i>vs.</i> 0.84 ± 0.24 Pa, p < 0.05; proximal bifurcation: 0.62 ± 0.22 Pa <i>vs.</i> 0.80 ± 0.21 Pa, p < 0.05). The receiver operating characteristic curve showed that a model combining with age, body mass index and WSS<sub>mean</sub> at the proximal carotid bifurcation had diagnostic value for detecting CVD in T2DM patients (area under the curve: 0.862, p < 0.05).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">WSS<sub>mean</sub> has potential value for evaluation of atherosclerosis, as well as in detecting the occurrence of CVD in T2DM patients. Ultrasound V-Flow imaging may be an effective tool for non-invasive evaluation of WSS in the clinic.</AbstractText><CopyrightInformation>Copyright © 2024 Li, Luo, Liu, Xie, Wang, Deng, Zhong, Liu, Cao, Du, Luo, Deng and Yin.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Li</LastName><ForeName>Zhaohuan</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Luo</LastName><ForeName>Anguo</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xuebing</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Shenghua</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yulin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Lan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhong</LastName><ForeName>Shimin</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yaoxia</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Geriatric Endocrinology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Xu</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Du</LastName><ForeName>Yigang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Ultrasound Research and Development, Shenzhen Mindray Bio-Medical Electronics Co., Ltd., Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luo</LastName><ForeName>Wen</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Clinical and Research, Shenzhen Mindray Bio-Medical Electronics Co., Ltd., Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Lixue</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Ultrasound and Non-invasive Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Ultrasound in Cardiac Electrophysiology and Biomechanics Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cardiovascular Disease, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017536" MajorTopicYN="N">Carotid Artery, Common</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014463" MajorTopicYN="N">Ultrasonography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013314" MajorTopicYN="N">Stress, Mechanical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001783" MajorTopicYN="N">Blood Flow Velocity</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002339" MajorTopicYN="N">Carotid Arteries</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059168" MajorTopicYN="N">Carotid Intima-Media Thickness</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cardiovascular diseases</Keyword><Keyword MajorTopicYN="N">carotid artery</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword><Keyword MajorTopicYN="N">vector flow imaging</Keyword><Keyword MajorTopicYN="N">wall shear stress</Keyword></KeywordList><CoiStatement>Authors YD and WL were employed by Shenzhen Mindray Bio-Medical Electronics Co., Ltd. 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(2016) 23:297–308. doi: 10.5551/jat.31377fi 2</Citation><ArticleIdList><ArticleId IdType="doi">10.5551/jat.31377</ArticleId><ArticleId IdType="pubmed">26477886</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39639901</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">2296-2565</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in public health</Title><ISOAbbreviation>Front Public Health</ISOAbbreviation></Journal><ArticleTitle>Health economic evaluation of structured education programs for patients with diabetes: a systematic review.</ArticleTitle><Pagination><StartPage>1467178</StartPage><MedlinePgn>1467178</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1467178</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fpubh.2024.1467178</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">Diabetes structured education programs have been demonstrated to effectively improve glycemic control and self-management behaviors. However, evidence on the health economic evaluation of these programs is limited.</AbstractText><AbstractText Label="OBJECTIVES" NlmCategory="UNASSIGNED">To systematically review the health economic evaluation of structured education programs for patients with type 1 and type 2 diabetes mellitus.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">The English databases PUBMED, WEB OF SCIENCE, OVID, COCHRANE LIBRARY, EMBASE, and EBSCO, along with the Chinese databases CNKI, WANFANG, VIP, and SINOMED, were searched from their inception to September 2024. The quality of the literature was assessed using the CHEERS 2022 checklist. A descriptive analysis was performed on the studies included in the review, with all currencies converted to international dollars. An incremental cost-effectiveness ratio of less than one times the <i>per capita</i> GDP was considered highly cost-effective, while a ratio between one and three times the <i>per capita</i> GDP was considered cost-effective.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 28 studies from upper-middle-income and high-income countries were included. The average quality score of the included studies was 18.6, indicating a moderate level of reporting quality. Among these, eleven studies demonstrated that diabetes structured education programs were highly cost-effective and twelve were found to be cost-effective. In contrast, three studies were deemed not cost-effective, and two studies provided uncertain results. The ranges of the incremental cost-effectiveness ratios for short-term, medium-term, and long-term studies were - 520.60 to 65,167.00 dollars, -24,952.22 to 14,465.00 dollars, and -874.00 to 236,991.67 dollars, respectively.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">This study confirms the cost-effectiveness of structured education programs for diabetes and highlights their importance for patients with type 2 diabetes who have HbA1c levels exceeding 7% and are receiving non-insulin therapy. Additionally, the potential advantages of incorporating telecommunication technologies into structured diabetes education were emphasized. These findings offer valuable insights and guidance for decision-making in diabetes management and clinical practice, contributing to the optimization of medical resource allocation and the improvement of health status and quality of life for patients.</AbstractText><CopyrightInformation>Copyright © 2024 Ye, Zhou, Yang, Tao and Jiang.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Caihua</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>International Nursing School, Hainan Medical University, Haikou, Hainan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Qiwei</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>International Nursing School, Hainan Medical University, Haikou, Hainan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Wenfei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>International Nursing School, Hainan Medical University, Haikou, Hainan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Tao</LastName><ForeName>Libo</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Center for Health Policy and Technology Evaluation, Peking University Health Science Center, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Jiang</LastName><ForeName>Xinjun</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>International Nursing School, Hainan Medical University, Haikou, Hainan, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Public Health</MedlineTA><NlmUniqueID>101616579</NlmUniqueID><ISSNLinking>2296-2565</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003362" MajorTopicYN="Y">Cost-Benefit Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010353" MajorTopicYN="Y">Patient Education as Topic</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="N">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cost-effectiveness analysis</Keyword><Keyword MajorTopicYN="N">diabetes</Keyword><Keyword MajorTopicYN="N">health economic evaluation</Keyword><Keyword MajorTopicYN="N">structured education</Keyword><Keyword MajorTopicYN="N">systematic review</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>4</Hour><Minute>35</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>11</Month><Day>21</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39639901</ArticleId><ArticleId IdType="pmc">PMC11617538</ArticleId><ArticleId IdType="doi">10.3389/fpubh.2024.1467178</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Zimmet P, Alberti KG, Shaw J. 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Patients diagnosed with diabetes mellitus have an increased risk of the cardiovascular and neurological diseases. However, recent evidence demonstrated that different antidiabetic drugs may delay cognitive impairment and improve cardiovascular outcomes. This review examines the impact of antidiabetic drugs on the HBA in patients with diabetes.</AbstractText><AbstractText Label="RECENT FINDINGS" NlmCategory="RESULTS">Metformin improves the cardiovascular and cognitive outcomes through adenosine 5'-monophosphate-activated protein kinase activation. Sodium-glucose cotransporter-2 inhibitors reduce inflammation, oxidative stress by inhibiting the NLRP3 inflammasome thereby reducing the incidence of heart failure and formation of beta-amyloid and neurofibrillary tangles in the brain. Dipeptidyl peptidase-4 inhibitors exhibit neuroprotective effects in Alzheimer's disease by reducing amyloid-beta and tau pathology and inflammation but may exacerbate heart failure risk due to increased sympathetic activity and prolonged β-adrenergic stimulation. Glucagon-like peptide-1 receptor agonists exhibit neuroprotective effects in Alzheimer's and Parkinson's diseases by reducing neuroinflammation, but may increase sympathetic activity, potentially elevating heart rate and blood pressure, despite their cardioprotective benefits.</AbstractText><AbstractText Label="SUMMARY" NlmCategory="CONCLUSIONS">Antidiabetes medications have the potential to improve cardiovascular and cognitive outcomes; however, additional studies are required to substantiate these effects.</AbstractText><CopyrightInformation>Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ong</LastName><ForeName>Leong Tung</ForeName><Initials>LT</Initials><AffiliationInfo><Affiliation>Department of Cardiology, National University Heart Centre, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sia</LastName><ForeName>Ching-Hui</ForeName><Initials>CH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Curr Opin Endocrinol Diabetes Obes</MedlineTA><NlmUniqueID>101308636</NlmUniqueID><ISSNLinking>1752-296X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>9100L32L2N</RegistryNumber><NameOfSubstance UI="D008687">Metformin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="Y">Brain</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008687" MajorTopicYN="N">Metformin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054873" MajorTopicYN="N">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="N">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>18</Day><Hour>12</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>4</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39639832</ArticleId><ArticleId IdType="doi">10.1097/MED.0000000000000896</ArticleId><ArticleId IdType="pii">01266029-990000000-00117</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Hu JR, Abdullah A, Nanna MG, Soufer R. 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Endocr Connect 2015; 4:R16–24.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39639712</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1940-4034</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><PubDate><Year>2024</Year><Season>Jan-Dec</Season></PubDate></JournalIssue><Title>Journal of cardiovascular pharmacology and therapeutics</Title><ISOAbbreviation>J Cardiovasc Pharmacol Ther</ISOAbbreviation></Journal><ArticleTitle>Impact of SGLT2 Inhibitors on Left Ventricular Remodeling in Diabetic Patients with Acute Myocardial Infarction.</ArticleTitle><Pagination><StartPage>10742484241301191</StartPage><MedlinePgn>10742484241301191</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1177/10742484241301191</ELocationID><Abstract><AbstractText Label="OBJECTIVE">To assess the effect of sodium-glucose cotransporter 2 inhibitors (SGLT2-I) on cardiac remodeling and prognosis in type 2 diabetes mellitus (T2DM) patients presenting with acute myocardial infarction (AMI).</AbstractText><AbstractText Label="METHODS">In this single-center retrospective active-comparator study, consecutive diabetic AMI patients undergoing percutaneous coronary intervention (PCI) between 2021 and 2023 were enrolled. Patients were divided into SGLT2-I users and non-SGLT2-I users based on discharge medications. The primary endpoint was the left ventricular remodeling index (LVRI), defined as the relative change in LV end-diastolic volume after six months. The secondary outcomes included major adverse cardiovascular events (MACE), comprising all-cause mortality, hospitalization for heart failure, nonfatal MI, and nonfatal stroke.</AbstractText><AbstractText Label="RESULTS">The study comprised 423 T2DM AMI patients(with or without ST-segment elevation), with 239 SGLT2-I users and 184 non-SGLT2-I users. At six months, LVRI was significantly lower in the SGLT2-I users compared to the non-SGLT2-I users (3.49 ± 19.71 vs 7.06 ± 15.15, <i>P</i> = .042). The non-SGLT2-I users exhibited a higher prevalence of positive LVR (LVRI > 0%) (64.67% vs 50.63%, <i>P</i> = .004) and pathological LVR (LVRI > 20%) (19.57% vs 12.13%, <i>P</i> = .036). Multivariate logistic regression indicated that SGLT2-I was associated with a reduced risk of LVR (OR 0.6; 95%CI 0.38-0.97; <i>P</i> = .035). During a mean follow-up of 25 ± 8 months, Kaplan-Meier analysis demonstrated a lower rate of MACE-free survival in the non-SGLT2-I users (<i>P</i> = .005).</AbstractText><AbstractText Label="CONCLUSIONS">SGLT2-I protects against LVR and lowers the risk of adverse cardiovascular outcomes in T2DM AMI patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Jun</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0003-1545-6556</Identifier><AffiliationInfo><Affiliation>Department of Emergency Internal Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Feng</ForeName><Initials>F</Initials><Identifier Source="ORCID">0009-0005-5343-6910</Identifier><AffiliationInfo><Affiliation>Department of Emergency Internal Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zuo</LastName><ForeName>Heping</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Emergency Internal Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Electrocardiographic Diagnosis, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yulin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Emergency Internal Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Emergency Internal Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Cai</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Emergency Internal Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Chunlin</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Emergency Surgery, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Jinglin</ForeName><Initials>J</Initials><Identifier Source="ORCID">0009-0009-7254-2128</Identifier><AffiliationInfo><Affiliation>Department of Emergency Internal Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>He</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Emergency Surgery, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Cardiovasc Pharmacol Ther</MedlineTA><NlmUniqueID>9602617</NlmUniqueID><ISSNLinking>1074-2484</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020257" MajorTopicYN="Y">Ventricular Remodeling</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="Y">Ventricular Function, Left</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D062645" MajorTopicYN="Y">Percutaneous Coronary Intervention</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="Y">Myocardial Infarction</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">SGLT2-I</Keyword><Keyword MajorTopicYN="N">T2DM</Keyword><Keyword MajorTopicYN="N">acute myocardial infarction</Keyword><Keyword MajorTopicYN="N">cardiac remodeling</Keyword></KeywordList><CoiStatement>Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>2</Hour><Minute>52</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39639712</ArticleId><ArticleId IdType="doi">10.1177/10742484241301191</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39639620</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>06</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1660-9379</ISSN><JournalIssue CitedMedium="Print"><Volume>20</Volume><Issue>898</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>Revue medicale suisse</Title><ISOAbbreviation>Rev Med Suisse</ISOAbbreviation></Journal><ArticleTitle>[SGLT2 inhibitors : promises, but for whom ?].</ArticleTitle><Pagination><StartPage>2307</StartPage><EndPage>2311</EndPage><MedlinePgn>2307-2311</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.53738/REVMED.2024.20.898.2307</ELocationID><Abstract><AbstractText>In type 2 diabetes, the launch of gliflozins (or SGLT2i), like each new therapeutic class, is generating a great deal of hope and is being heavily marketed. The pivotal studies show a beneficial effect on the risk of hospitalization for heart failure and, to a lesser extent, on the decline in renal function. The impact on physiological factors (weight, glycated hemoglobin, blood pressure) is modest, and the side-effect profile is relatively heavy, particularly in the elderly (frequent urogenital infections, ketoacidosis, etc.). The aim of this article is first and foremost to take a critical look at the interpretation of clinical studies and to identify populations where a favorable benefit/risk balance cannot be guaranteed.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lanfranchi</LastName><ForeName>Camille</ForeName><Initials>C</Initials><Identifier Source="ORCID">0009-0002-1927-4645</Identifier><AffiliationInfo><Affiliation>Pharmacie interjurassienne, Hôpitaux et institutions de soins du canton du Jura, du Jura bernois et du canton de Neuchâtel, 2740 Moutier.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jolivot</LastName><ForeName>Pierre-Alain</ForeName><Initials>PA</Initials><Identifier Source="ORCID">0009-0002-6238-0910</Identifier><AffiliationInfo><Affiliation>Pharmacie interjurassienne, Hôpitaux et institutions de soins du canton du Jura, du Jura bernois et du canton de Neuchâtel, 2740 Moutier.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wermeille</LastName><ForeName>Joël</ForeName><Initials>J</Initials><Identifier Source="ORCID">0009-0005-9767-0282</Identifier><AffiliationInfo><Affiliation>Pharmacie interjurassienne, Hôpitaux et institutions de soins du canton du Jura, du Jura bernois et du canton de Neuchâtel, 2740 Moutier.</Affiliation></AffiliationInfo></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Inhibiteurs du SGLT2 : des promesses, mais pour qui ?</VernacularTitle></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Rev Med Suisse</MedlineTA><NlmUniqueID>101219148</NlmUniqueID><ISSNLinking>1660-9379</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="fre"><AbstractText>Dans le diabète de type 2, l’arrivée sur le marché des gliflozines (ou iSGLT2) comme chaque nouvelle classe thérapeutique, suscite beaucoup d’espoir et fait l’objet d’un marketing important. Les études déterminantes (pivots), montrent un effet bénéfique sur le risque d’hospitalisation pour insuffisance cardiaque et dans une proportion moindre, sur le déclin de la fonction rénale. L’impact sur les facteurs physiologiques (poids, hémoglobine glyquée, tension artérielle) est modeste et leur profil d’effets indésirables est relativement chargé en particulier chez la personne âgée (infections urogénitales fréquentes, acidocétose, etc.). L’objectif de cet article est avant tout de poser un regard critique sur l’interprétation des études déterminantes et d’identifier les populations chez qui la balance bénéfice/risque devrait être questionnée.</AbstractText></OtherAbstract><CoiStatement>Les auteurs n’ont déclaré aucun conflit d’intérêts en relation avec cet article.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>2</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39639620</ArticleId><ArticleId IdType="doi">10.53738/REVMED.2024.20.898.2307</ArticleId><ArticleId IdType="pii">RMS0898-010</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39639300</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>08</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1472-6963</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>05</Day></PubDate></JournalIssue><Title>BMC health services research</Title><ISOAbbreviation>BMC Health Serv Res</ISOAbbreviation></Journal><ArticleTitle>Prescribing patterns before the initiation of novel antidiabetic medicines in public, occupational, and private healthcare: a register study reflecting the guidelines of care in type 2 diabetes.</ArticleTitle><Pagination><StartPage>1553</StartPage><MedlinePgn>1553</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1553</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12913-024-12010-y</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Disparities in access to healthcare has been implied before in Finland, a country with universal healthcare but de facto tiered primary care. Less is however known about the content of care provided in different settings. Previous studies indicate potential disparities in prescribing newer medicines between healthcare sectors. We compared the preceding prescribing patterns of patients who initiated a sodium-glucose co-transporter 2 (SGLT2) inhibitor or a glucagon-like peptide-1 (GLP-1) analogue in public, occupational, and private healthcare.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We used logistic models and patient-level register data from the city of Oulu, Finland, during 2014-2018. Among patients who initiated SGLT2 inhibitors or GLP-1 analogues, we studied whether it was a first-line treatment or if other antidiabetic medicines preceded the use. In addition, prior use of statins (a lipid-lowering medicine) and insulins were studied. Clinical guidelines for type 2 diabetes recommend in most cases metformin in first-line, and insulin only at later stages or in case of severe hyperglycaemia. Using a lipid-lowering medicine is typically recommended for all.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The examined novel antidiabetic medicines were seldom initiated in first-line, and no significant differences were observed for preceding statin use across sectors, net of patient characteristics. However, patients in the public sector were more likely to have used insulin previously compared to patients in occupational sector.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Before the initiation of the examined novel antidiabetic medicines, no marked differences across sectors in the use of other antidiabetic medicines or statins were observed. The higher likelihood of prior insulin use in the public sector might reflect initiation at a later stage and/or unobserved differences in clinical characteristics across patient populations.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rättö</LastName><ForeName>Hanna</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Research Unit, The Social Insurance Institution of Finland, Helsinki, Finland. hanna.ratto@kela.fi.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>INVEST Research Flagship Centre, University of Turku, Turku, Finland. hanna.ratto@kela.fi.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nurminen</LastName><ForeName>Mikko</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Research Unit, The Social Insurance Institution of Finland, Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aaltonen</LastName><ForeName>Katri</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Research Unit, The Social Insurance Institution of Finland, Helsinki, Finland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>INVEST Research Flagship Centre, University of Turku, Turku, Finland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2/26/2021</GrantID><Agency>The Social Insurance Institution of Finland</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Health Serv Res</MedlineTA><NlmUniqueID>101088677</NlmUniqueID><ISSNLinking>1472-6963</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005387" MajorTopicYN="N" Type="Geographic">Finland</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010818" MajorTopicYN="Y">Practice Patterns, Physicians'</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012042" MajorTopicYN="Y">Registries</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="N">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017149" MajorTopicYN="N">Private Sector</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017150" MajorTopicYN="N">Public Sector</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017410" MajorTopicYN="N">Practice Guidelines as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Care guideline</Keyword><Keyword MajorTopicYN="N">Diabetes</Keyword><Keyword MajorTopicYN="N">Healthcare</Keyword><Keyword MajorTopicYN="N">Novel medicine</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: This study was based only on administrative, secondary register data, and no human subjects were contacted to collect the data. From purely register-based studies, no Ethics Board approval is required in Finland [61]. According to the General Data Protection Regulation of the European Union and the Finnish Data Protection Act, processing of personal data is permitted without informed consent of study subjects if the task is carried out in the public interest, such as scientific research [62, 63]. The data used in the study were fully pseudonymised before we accessed them, and all data preparation and linkage in the study were done with pseudo-identifiers. The study was conducted following good scientific practice, data protection guidelines and ethical standards. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>4</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>5</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>23</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>5</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39639300</ArticleId><ArticleId IdType="pmc">PMC11619279</ArticleId><ArticleId IdType="doi">10.1186/s12913-024-12010-y</ArticleId><ArticleId IdType="pii">10.1186/s12913-024-12010-y</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Cho NH, Shaw JE, Karuranga S, Huang Y, da Rocha Fernandes JD, Ohlrogge AW, Malanda B. 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English translation.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39639251</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>08</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2458</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>05</Day></PubDate></JournalIssue><Title>BMC public health</Title><ISOAbbreviation>BMC Public Health</ISOAbbreviation></Journal><ArticleTitle>The effect of life skills training on reducing domestic violence and improving treatment adherence in women with diabetes experiencing intimate partner violence: a randomized clinical trial based on the theory of self-efficacy.</ArticleTitle><Pagination><StartPage>3390</StartPage><MedlinePgn>3390</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">3390</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12889-024-20913-y</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Intimate partner violence (IPV) is a global health problem and the cause of chronic diseases, such as diabetes. It has a negative effect on adherence to treatment, decreases self-efficacy beliefs, and intensifies stress in women. Therefore, this study aimed to investigate the effect of life skills training based on the self-efficacy theory on IPV and adherence to treatment in women with type 2 diabetes.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">This trial was conducted using a pretest-posttest design and follow-up after one month. The samples included 100 women selected by convenience sampling with random block allocation with type 2 diabetes and IPV. The intervention consisted of 8 sessions over one month of life skills training based on self-efficacy theory. Participants completed questionnaires at pre-test, post-test and follow-up, including a demographic information form and questionnaires on IPV and treatment adherence. Considered statistically significant at P < 0. 05.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The mean changes in IPV scores from the pre-test to the post-test were - 8.38 ± 4.06 and - 0.06 ± 3.09 in the intervention and control groups, respectively. Also, the reduction in the intervention group was significantly more than in the control group (P < 0.001; 95%CI=-9.75; -6.89). The mean changes in IPV scores from post-test to follow-up were - 1.36 ± 3.47 and 1.50 ± 4.14 in intervention and control groups, respectively, indicating a statistically significant difference between the two groups (P < 0.001; 95%CI=-4.38; -1.34). The mean changes in adherence scores from the pre-test to the post-test were 11.40 ± 4.23 and 0.68 ± 3.49 in the intervention and control groups, respectively. The increase was significantly higher in the intervention group than in the control group (P < 0.001; 95%CI = 9.18; 12.26). The mean changes in adherence scores from post-test to follow-up were 2.68 ± 5.06 and - 0.86 ± 2.43 in the intervention and control groups, respectively. The difference between the two groups was statistically significant (P < 0.001; 95%CI = 1.95; 5.12).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Life skills training based on self-efficacy theory reduced IPV and improved treatment compliance in women with diabetes under IPV. It is recommended that this training be taught to other patients with chronic conditions as a means of violence prevention and treatment adherence.</AbstractText><AbstractText Label="TRIAL REGISTRATION" NlmCategory="BACKGROUND">The trial was registered with the Iranian Registry of Clinical Trials (IRCT) on 13 October 2022 and can be found on the Iranian Registry of Clinical Trials platform. IRCT registration number: IRCT20090522001930N6.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rezaee</LastName><ForeName>Shahrbanoo</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Student Research Committee, Faculty of Nursing and Midwifery, Bushehr University of Medical Sciences, Bushehr, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bagherzadeh</LastName><ForeName>Razieh</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Midwifery, Nursing and Midwifery Faculty, Bushehr University of Medical Sciences, Bushehr, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reisi</LastName><ForeName>Mahnoush</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Health Education and Health Promotion, Faculty of Health, Bushehr University of Medical Sciences, Bushehr, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fotovat</LastName><ForeName>Leila</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Student Mental Health Counseling Office, Student Cultural Vice-Chancellor, Bushehr University of Medical Sciences, Bushehr, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vahedparast</LastName><ForeName>Hakimeh</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Medical-Surgical Nursing, Nursing and Midwifery Faculty, Bushehr University of Medical Sciences, P.O.Box. 7518759577, Salmane-farsi Blvd, Bushehr, Iran. h.vahedparast@bpums.ac.ir.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Public Health</MedlineTA><NlmUniqueID>100968562</NlmUniqueID><ISSNLinking>1471-2458</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020377" MajorTopicYN="Y">Self Efficacy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000066511" MajorTopicYN="Y">Intimate Partner Violence</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011795" MajorTopicYN="N">Surveys and Questionnaires</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000074822" MajorTopicYN="N">Treatment Adherence and Compliance</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017579" MajorTopicYN="N">Domestic Violence</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Intimate partner violence</Keyword><Keyword MajorTopicYN="N">Life skills training</Keyword><Keyword MajorTopicYN="N">Self-efficacy</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword><Keyword MajorTopicYN="N">Women</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: This research was approved by the Ethics Committee of Bushehr University of Medical Sciences (reference number IR.BPUMS.REC.1401.063). All participants were required to sign a written informed consent form. The participants were informed of the research objectives and methodology and were assured of the confidentiality of their data. Furthermore, it was emphasised that participation in the study was entirely voluntary and that participants were free to withdraw from the study at any time. To safeguard the confidentiality of those involved in the research, the objectives and methodology were presented in a private setting by a female researcher to participants who met the eligibility criteria. Once consent had been obtained, the participants completed the IPV questionnaire in the absence of any other individual. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>4</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>5</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>23</Hour><Minute>50</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>5</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39639251</ArticleId><ArticleId IdType="pmc">PMC11622502</ArticleId><ArticleId IdType="doi">10.1186/s12889-024-20913-y</ArticleId><ArticleId IdType="pii">10.1186/s12889-024-20913-y</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Lye M-S, Zarghami M, Charati JY, Abdollahi F. 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Am Psychol. 1982;37(2):122–47.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39639039</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>03</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-1723</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>05</Day></PubDate></JournalIssue><Title>Nature communications</Title><ISOAbbreviation>Nat Commun</ISOAbbreviation></Journal><ArticleTitle>Healthcare utilization, mortality, and cardiovascular events following GLP1-RA initiation in chronic kidney disease.</ArticleTitle><Pagination><StartPage>10623</StartPage><MedlinePgn>10623</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">10623</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41467-024-54009-3</ELocationID><Abstract><AbstractText>Treatment with glucagon-like peptide-1 receptor agonists (GLP1-RA) in patients with type 2 diabetes (T2D) and chronic kidney disease (CKD) may attenuate kidney disease progression and cardiovascular events but their real-world impact on healthcare utilization and mortality in this population are not well-defined. Here, we emulate a clinical trial that compares outcomes following initiation of GLP1-RA vs Dipeptidyl peptidase-4 inhibitors (DPP4i), as active comparators, in U.S. veterans aged 35 years of older with moderate to advanced CKD during fiscal years 2006 to 2021. Primary outcome was rate of acute healthcare utilization. Secondary outcomes were all-cause mortality and a composite of acute cardiovascular events. After propensity score matching (16,076 pairs) and 2.2 years mean follow-up duration, use of GLP1-RA in patients with moderate to advanced CKD was associated with lower annual rate of acute healthcare utilization and all-cause mortality. There was no significant difference in acute cardiovascular events.</AbstractText><CopyrightInformation>© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Shuyao</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Division of Endocrinology, University of Texas Southwestern Medical Center, Dallas, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sidra</LastName><ForeName>Fnu</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Division of Endocrinology, University of Texas Southwestern Medical Center, Dallas, TX, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Jones Center for Diabetes & Endocrine Wellness, Macon, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alvarez</LastName><ForeName>Carlos A</ForeName><Initials>CA</Initials><AffiliationInfo><Affiliation>Department of Pharmacy Practice and Center for Excellence in Real World Evidence, Texas Tech University Health Science Center, Dallas, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kinaan</LastName><ForeName>Mustafa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Endocrinology, Diabetes, and Metabolism Fellowship, UCF HCA Healthcare GME, Orlando, FL, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Internal Medicine, University of Central Florida, College of Medicine, Orlando, FL, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Lingvay</LastName><ForeName>Ildiko</ForeName><Initials>I</Initials><Identifier Source="ORCID">0000-0001-7006-7401</Identifier><AffiliationInfo><Affiliation>Department of Internal Medicine, Division of Endocrinology, University of Texas Southwestern Medical Center, Dallas, TX, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Peter O'Donnell Jr. School of Public Health, University of Texas Southwestern Medical Center, Dallas, TX, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Mansi</LastName><ForeName>Ishak A</ForeName><Initials>IA</Initials><Identifier Source="ORCID">0000-0001-6122-3716</Identifier><AffiliationInfo><Affiliation>Department of Internal Medicine, University of Central Florida, College of Medicine, Orlando, FL, USA. Ishak.mansi@va.gov.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Education Services, Orlando VA Healthcare System, Orlando, FL, USA. Ishak.mansi@va.gov.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nat Commun</MedlineTA><NlmUniqueID>101528555</NlmUniqueID><ISSNLinking>2041-1723</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="Y">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054873" MajorTopicYN="N">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010342" MajorTopicYN="N">Patient Acceptance of Health Care</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Competing interests: I.L. received research funding (paid to institution) from NovoNordisk, Sanofi, Merck, Pfizer, Mylan, Boehringer-Ingelheim. IL received advisory/consulting fees and/or other support from: Novo Nordisk, Eli Lilly, Sanofi, Astra Zeneca, Boehringer-Ingelheim, Cytoki Pharma, Johnson and Johnson, Intercept, TARGETPharma, Merck, Pfizer, Valeritas, Zealand Pharma, Shionogi, Carmot Therapeutics, Structure Therapeutics, Bayer, Translational Medical Academy, Mediflix, Biomea, Metsera, Regeneron, The Comm Group, and WebMD. I.L. serves on the Data Safety Monitoring Board for JAEB. C.A.A. received research funding (paid to the institution) from Merck, Bristol Myers Squibb, and Boehringer-Ingelheim. C.A.A. received funding from the National Institutes of Health National Center for Advancing Translational Sciences (grant #UL1TR003163). 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Analg.127, 1066–1073 (2018).</Citation><ArticleIdList><ArticleId IdType="pubmed">29324498</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39638855</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>05</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Monitoring individualized glucose levels predicts risk for bradycardia in type 2 diabetes patients with chronic kidney disease: a pilot study.</ArticleTitle><Pagination><StartPage>30290</StartPage><MedlinePgn>30290</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">30290</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-024-81983-x</ELocationID><Abstract><AbstractText>Patients with diabetes mellitus (DM) and chronic kidney disease (CKD) exhibit an elevated risk for cardiac arrhythmias, such as bradycardia, which may potentially lead to sudden cardiac death (SCD). While hypoglycemia, defined as a critical drop in glucose levels below the normal range, has long been associated with adverse cardiovascular events, recent studies have highlighted the need for a comprehensive reevaluation of its direct impact on cardiovascular outcomes, particularly in high-risk populations such as those with DM and CKD. In this study, we investigated the association between glucose levels and bradycardia by simultaneously monitoring interstitial glucose (IG) and ECG for 7 days in insulin-treated patients with DM and CKD. We identified bradycardia episodes in 19 of 85 patients (22%) and associated these episodes with personalized low, medium, and high relative glucose levels. Our analysis revealed a significant increase in bradycardia frequency during periods of lowest relative glucose, particularly between 06:00-09:00 and 12:00-15:00. Furthermore, leveraging a Random Forests classifier, we achieved a promising area under the curve (AUC) of 0.94 for predicting bradyarrhythmias using glucose levels and heart rate variability features. Contrary to previous findings, only 4% of bradycardia episodes in our study population occurred at glucose levels of 70 mg/dL or lower, with 28% observed at levels exceeding 180 mg/dL. Our findings not only highlight the strong correlation between relative glucose levels, heart rate parameters, and bradycardia onset but also emphasize the need for a more personalized definition of hypoglycemia to understand its relationship with bradyarrhythmias in high-risk DM and CKD patient populations.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Farhadi Ghalati</LastName><ForeName>Pejman</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Institute for Computational Biomedicine, RWTH Aachen University, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>E Samadi</LastName><ForeName>Moein</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute for Computational Biomedicine, RWTH Aachen University, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Verket</LastName><ForeName>Marlo</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine I, University Hospital RWTH, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Balfanz</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine I, University Hospital RWTH, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Müller-Wieland</LastName><ForeName>Dirk</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine I, University Hospital RWTH, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jonas</LastName><ForeName>Stephan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute for Digital Medicine, University Clinic Bonn, Bonn, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Napp</LastName><ForeName>Andreas</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine I, University Hospital RWTH, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wanner</LastName><ForeName>Christoph</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ketteler</LastName><ForeName>Markus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Nephrology, Coburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vassiliadou</LastName><ForeName>Athina</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Nephrology and Diabetology, Kliniken Maria-Hilf GmbH, Mönchengladbach, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heidenreich</LastName><ForeName>Stefan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>KFH Nephrology Center, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deserno</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Peter L. Reichertz Institute for Medical Informatics of TU Braunschweig and Hannover Medical School, Braunschweig, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hetzel</LastName><ForeName>Gudrun</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Nephrology, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fliser</LastName><ForeName>Danilo</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine IV, Saarland University Medical Centre, Homburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kelm</LastName><ForeName>Malte</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Pulmonology and Vascular Medicine, HHU Düsseldorf, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Floege</LastName><ForeName>Jürgen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine II, University Hospital Aachen, RWTH Aachen University, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marx</LastName><ForeName>Nikolaus</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine I, University Hospital RWTH, Aachen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schuppert</LastName><ForeName>Andreas</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute for Computational Biomedicine, RWTH Aachen University, Aachen, Germany. aschuppert@ukaachen.de.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001919" MajorTopicYN="Y">Bradycardia</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="Y">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010865" MajorTopicYN="N">Pilot Projects</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="N">Heart Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007003" MajorTopicYN="N">Hypoglycemia</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Bradycardia</Keyword><Keyword MajorTopicYN="N">Chronic kidney disease</Keyword><Keyword MajorTopicYN="N">Diabetes mellitus</Keyword><Keyword MajorTopicYN="N">Glucose monitoring</Keyword><Keyword MajorTopicYN="N">Hypoglycemia</Keyword><Keyword MajorTopicYN="N">Machine learning</Keyword><Keyword MajorTopicYN="N">Personalized medicine</Keyword></KeywordList><CoiStatement>Declarations. 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Scikit-learn: Machine learning in python. the Journal of machine Learning research12, 2825–2830 (2011).</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39638769</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1463-1326</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>2</Issue><PubDate><Year>2025</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Diabetes, obesity & metabolism</Title><ISOAbbreviation>Diabetes Obes Metab</ISOAbbreviation></Journal><ArticleTitle>Effectiveness and cost-effectiveness of an app and rewards-based intervention in type 2 diabetes: A randomised controlled trial.</ArticleTitle><Pagination><StartPage>729</StartPage><EndPage>739</EndPage><MedlinePgn>729-739</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/dom.16067</ELocationID><Abstract><AbstractText Label="AIM" NlmCategory="OBJECTIVE">Digital health interventions and economic incentives have shown promise in facilitating diabetes self-management, though evidence is limited. Therefore, this study aimed to evaluate the effectiveness and cost-effectiveness of a comprehensive app-based diabetes self-management programme with rewards for healthy behaviours and health outcomes.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">The TRIal to slow the Progression Of Diabetes (TRIPOD) study was an open-label, parallel-group, randomised controlled trial conducted at Duke-NUS Medical School, Singapore. Adults with Type 2 Diabetes (diabetes), HbA<sub>1c</sub> of 7.5%-11.0% (inclusive) and taking at least one oral diabetes medication were eligible. In total, 269 participants were randomised across three arms [Usual care (UC): 117, diabetes management programme (DMP) (intervention without rewards): 36, DMP+ (intervention with rewards): 116]. Data were analysed using intention-to-treat analysis with change in HbA<sub>1c</sub> at month 12 between DMP+ and UC as the primary outcome. Cost-effectiveness of DMP+ relative to UC was also calculated.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Mean HbA<sub>1c</sub> improved by 0.1% in UC and by 0.5% in DMP+ at 12 months, revealing a mean difference of 0.4% (95% confidence interval (CI): -0.70, -0.08, p = 0.015). The odds ratio of HbA<sub>1c</sub> improvements of >0.5% was 2.12 (95% CI: 1.17, 3.85, p = 0.013) for DMP+ relative to UC. The incremental cost-effectiveness ratio of DMP+ relative to UC was SGD8,516 (USD6,531) per quality-adjusted life year gained if effectiveness could be maintained with a single year of intervention.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">A comprehensive app-based diabetes self-management programme with rewards for healthy behaviours and health outcomes (DMP+) cost-effectively improved glycaemic control in Type 2 diabetes patients. Organizations focusing on value-based healthcare should consider subsidising similar interventions.</AbstractText><CopyrightInformation>© 2024 John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Finkelstein</LastName><ForeName>Eric Andrew</ForeName><Initials>EA</Initials><Identifier Source="ORCID">0000-0001-6443-9686</Identifier><AffiliationInfo><Affiliation>Health Services & Systems Research, Duke-NUS Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gardner</LastName><ForeName>Daphne Su-Lyn</ForeName><Initials>DS</Initials><Identifier Source="ORCID">0000-0001-5349-7442</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology, Singapore General Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tham</LastName><ForeName>Kwang Wei</ForeName><Initials>KW</Initials><Identifier Source="ORCID">0000-0003-1904-5711</Identifier><AffiliationInfo><Affiliation>Endocrinology Services, Woodlands Health, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gandhi</LastName><ForeName>Mihir</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-8902-2710</Identifier><AffiliationInfo><Affiliation>Centre for Quantitative Medicine, Duke-NUS Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biostatistics, Singapore Clinical Research Institute, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheung</LastName><ForeName>Yin Bun</ForeName><Initials>YB</Initials><Identifier Source="ORCID">0000-0003-0517-7625</Identifier><AffiliationInfo><Affiliation>Health Services & Systems Research, Duke-NUS Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centre for Quantitative Medicine, Duke-NUS Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bairavi</LastName><ForeName>Joann</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-9497-3994</Identifier><AffiliationInfo><Affiliation>Health Services & Systems Research, Duke-NUS Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chun Fan</ForeName><Initials>CF</Initials><Identifier Source="ORCID">0000-0002-1375-5328</Identifier><AffiliationInfo><Affiliation>Centre for Quantitative Medicine, Duke-NUS Medical School, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Ngiap Chuan</ForeName><Initials>NC</Initials><Identifier Source="ORCID">0000-0002-5946-1149</Identifier><AffiliationInfo><Affiliation>Department of Research, SingHealth Polyclinics, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yeoh</LastName><ForeName>Ester</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0002-2686-9412</Identifier><AffiliationInfo><Affiliation>Diabetes Centre, Admiralty Medical Centre, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Aspen Diabetes & Endocrine Clinic, Mount Elizabeth Novena Specialist Centre, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Phong Ching</ForeName><Initials>PC</Initials><Identifier Source="ORCID">0000-0002-9446-2032</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology, Singapore General Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Emily Tse Lin</ForeName><Initials>ETL</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Singapore General Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adamjee</LastName><ForeName>Thofique</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of General Medicine, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bee</LastName><ForeName>Yong Mong</ForeName><Initials>YM</Initials><Identifier Source="ORCID">0000-0002-5482-2646</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology, Singapore General Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goh</LastName><ForeName>Su-Yen</ForeName><Initials>SY</Initials><Identifier Source="ORCID">0000-0003-3758-9982</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology, Singapore General Hospital, Singapore, Singapore.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NMRC/HSRG/0079/2017</GrantID><Agency>National Medical Research Council</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Diabetes Obes Metab</MedlineTA><NlmUniqueID>100883645</NlmUniqueID><ISSNLinking>1462-8902</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C517652">hemoglobin A1c protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003362" MajorTopicYN="Y">Cost-Benefit Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D063731" MajorTopicYN="Y">Mobile Applications</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012201" MajorTopicYN="Y">Reward</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073278" MajorTopicYN="Y">Self-Management</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012846" MajorTopicYN="N" Type="Geographic">Singapore</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015438" MajorTopicYN="N">Health Behavior</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019057" MajorTopicYN="N">Quality-Adjusted Life Years</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cost‐effectiveness</Keyword><Keyword MajorTopicYN="N">effectiveness</Keyword><Keyword MajorTopicYN="N">glycaemic control</Keyword><Keyword MajorTopicYN="N">randomised trial</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>7</Day><Hour>0</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>5</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>22</Hour><Minute>42</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39638769</ArticleId><ArticleId IdType="doi">10.1111/dom.16067</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Cheah JS, Yeo PP, Thai AC, et al. 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This study investigated the hypoglycemic effects and underlying mechanisms of pure Hovenia dulcis (Guaizao) polysaccharide (HDPs-2A) in rats subjected to a high-fat and high-sugar diet combined with streptozotocin-induced T2DM. Oral administration of HDPs-2A resulted in significant increases in body weight and liver glycogen levels compared to untreated controls. Moreover, a reduction in fasting blood glucose levels, alleviation of hyperinsulinemia, enhanced glucose tolerance, and improved insulin resistance were observed in the HDPs-2A-treated group. HDPs-2A also effectively reversed diabetes-induced dyslipidemia, as evidenced by decreased total cholesterol and triglyceride levels, alongside increased high-density lipoprotein cholesterol levels. Histopathological analyses confirmed that HDPs-2A partially repaired liver tissue damage by mitigating oxidative stress responses in the liver. Additionally, treatment with HDPs-2A significantly elevated short-chain fatty acid levels in T2DM rats. Real-time quantitative PCR and Western blot analyses indicated that HDPs-2A significantly enhanced the expression of InsR, IRS2, PI3K, Akt, and GLUT4, suggesting that HDPs-2A regulates insulin resistance and glycometabolism through the activation of the PI3K/Akt signaling pathway. Furthermore, HDPs-2A appeared to modulate the expression of GS, GSK-3β, and FoxO1 to improve glucose metabolism and reduce insulin resistance. It also improved glucose metabolism by activating the AMPK pathway and modulating G6Pase and PEPCK expression. This study provides novel insights into the antidiabetic effects of HDPs, positioning them as promising nutritional agents for the management of T2DM.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Bing</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>College of Food Science and Technology, Hebei Agricultural University, 289 Lingyusi Road, Baoding, Hebei 071001, PR China. Electronic address: yangbing4329@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ruyan</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>College of Food Science and Technology, Hebei Agricultural University, 289 Lingyusi Road, Baoding, Hebei 071001, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xinyu</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>College of Food Science and Technology, Hebei Agricultural University, 289 Lingyusi Road, Baoding, Hebei 071001, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Wanjia</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>College of Food Science and Technology, Hebei Agricultural University, 289 Lingyusi Road, Baoding, Hebei 071001, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kan</LastName><ForeName>Jianquan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Food Science, Southwest University, 2 Tiansheng Road, Beibei, Chongqing 400715, PR China. Electronic address: kanjianquan@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Biol Macromol</MedlineTA><NlmUniqueID>7909578</NlmUniqueID><ISSNLinking>0141-8130</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011134">Polysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011134" MajorTopicYN="Y">Polysaccharides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006943" MajorTopicYN="Y">Hyperglycemia</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Glycolipid metabolism</Keyword><Keyword MajorTopicYN="N">Hovenia dulcis</Keyword><Keyword MajorTopicYN="N">Insulin resistance</Keyword><Keyword MajorTopicYN="N">Polysaccharide</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare no competing financial interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>10</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>12</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>8</Day><Hour>6</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>5</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>19</Hour><Minute>18</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39638196</ArticleId><ArticleId IdType="doi">10.1016/j.ijbiomac.2024.138338</ArticleId><ArticleId IdType="pii">S0141-8130(24)09149-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39637763</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7123</ISSN><JournalIssue CitedMedium="Internet"><Volume>343</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Psychiatry research</Title><ISOAbbreviation>Psychiatry Res</ISOAbbreviation></Journal><ArticleTitle>The relationship between depression and insulin resistance in the population without diabetes: Results from the 2005-2016 NHANES.</ArticleTitle><Pagination><StartPage>116311</StartPage><MedlinePgn>116311</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.psychres.2024.116311</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0165-1781(24)00596-1</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Insulin resistance (IR), a precursor of type 2 diabetes and other metabolic disorders, is becoming more common owing to rising obesity rates. Depression, which affects 4.4 % of the global population, has been linked to IR; however, the findings are inconsistent. The roles of moderating factors in the depression-IR relationship remain underexplored, creating a gap in the current understanding.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Data from six cycles of the National Health and Nutrition Examination Survey (NHANES, 2005-2016), including 6636 participants without diabetes, were analyzed. Depression was assessed using the Patient Health Questionnaire-9 (PHQ-9), with scores of 5-9 and 10-27 defined as mild and moderate-to-severe depression, respectively. IR was measured using the HOMA2-IR model, with IR defined as a value of ≥ 2.3. Weighted generalized linear models (GLMs) were used to investigate the relationship between depression and IR. Stratified analyses were used to evaluate the potential moderators.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">After adjusting for demographic factors and metabolic indicators, the results of GLMs analysis showed that moderate-to-severe depression significantly increased the odds of IR (OR = 1.65, 95 % CI: 1.04-2.61, p = 0.035), especially in non-Hispanic White individuals (OR = 2.64, 95 % CI: 1.39-5.00, p = 0.004). Antidepressant use also reduced this association.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Moderate-to-severe depression was significantly associated with IR, and race/ethnicity and antidepressant use were important moderators. These findings underscore the need for targeted interventions to address both mental and metabolic health risks in high-risk populations.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Nanchong Psychosomatic Hospital, Nanchong 637700, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Siyu</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Nanchong Psychosomatic Hospital, Nanchong 637700, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xian</LastName><ForeName>Xiaohua</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Nanchong Psychosomatic Hospital, Nanchong 637700, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xian</LastName><ForeName>Yin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Nanchong Psychosomatic Hospital, Nanchong 637700, PR China. Electronic address: xianyin@ncsxyy.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Psychiatry Res</MedlineTA><NlmUniqueID>7911385</NlmUniqueID><ISSNLinking>0165-1781</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009749" MajorTopicYN="Y">Nutrition Surveys</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003863" MajorTopicYN="Y">Depression</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014481" MajorTopicYN="N" Type="Geographic">United States</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Antidepressants</Keyword><Keyword MajorTopicYN="N">Depression, Insulin resistance</Keyword><Keyword MajorTopicYN="N">Modulatory effect</Keyword><Keyword MajorTopicYN="N">NHANES</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>10</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>0</Hour><Minute>41</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>6</Day><Hour>5</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>18</Hour><Minute>11</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39637763</ArticleId><ArticleId IdType="doi">10.1016/j.psychres.2024.116311</ArticleId><ArticleId IdType="pii">S0165-1781(24)00596-1</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39635824</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-6348</ISSN><JournalIssue CitedMedium="Internet"><Volume>40</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>05</Day></PubDate></JournalIssue><Title>International journal of technology assessment in health care</Title><ISOAbbreviation>Int J Technol Assess Health Care</ISOAbbreviation></Journal><ArticleTitle>Expanding access to sodium-glucose cotransporter 2 inhibitors (SGLT2i) in the Ministry of Health Malaysia - a multiple HTA approach.</ArticleTitle><Pagination><StartPage>e69</StartPage><MedlinePgn>e69</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e69</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1017/S0266462324000643</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">Ministry of Health (MOH) Malaysia stakeholders seek primary care access to sodium-glucose cotransporter 2 inhibitor (SGLT2i). Addressing this required a complex decision, selecting among three SGLT2i for two different indications and two practice settings. The options include expanding the existing SGLT2i (empagliflozin) in the MOH Medicines Formulary to primary care and/or having dapagliflozin and/or luseogliflozin as alternatives. This study aimed to conduct a multiple health technology assessment (HTA) to determine the SGLT2i of choice for the MOH setting.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The clinical benefits of SGLT2i were assessed through a systematic literature review and affordability was assessed through the development of three budget impact analysis models simulating seventy scenarios. Each model varied by prescribing indications, restrictions, and SGLT2i involved (M1: glycemic control, HbA1c between 6.5 percent and 10 percent, empagliflozin-dapagliflozin-luseogliflozin; M2: cardiovascular benefits, HbA1c less than 10 percent, empagliflozin-dapagliflozin; M3: a composite of M1 and M2). The outcome of the HTA was presented to the MOH decision-makers.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Although there was no significant difference in glycemic control between the SGLT2i, differences exist in cardiovascular benefits conferred. Despite having scenarios with lower net budget impact (NBI) in the M1, M2, and M3 models, decision-makers decided to expand empagliflozin use to primary care setting and add dapagliflozin for hospital-only setting for both indications [NBI of $4.38 mil] due to empagliflozin's advantage in reducing risk for cardiovascular death and prior experience of its use in MOH.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The multiple HTA approach guided the complex decision-making process by providing a holistic understanding of the decision's impact.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Choo</LastName><ForeName>Coleen Siew Bee</ForeName><Initials>CSB</Initials><Identifier Source="ORCID">0009-0003-0942-5726</Identifier><AffiliationInfo><Affiliation>Pharmaceutical Services Programme, Ministry of Health MalaysiaPetaling Jaya, Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yong</LastName><ForeName>Yee Vern</ForeName><Initials>YV</Initials><AffiliationInfo><Affiliation>Dato' Keramat Primary Healthcare Clinic, Ministry of Health MalaysiaKuala Lumpur, Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chandriah</LastName><ForeName>Haarathi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Pharmaceutical Services Programme, Ministry of Health MalaysiaPetaling Jaya, Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahmad</LastName><ForeName>Nur Sufiza</ForeName><Initials>NS</Initials><AffiliationInfo><Affiliation>Pharmaceutical Services Programme, Ministry of Health MalaysiaPetaling Jaya, Malaysia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Int J Technol Assess Health Care</MedlineTA><NlmUniqueID>8508113</NlmUniqueID><ISSNLinking>0266-4623</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001559">Benzhydryl Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>1ULL0QJ8UC</RegistryNumber><NameOfSubstance UI="C529054">dapagliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>HDC1R2M35U</RegistryNumber><NameOfSubstance UI="C570240">empagliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001559" MajorTopicYN="Y">Benzhydryl Compounds</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003362" MajorTopicYN="N">Cost-Benefit Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="Y">Glucosides</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008296" MajorTopicYN="N" Type="Geographic">Malaysia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011320" MajorTopicYN="N">Primary Health Care</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019057" MajorTopicYN="N">Quality-Adjusted Life Years</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000191" MajorTopicYN="N">economics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013673" MajorTopicYN="Y">Technology Assessment, Biomedical</DescriptorName><QualifierName UI="Q000458" MajorTopicYN="N">organization & administration</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">SGLT2i</Keyword><Keyword MajorTopicYN="N">decision-making</Keyword><Keyword MajorTopicYN="N">technology assessment</Keyword></KeywordList><CoiStatement>The authors reported no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>17</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>17</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>3</Minute></PubMedPubDate><PubMedPubDate 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Available from: https://www.ace-hta.gov.sg/healthcare-professionals/ace-technology-guidances.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39635750</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2299-2847</ISSN><JournalIssue CitedMedium="Internet"><Volume>96</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Month>May</Month><Day>09</Day></PubDate></JournalIssue><Title>Polski przeglad chirurgiczny</Title><ISOAbbreviation>Pol Przegl Chir</ISOAbbreviation></Journal><ArticleTitle>Analysis of quality of life in patients with clinically severe obesity and type 2 diabetes mellitus after laparoscopic sleeve gastrectomy - a 12-month prospective observational study.</ArticleTitle><Pagination><StartPage>20</StartPage><EndPage>30</EndPage><MedlinePgn>20-30</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.5604/01.3001.0054.5125</ELocationID><Abstract><AbstractText>&lt;b&gt;Introduction:&lt;/b&gt; Due to a short history of laparoscopic sleeve gastrectomy (LSG) as an independent bariatric procedure, we stilllack studies providing analysis of the quality of life (QoL) in patients with type 2 diabetes mellitus (DM2).&lt;b&gt;Aim:&lt;/b&gt; We aimed to assess the influence of LSG on QoL in obese patients with DM2.&lt;b&gt;Material and Methods:&lt;/b&gt; Prospective, observational study included patients with: morbid obesity, body mass index (BMI) ≥ 35 kg/m and ≤ 50 kg/m&lt;sup&gt;2&lt;/sup&gt;, DM2 shorter than 10 years, qualified for LSG. Bariatric Analysis and Reporting Outcome System (BAROS) that included the Moorehead-Ardelt Quality of Life Questionnaire II (MA-QoLQII) score, and the SF-36 Health Survey (SF-36) questionnaire were used for repetitive assessment of QoL before LSG and after one and 12 months following surgery. Selected clinical and biochemical parameters were also repeatedly measured.&lt;b&gt;Results:&lt;/b&gt; Thirty-three patients were included in the study (23 females). Patients' mean age was 45 10 years. BAROS significantly increased before LSG, one month, and one year after surgery (0.63 1.12, 2.94 1.90, and 4.97 2.08, respectively). The MA-QoLQII score significantly rose with an increase of excess body mass index loss (EBMIL) (P = 0.002) and remission of DM2 (P = 0.049), while inversely correlated with Homeostatic Model Assessment for Insulin Resistance index (HOMA-IR) (P = 0.003). Degenerative joint disease (P = 0.025) and average time of low glucose concentration in continuous glucose monitoring (CGM) (P = 0.005) had an inverse correlation with SF-36 Physical Component Summaries (PCS), standardized for cardiovascular comorbidity, EBMIL and HOMA-IR (P = 0.839; P = 0.086; P = 0.571, respectively). EBMIL (P = 0.003), remission of DM2 (P &lt; 0.001) had a positive correlation with Mental Component Summaries (MCS), while HOMA-IR (P &lt; 0.001) and count of low glucose concentration events (P = 0.022) had an inverse correlation with MCS, while standardized for average glucose concentration in CGM after 12 months (P = 0.586).&lt;b&gt;Discussion:&lt;/b&gt; Significant improvement in QoL was observed in patients with DM2 after LSG. Remission of DM2, higher EBMIL, lower HOMA-IR, fewer and shorter low glucose concentration events in CGM after 12 months were factors that increased selected QoL scores.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wysocki</LastName><ForeName>Michał</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of General Surgery and Surgical Oncology, Ludwik Rydygier Memorial Hospital in Cracow, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mizera</LastName><ForeName>Magdalena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>2nd Department of General Surgery, Jagiellonian University Medical College, Cracow, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karpińska</LastName><ForeName>Izabela</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>2nd Department of General Surgery, Jagiellonian University Medical College, Cracow, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ptaszkiewicz</LastName><ForeName>Kuba</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>2nd Department of General Surgery, Jagiellonian University Medical College, Cracow, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Małczak</LastName><ForeName>Piotr</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>2nd Department of General Surgery, Jagiellonian University Medical College, Cracow, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pisarska-Adamczyk</LastName><ForeName>Magdalena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical Education, Jagiellonian University Medical College, Cracow, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kania</LastName><ForeName>Michał</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Metabolic Diseases and Diabetology, Jagiellonian University Medical College, Cracow, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Major</LastName><ForeName>Piotr</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>2nd Department of General Surgery, Jagiellonian University Medical College, Cracow, Poland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Poland</Country><MedlineTA>Pol Przegl Chir</MedlineTA><NlmUniqueID>0376426</NlmUniqueID><ISSNLinking>0032-373X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011788" MajorTopicYN="Y">Quality of Life</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009767" MajorTopicYN="Y">Obesity, Morbid</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005743" MajorTopicYN="Y">Gastrectomy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010535" MajorTopicYN="Y">Laparoscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050110" MajorTopicYN="N">Bariatric Surgery</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015992" MajorTopicYN="N">Body Mass Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011795" MajorTopicYN="N">Surveys and Questionnaires</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Bariatric Analysis and Reporting Outcome System</Keyword><Keyword MajorTopicYN="N">SF-36 Health Survey</Keyword><Keyword MajorTopicYN="N">diabetes mellitus</Keyword><Keyword MajorTopicYN="N">laparoscopic sleeve gastrectomy</Keyword><Keyword MajorTopicYN="N">morbid obesity</Keyword><Keyword MajorTopicYN="N">quality of life</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>17</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>5</Hour><Minute>55</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39635750</ArticleId><ArticleId IdType="doi">10.5604/01.3001.0054.5125</ArticleId><ArticleId IdType="pii">01.3001.0054.5125</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39634184</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>Mapping the mitochondrial landscape in T2DM: key findings from 2003-2023.</ArticleTitle><Pagination><StartPage>1474232</StartPage><MedlinePgn>1474232</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1474232</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1474232</ELocationID><Abstract><AbstractText Label="BACKGOUND" NlmCategory="UNASSIGNED">T2DM, a chronic metabolic disorder, poses a significant threat to global public health. Mitochondria play a crucial role in the pathogenesis of T2DM. This study intends to investigate the correlation between mitochondria and T2DM over the past two decades (2003-2023) through bibliometric analysis. Its objectives are to pinpoint trends, emphasize research priorities, and establish a foundation for future investigations.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">A literature search was conducted using the SCI-E database. All recorded results were downloaded in plain text format for further analysis. The following terms were analyzed using Vosviewer 1.6.18, citespace 6.3r1, bibliometrix in RStudio (v.4.4.1), and Microsoft Excel 2021: country, institution, author, journal, references, and keywords.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">From January 1, 2003 to December 31, 2023, a total of 2,732 articles were retrieved. The United States, China, and Italy contributed most of the records. UNIVERSITY OF CALIFORNIA SYSTEM, INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICAL INSERM, and US DEPARTMENT OF VETERANS AFFAIRS were the top 3 most productive institutions. rocha milagros, victor victor m had the most publications, followed by roden michael, and petersen kf had the most citations together. DIABETES published the most articles on research on this topic, followed by AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, DIABETOLOGIA. The key points of this topic are the relationship between mitochondria and T2DM, the skeletal muscle mitochondrial changes observed in T2DM, and the impact of mitochondrial dysfunction on T2DM. Over the past five years, particle dynamics, mitochondrial dysfunction, and mechanism research have emerged as significant focal points in this field.</AbstractText><AbstractText Label="CONCLUDE" NlmCategory="UNASSIGNED">This paper successfully identified the key areas and emerging trends in the relationship between mitochondria and T2DM, thereby offering valuable insights for future research.</AbstractText><CopyrightInformation>Copyright © 2024 Tan, Liu, Zhou, Gao, Fang, Wang and Chen.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Yi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Departments of Acupuncture and Massage, Changchun University of Chinese Medicine, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Mingjun</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Departments of Acupuncture and Massage, Changchun University of Chinese Medicine, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Xinfeng</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Departments of Acupuncture and Massage, Changchun University of Chinese Medicine, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Tianjiao</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>The Affliated Hospital of Changchun University of Chinese Medicine, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Jinxu</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Departments of Acupuncture and Massage, Changchun University of Chinese Medicine, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Sixian</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Departments of Acupuncture and Massage, Changchun University of Chinese Medicine, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Shaotao</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Departments of Acupuncture and Massage, Changchun University of Chinese Medicine, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015706" MajorTopicYN="Y">Bibliometrics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="Y">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">CiteSpace</Keyword><Keyword MajorTopicYN="N">T2DM</Keyword><Keyword 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Acute pancreatitis (AP) can be triggered by various factors and is a potentially life-threatening condition. Although T2DM has been shown to have a close relationship with AP, the common mechanisms underlying the two conditions remain unclear.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">We identified common differentially expressed genes (DEGs) in T2DM and AP and used functional enrichment analysis and Mendelian randomization to understand the underlying mechanisms. Subsequently, we used several machine learning algorithms to identify candidate biomarkers and construct a diagnostic nomogram for T2DM and AP. The diagnostic performance of the model was evaluated using ROC, calibration, and DCA curves. Furthermore, we investigated the potential roles of core genes in T2DM and AP using GSEA, xCell, and single-cell atlas and by constructing a ceRNA network. Finally, we identified potential small-molecule compounds with therapeutic effects on T2DM and AP using the CMap database and molecular docking.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 26 DEGs, with 14 upregulated and 12 downregulated genes, were common between T2DM and AP. According to functional and DisGeNET enrichment analysis, these DEGs were mainly enriched in immune effector processes, blood vessel development, dyslipidemia, and hyperlipidemia. Mendelian randomization analyses further suggested that lipids may be a potential link between AP and T2DM. Machine learning algorithms revealed ARHGEF9 and SLPI as common genes associated with the two diseases. ROC, calibration, and DCA curves showed that the two-gene model had good diagnostic efficacy. Additionally, the two genes were found to be closely associated with immune cell infiltration. Finally, imatinib was identified as a potential compound for the treatment of T2DM and AP.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">This study suggests that abnormal lipid metabolism is a potential crosstalk mechanism between T2DM and AP. In addition, we established a two-gene model for the clinical diagnosis of T2DM and AP and identified imatinib as a potential therapeutic agent for both diseases.</AbstractText><CopyrightInformation>Copyright © 2024 Zhong, Yang, Shang, Yang, Li, Liu, Zhang, Liu and Jiang.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Zhong</LastName><ForeName>Lei</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Yang</LastName><ForeName>Xi</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Plastic Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Shang</LastName><ForeName>Yuxuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Plastic Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yao</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Junchen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Shuo</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolic Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yunshu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jifeng</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Xingchi</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010195" MajorTopicYN="Y">Pancreatitis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019295" MajorTopicYN="Y">Computational Biology</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="Y">Biomarkers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D062105" MajorTopicYN="N">Molecular Docking Simulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057182" MajorTopicYN="N">Mendelian Randomization Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000208" MajorTopicYN="N">Acute Disease</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">acute pancreatitis</Keyword><Keyword MajorTopicYN="N">biomarker</Keyword><Keyword MajorTopicYN="N">machine learning</Keyword><Keyword MajorTopicYN="N">molecular docking</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate 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Traditional dietary interventions, such as low-calorie or low-carbohydrate diets, typically overlook individual variability in postprandial glycemic responses (PPGRs), which can lead to suboptimal management of the disease. Recent advancements suggest that personalized nutrition, tailored to individual metabolic profiles, may enhance the effectiveness of T2D management.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">This study aims to present the development and application of a Digital Twin (DT) technology-a machine learning (ML)-powered platform designed to predict and modulate PPGRs in T2D patients. By integrating continuous glucose monitoring (CGM), dietary data, and other physiological inputs, the DT provides individualized dietary recommendations to improve insulin sensitivity, reduce hyperinsulinemia, and support the remission of T2D.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">We developed a sophisticated DT platform that synthesizes real-time data from CGM, dietary logs, and other biometric inputs to create personalized metabolic models for T2D patients. The intervention is delivered via a mobile application, which dynamically adjusts dietary recommendations based on predicted PPGRs. This methodology is validated through a randomized controlled trial (RCT) assessing its impact on various metabolic markers, including HbA1c, metabolic-associated fatty liver disease (MAFLD), blood pressure, body weight, ASCVD risk, albuminuria, and diabetic retinopathy.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Preliminary data from the ongoing RCT and real-world study demonstrate the DT's capacity to generate significant improvements in glycemic control and metabolic health. The DT-driven personalized nutrition plan has been associated with reductions in HbA1c, enhanced beta-cell function, and normalization of hyperinsulinemia, supporting sustained T2D remission. Additionally, the DT's predictions have contributed to improvements in MAFLD markers, blood pressure, and cardiovascular risk factors, highlighting its potential as a comprehensive management tool.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">The DT technology represents a novel and scalable approach to personalized nutrition in T2D management. By addressing individual variability in PPGRs, this method offers a promising alternative to conventional dietary interventions, with the potential to improve long-term outcomes and reduce the global burden of T2D.</AbstractText><CopyrightInformation>Copyright © 2024 Shamanna, Joshi, Thajudeen, Shah, Poon, Mohamed and Mohammed.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shamanna</LastName><ForeName>Paramesh</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Bangalore Diabetes Center, Bangalore, Karnataka, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Joshi</LastName><ForeName>Shashank</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Diabetology and Endocrinology, Lilavati Hospital and Research Center, Mumbai, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thajudeen</LastName><ForeName>Mohamed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Twin Health, Mountain View, CA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shah</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Twin Health, Mountain View, CA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Poon</LastName><ForeName>Terrence</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Twin Health, Mountain View, CA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohamed</LastName><ForeName>Maluk</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Twin Health, Mountain View, CA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohammed</LastName><ForeName>Jahangir</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Twin Health, Mountain View, CA, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000178" MajorTopicYN="N">diet therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057285" MajorTopicYN="Y">Precision Medicine</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000085002" MajorTopicYN="Y">Glycemic Control</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069550" MajorTopicYN="N">Machine Learning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015190" MajorTopicYN="N">Blood Glucose Self-Monitoring</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012074" MajorTopicYN="N">Remission Induction</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019518" MajorTopicYN="N">Postprandial Period</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000082222" MajorTopicYN="N">Digital Technology</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">digital twin technology</Keyword><Keyword MajorTopicYN="N">machine learning</Keyword><Keyword MajorTopicYN="N">personalized nutrition</Keyword><Keyword MajorTopicYN="N">predictive glycemic control</Keyword><Keyword MajorTopicYN="N">type 2 diabetes remission</Keyword></KeywordList><CoiStatement>PS, MT, LS, TP, MM and JM are employees of Twin Health Inc. 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(2019) 21:S2–35. doi: 10.1089/dia.2019.0019</Citation><ArticleIdList><ArticleId IdType="doi">10.1089/dia.2019.0019</ArticleId><ArticleId IdType="pubmed">31169427</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39634174</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>Factors related to type 2 diabetic retinopathy and their clinical application value.</ArticleTitle><Pagination><StartPage>1484197</StartPage><MedlinePgn>1484197</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1484197</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1484197</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">To compare the differences in clinical-related factors between patients with type 2 diabetes (T2DM) and those without diabetic retinopathy (DR) and to explore the risk factors or protective factors affecting DR in T2DM patients.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">We performed a retrospective analysis of 380 patients with type 2 diabetes admitted to Handan Central Hospital from June 2023 to May 2024. Clinical data collected included baseline characteristics, hematological tests, metabolic indicators, and information on diabetic complications and comorbidities.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Our findings identified intervention, neck vascular disease, bilateral lower limb venous thrombosis, high creatinine, high glomerular filtration rate, high chloride, high fasting C-peptide, and high lactate dehydrogenase as risk factors for DR. In contrast, High 2-hour postprandial C-peptide is a protective factor for diabetic retinopathy. A logistic regression model was constructed using stepwise regression to predict DR occurrence, achieving an accuracy of 0.80 and an AUC of 0.83.</AbstractText><CopyrightInformation>Copyright © 2024 Lian and Zhu.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lian</LastName><ForeName>Xue-Nan</ForeName><Initials>XN</Initials><AffiliationInfo><Affiliation>School of Graduate Studies, Hebei North University, Zhangjiakou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Endocrinology, Handan Central Hospital, Handan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Ming-Ming</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Handan Central Hospital, Handan, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003930" MajorTopicYN="Y">Diabetic Retinopathy</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">diabetic retinopathy</Keyword><Keyword MajorTopicYN="N">lactate dehydrogenase</Keyword><Keyword MajorTopicYN="N">logistic regression</Keyword><Keyword MajorTopicYN="N">protective factors</Keyword><Keyword MajorTopicYN="N">risk factors</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>17</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>5</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>1</Month><Day>1</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39634174</ArticleId><ArticleId IdType="pmc">PMC11614660</ArticleId><ArticleId IdType="doi">10.3389/fendo.2024.1484197</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Wang L, Gao P, Zhang M, Huang Z, Zhang D, Deng Q, et al. . 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Recently, the mechanism of ferroptosis in the pathophysiology of various diseases, including DCM, has attracted widespread attention. Here, we explored the role of PACS2 in ferroptosis in DCM through its downregulation of PACS2 expression.</AbstractText><AbstractText Label="METHODS AND RESULTS">Cardiomyocytes were treated with high glucose and palmitic acid (HGPA), and the detection of cardiomyocyte iron ions, lipid peroxides, and reactive oxygen species (ROS) revealed clear ferroptosis during these treatments. Silencing PACS2 downregulated CPT1A expression and upregulated DHODH expression significantly, reversing HGPA-induced ferroptosis. Further silencing of PACS2 with a CPT1A agonist exacerbated cardiomyocyte ferroptosis while promoting mitochondrial damage in cardiomyocytes. Using a mouse model of type 2 diabetes induced by streptozotocin (STZ) and a high-fat diet (HFD), we found that PACS2 deletion reversed these treatment-induced increases in cellular iron ions, impaired cardiac function, mitochondrial damage and ferroptosis in cardiac muscle tissues.</AbstractText><AbstractText Label="CONCLUSIONS">The PACS2/CPT1A/DHODH signalling pathway may be involved in ferroptosis in DCM by regulating cardiomyocyte mitochondrial function.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xiang</LastName><ForeName>Hong</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha, Hunan, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Center for Experimental Medicine, The Third Xiangya Hospital of Central South University, Changsha, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lyu</LastName><ForeName>Qi</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Shuhua</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, School of Life Sciences of Central South University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ouyang</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Third Xiangya Hospital of Central South University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Di</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Quanjun</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Third Xiangya Hospital of Central South University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Long</LastName><ForeName>HaiJiao</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Third Xiangya Hospital of Central South University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>Xinru</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Third Xiangya Hospital of Central South University, Changsha, Hunan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xiaoping</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha, Hunan, China. Xiaoping.Yang@hunnu.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Hongwei</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Center for Experimental Medicine, The Third Xiangya Hospital of Central South University, Changsha, China. hongweilu@csu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology, Third Xiangya Hospital of Central South University, Changsha, Hunan, China. hongweilu@csu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cardiovasc 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effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058065" MajorTopicYN="Y">Diabetic Cardiomyopathies</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="Y">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal 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MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019308" MajorTopicYN="N">Palmitic Acid</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetic cardiomyopathy</Keyword><Keyword MajorTopicYN="N">Ferroptosis</Keyword><Keyword MajorTopicYN="N">Mitochondria</Keyword></KeywordList><CoiStatement>Declarations. Competing interests: The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>4</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>4</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39633391</ArticleId><ArticleId IdType="pmc">PMC11619700</ArticleId><ArticleId IdType="doi">10.1186/s12933-024-02514-6</ArticleId><ArticleId IdType="pii">10.1186/s12933-024-02514-6</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Saeedi P, Petersohn I, Salpea P, Malanda B, Karuranga S, Unwin N, Colagiuri S, Guariguata L, Motala AA, Ogurtsova K, et al. 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Redox Biol. 2017;11:637–45.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5284490</ArticleId><ArticleId IdType="pubmed">28131082</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39633380</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>19</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1472-6823</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>05</Day></PubDate></JournalIssue><Title>BMC endocrine disorders</Title><ISOAbbreviation>BMC Endocr Disord</ISOAbbreviation></Journal><ArticleTitle>Glycemic control and associated factors in patients with type 2 diabetes in Southwest Ethiopia: a prospective observational study.</ArticleTitle><Pagination><StartPage>262</StartPage><MedlinePgn>262</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">262</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12902-024-01795-y</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Diabetes, a known syndrome marked by hyperglycemia and glucose intolerance, is increasing at an alarming rate worldwide. Over half a billion people worldwide have DM, and most live in low- and middle-income countries. Poor glycemic control is a public health concern in type 2 diabetes mellitus. Glycemic control and identifying factors associated with poor glycemic control can help healthcare providers design programs that improve glycemic control and the quality of services provided to patients.</AbstractText><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">This study was designed to assess the level of glycemic control and associated factors in patients with type 2 diabetes in Jimma Medical Center, Southwest Ethiopia.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">This institution-based prospective observational study was conducted among 420 patients with type 2 diabetes at Jimma Medical Center's diabetic clinics. A pretested structured interviewer-administered questionnaire was used to collect data, and a checklist was used to assess patient documents. The data were analyzed using SPSS version 26. The variables linked to poor glycemic control were investigated using binary logistic regression. Variables with p values less than 0.05 were considered statistically significant.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Six-month follow-ups were conducted among 420 patients with type 2 diabetes, among whom 220 (52.38%) were women. The median age of the participants was 54(IQR = 40-60 years old). The proportion of respondents with uncontrolled fasting blood glucose was 58.1%. Sex (AOR = 2.576, 95% CI [2.80-11.479], P = 0.001), age(≥ 60) (AOR = 2.024, 95% CI [1.794-4.646], P = 0.002), diabetes duration > 10 years (AOR = 3.036, 95% CI [2.616-8.306], P = 0.003), type 2 diabetes mellitus on insulin + oral antidiabetic (OADs) (AOR = 2.08, 95% CI [298-3.918], P = 0.004), obesity (AOR = 2.18, 95% CI [(1.218-4.218)], P = 0.003), diabetic complications (AOR = 3.193, 95% CI [2.324-6.05], p = 0.002) and poor self-care practices (AOR = 3.034, 95% CI [5.821-7.02], P = 0.005) were found to be significantly associated with poor glycemic control.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">At the Jimma Medical Center, the prevalence of poor glycemic control was high. Based on these findings, teaching and counseling provided by healthcare providers should focus on improving diabetes self-care activities, weight reduction, and diabetic complications to achieve good glycemic control.</AbstractText><AbstractText Label="CLINICAL TRIAL NUMBER" NlmCategory="BACKGROUND">Not applicable.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Garedo</LastName><ForeName>Aster Wakjira</ForeName><Initials>AW</Initials><AffiliationInfo><Affiliation>School of Pharmacy, Jimma University, Jimma, Ethiopia. asterwakjira@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Drug Quality and Registration (DruQuaR) group, Faculty of Pharmaceutical Sciences, Ghent University, Ghent, Belgium. asterwakjira@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tesfaye</LastName><ForeName>Gorfineh Teshome</ForeName><Initials>GT</Initials><AffiliationInfo><Affiliation>Jimma University Medical Center, Jimma, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tamrat</LastName><ForeName>Rahel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Jimma University School of Medical Laboratory, Jimma, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wynendaele</LastName><ForeName>Evelien</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Translational Research in Immunosenescence, Gerontology and Geriatrics (TRIGG) group, Ghent University Hospital, Ghent, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Drug Quality and Registration (DruQuaR) group, Faculty of Pharmaceutical Sciences, Ghent University, Ghent, Belgium.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Endocr Disord</MedlineTA><NlmUniqueID>101088676</NlmUniqueID><ISSNLinking>1472-6823</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005002" MajorTopicYN="N" Type="Geographic">Ethiopia</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000085002" MajorTopicYN="Y">Glycemic Control</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes mellitus</Keyword><Keyword MajorTopicYN="N">Ethiopia</Keyword><Keyword MajorTopicYN="N">Glycemic control</Keyword><Keyword MajorTopicYN="N">Risk factors</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: The International Council on Harmonization Guidelines for Good Clinical Practice and the Declaration of Helsinki were followed when conducting the study. The Jimma University Institutional Review Board (IRB) granted ethical approval as per protocol (IRB000/249/2023) prior to data collection. A research aim explanation was produced and distributed to all eligible participants in the form of an information sheet. We obtained informed consent from each participant. Parents or legal guardians provided informed consent for participants aged below 18 years. Patient confidentiality was maintained by utilizing the patients’ identification cards. Consent to publish: Not applicable. 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Sci Rep. 2020;10:17545. 10.1038/s41598-020-74000-4.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7567832</ArticleId><ArticleId IdType="pubmed">33067519</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39633372</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1475-2840</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>Cardiovascular diabetology</Title><ISOAbbreviation>Cardiovasc Diabetol</ISOAbbreviation></Journal><ArticleTitle>SGLT2 inhibitor downregulates ANGPTL4 to mitigate pathological aging of cardiomyocytes induced by type 2 diabetes.</ArticleTitle><Pagination><StartPage>430</StartPage><MedlinePgn>430</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">430</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12933-024-02520-8</ELocationID><Abstract><AbstractText Label="BACKGROUND">Senescence is recognized as a principal risk factor for cardiovascular diseases, with a significant association between the senescence of cardiomyocytes and inferior cardiac function. Furthermore, type 2 diabetes exacerbates this aging process. Sodium-glucose co-transporter 2 inhibitor (SGLT2i) has well-established cardiovascular benefits and, in recent years, has been posited to possess anti-aging properties. However, there are no reported data on their improvement of cardiomyocytes function through the alleviation of aging. Consequently, our study aims to investigate the mechanism by which SGLT2i exerts anti-aging and protective effects at the cardiac level through its action on the FOXO1-ANGPTL4 pathway.</AbstractText><AbstractText Label="METHODS">To elucidate the underlying functions and mechanisms, we established both in vivo and in vitro disease models, utilizing mice with diabetic cardiomyopathy (DCM) induced by type 2 diabetes mellitus (T2DM) through high-fat diet combined with streptozotocin (STZ) administration, and AC16 human cardiomyocyte cell subjected to stimulation with high glucose (HG) and palmitic acid (PA). These models were employed to assess the changes in the senescence phenotype of cardiomyocytes and cardiac function following treatment with SGLT2i. Concurrently, we identified ANGPTL4, a key factor contributing to senescence in DCM, using RNA sequencing (RNA-seq) technology and bioinformatics methods. We further clarified ANGPTL4 role in promoting pathological aging of cardiomyocytes induced by hyperglycemia and hyperlipidemia through knockdown and overexpression of the factor, as well as analyzed the impact of SGLT2i intervention on ANGPTL4 expression. Additionally, we utilized chromatin immunoprecipitation followed by quantitative real-time PCR (ChIP-qPCR) to confirm that FOXO1 is essential for the transcriptional activation of ANGPTL4.</AbstractText><AbstractText Label="RESULTS">The therapeutic intervention with SGLT2i alleviated the senescence phenotype in cardiomyocytes of the DCM mouse model constructed by high-fat feeding combined with STZ, as well as in the AC16 model stimulated by HG and PA, while also improving cardiac function in DCM mice. We observed that the knockdown of ANGPTL4, a key senescence-promoting factor in DCM identified through RNA-seq technology and bioinformatics, mitigated the senescence of cardiomyocytes, whereas overexpression of ANGPTL4 exacerbated it. Moreover, SGLT2i improved the senescence phenotype by suppressing the overexpression of ANGPTL4. In fact, we discovered that SGLT2i exert their effects by regulating the upstream transcription factor FOXO1 of ANGPTL4. Under conditions of hyperglycemia and hyperlipidemia, compared to the control group without FOXO1, the overexpression of FOXO1 in conjunction with SGLT2i intervention significantly reduced both ANGPTL4 mRNA and protein levels. This suggests that the FOXO1-ANGPTL4 axis may be a potential target for the cardioprotective effects of SGLT2i.</AbstractText><AbstractText Label="CONCLUSIONS">Collectively, our study demonstrates that SGLT2i ameliorate the pathological aging of cardiomyocytes induced by a high glucose and high fat metabolic milieu by regulating the interaction between FOXO1 and ANGPTL4, thereby suppressing the transcriptional synthesis of the latter, and consequently restoring cardiac function.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wen</LastName><ForeName>Yun</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiaofang</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Guangzhou Key Laboratory of Basic and Translational Research on Chronic Diseases, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Han</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Haowen</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ruxin</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Caixia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duo</LastName><ForeName>Tianqi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jiaxin</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xian</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Meixin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Liangyan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Yongting</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Lihong</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, First Affiliated Hospital of Jinan University, Guangzhou, China. nd6688@163.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Academician Cooperative Laboratory of Basic and Translational Research on Chronic Diseases, The First Affiliated Hospital, Jinan University, Guangzhou, China. nd6688@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>82200417</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>2023A04J1280</GrantID><Agency>Science and Technology Projects in Guangzhou</Agency><Country/></Grant><Grant><GrantID>808026</GrantID><Agency>Talent introduction funding project of the First Affiliated Hospital of Jinan University</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cardiovasc Diabetol</MedlineTA><NlmUniqueID>101147637</NlmUniqueID><ISSNLinking>1475-2840</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000075803">Angiopoietin-Like Protein 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071161">Forkhead Box Protein O1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C407088">Angptl4 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467200">Foxo1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C490299">Slc5a2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C474772">ANGPTL4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051297">Sodium-Glucose Transporter 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="Y">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000075803" MajorTopicYN="Y">Angiopoietin-Like Protein 4</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058065" MajorTopicYN="Y">Diabetic Cardiomyopathies</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016922" MajorTopicYN="Y">Cellular Senescence</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="Y">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="Y">Down-Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071161" MajorTopicYN="Y">Forkhead Box Protein O1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051297" MajorTopicYN="N">Sodium-Glucose Transporter 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="N">Glucosides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ANGPTL4</Keyword><Keyword MajorTopicYN="N">Cellular senescence</Keyword><Keyword MajorTopicYN="N">Diabetic cardiomyopathy</Keyword><Keyword MajorTopicYN="N">FOXO1</Keyword><Keyword MajorTopicYN="N">SGLT2i</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: Jinan University Experimental Animal Welfare Ethics Committee approved all animal experiments in this study (IACUC-20220512-06). 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Front Endocrinol (Lausanne). 2021;12:705154.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC8488438</ArticleId><ArticleId IdType="pubmed">34616362</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39633354</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1472-6823</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>BMC endocrine disorders</Title><ISOAbbreviation>BMC Endocr Disord</ISOAbbreviation></Journal><ArticleTitle>The potential of insulin resistance indices to predict non-alcoholic fatty liver disease in patients with type 2 diabetes.</ArticleTitle><Pagination><StartPage>261</StartPage><MedlinePgn>261</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">261</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12902-024-01794-z</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The triglyceride-glucose (TyG) index and related parameters, as well as the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), have been developed as insulin resistance markers to identify individuals at risk for non-alcoholic fatty liver disease (NAFLD). However, its use for predicting NAFLD in patients with type 2 diabetes mellitus (T2DM) remains unclear. In this study, we aimed to observe the performance of insulin resistance indices in diagnosing NAFLD combined with T2DM and to compare their diagnostic values in clinical practice.</AbstractText><AbstractText Label="PATIENTS AND METHODS" NlmCategory="METHODS">Overall, 268 patients with T2DM from the Endocrinology Department of Jiangsu Provincial Hospital of Traditional Chinese Medicine were enrolled in this study and divided into two groups: an NAFLD group (T2DM with NAFLD) and a T2DM group (T2DM without NAFLD). General information and blood indicators of the participants were collected, and insulin resistance indices were calculated based on these data. Receiver operating characteristic (ROC) analysis was conducted to calculate the area under the curve (AUC) for insulin resistance-related indices, aiming to assess their ability to discriminate between T2DM patients with and without NAFLD.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">ROC analysis revealed that among the five insulin resistance-related indices, four parameters (TyG, TyG-body mass index [BMI], TyG-waist circumference [WC], and TyG- (waist-hip ratio [WHR]) exhibited high predictive performance for identifying NAFLD, except for HOMA-IR (AUCs:0.710,0.738,0.737 and 0.730, respectivly). TyG-BMI demonstrated superior predictive value, especially in males. For males, the AUC for TyG-BMI was 0.764 (95% confidence interval [CI] 0.691-0.827). The sensitivity and specificity for male NAFLD were 90.32% and 47.89%, respectively. Moreover, in the Generalized linear regression models, there were positive associations of TyG, TyG-BMI, TyG-WC, TyG-WHR, and HOMA-IR with controlled attenuation parameter (CAP), with β values of 21.30, 0.745, 0.247, and 2.549 (all P < 0.001), respectively.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">TyG-BMI is a promising predictor of NAFLD combined with T2DM, particularly in lean male patients.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Tian</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>School of Nursing, Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Cao</LastName><ForeName>Yutian</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The First Clinical Medical College of Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Wenhui</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The First Clinical Medical College of Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Aiyao</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>School of Nursing, Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xinyi</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The First Clinical Medical College of Nanjing University of Chinese Medicine, Nanjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dong</LastName><ForeName>Yinfeng</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Pathology and Pathophysiology, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, China. dongyf@njucm.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Xiqiao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China. zhouxiqiao@njucm.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The First Clinical Medical College of Nanjing University of Chinese Medicine, Nanjing, China. zhouxiqiao@njucm.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Endocr Disord</MedlineTA><NlmUniqueID>101088676</NlmUniqueID><ISSNLinking>1472-6823</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014280">Triglycerides</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065626" MajorTopicYN="Y">Non-alcoholic Fatty Liver Disease</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015992" MajorTopicYN="N">Body Mass Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014280" MajorTopicYN="N">Triglycerides</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055105" MajorTopicYN="N">Waist Circumference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012372" MajorTopicYN="N">ROC Curve</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">BMI</Keyword><Keyword MajorTopicYN="N">Non-alcoholic fatty liver disease</Keyword><Keyword MajorTopicYN="N">ROC curves</Keyword><Keyword MajorTopicYN="N">TyG index-related parameters</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: The study protocol was approved by the Ethics Committee of Jiangsu Province Hospital of Traditional Chinese Medicine, with a waiver of informed consent. All methods were conducted in accordance with relevant guidelines and regulations. Consent for publication: Not applicable. 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The additional biological contribution of COVID-19 to TB is less clear. The goal of this study was to determine if there is an association between COVID-19 in the past 18 months and a new TB episode, and the role played by type 2 diabetes mellitus (DM) comorbidity in this relationship.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A cross-sectional study was conducted among 112 new active TB patients and 373 non-TB controls, identified between June 2020 and November 2021 in communities along the Mexican border with Texas. Past COVID-19 was based on self-report or positive serology. Bivariable/multivariable analysis were used to evaluate the odds of new TB in hosts with past COVID-19 and/or DM status.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The odds of new TB were higher among past COVID-19 cases vs. controls, but only significant among DM patients (aOR 2.3). The odds of TB in people with DM was 2.7-fold higher among participants without past COVID-19 and increased to 7.9-fold among those with past COVID-19.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">DM interacts with past COVID-19 synergistically to magnify the risk of TB. Latent TB screening and prophylactic treatment, if positive, is recommended in past COVID-19 persons with DM. Future studies are warranted with a longitudinal design and larger sample size to confirm our findings.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Calles-Cabanillas</LastName><ForeName>Liz E</ForeName><Initials>LE</Initials><AffiliationInfo><Affiliation>School of Public Health, University of Texas Health Science Center at Houston, One West University Blvd, SPH Bldg, Brownsville, TX, 78520, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aguillón-Durán</LastName><ForeName>Genesis P</ForeName><Initials>GP</Initials><AffiliationInfo><Affiliation>School of Public Health, University of Texas Health Science Center at Houston, One West University Blvd, SPH Bldg, Brownsville, TX, 78520, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ayala</LastName><ForeName>Doris</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>School of Public Health, University of Texas Health Science Center at Houston, One West University Blvd, SPH Bldg, Brownsville, TX, 78520, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caso</LastName><ForeName>José A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>School of Public Health, University of Texas Health Science Center at Houston, One West University Blvd, SPH Bldg, Brownsville, TX, 78520, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garza</LastName><ForeName>Miguel</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Public Health, University of Texas Health Science Center at Houston, One West University Blvd, SPH Bldg, Brownsville, TX, 78520, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Joya-Ayala</LastName><ForeName>Mateo</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Health and Biomedical Sciences, University of Texas Rio Grande Valley, Edinburg, TX, 78541, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cruz-Gonzalez</LastName><ForeName>America M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Departamento Estatal de Micobacteriosis, Secretaría de Salud de Tamaulipas, Reynosa 88630, Matamoros 87370 and Ciudad Victoria 87000, Tamaulipas, México.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loera-Salazar</LastName><ForeName>Raul</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Departamento Estatal de Micobacteriosis, Secretaría de Salud de Tamaulipas, Reynosa 88630, Matamoros 87370 and Ciudad Victoria 87000, Tamaulipas, México.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Prieto-Martinez</LastName><ForeName>Ericka</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Departamento Estatal de Micobacteriosis, Secretaría de Salud de Tamaulipas, Reynosa 88630, Matamoros 87370 and Ciudad Victoria 87000, Tamaulipas, México.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rodríguez-Herrera</LastName><ForeName>Javier E</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Departamento Estatal de Micobacteriosis, Secretaría de Salud de Tamaulipas, Reynosa 88630, Matamoros 87370 and Ciudad Victoria 87000, Tamaulipas, México.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garcia-Oropesa</LastName><ForeName>Esperanza M</ForeName><Initials>EM</Initials><AffiliationInfo><Affiliation>Unidad Académica Reynosa-Aztlán, Universidad Autónoma de Tamaulipas, Reynosa, Mexico.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thomas</LastName><ForeName>John M</ForeName><Initials>JM</Initials><Suffix>3rd</Suffix><AffiliationInfo><Affiliation>South Texas Diabetes and Obesity Institute and Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, 78541, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Miryoung</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Public Health, University of Texas Health Science Center at Houston, One West University Blvd, SPH Bldg, Brownsville, TX, 78520, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Torrelles</LastName><ForeName>Jordi B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>Population Health and Host Pathogens Interactions Programs and International Center for the Advancement of Research & Education (I•CARE), Texas Biomedical Research Institute, San Antonio, TX, 78229, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Restrepo</LastName><ForeName>Blanca I</ForeName><Initials>BI</Initials><AffiliationInfo><Affiliation>School of Public Health, University of Texas Health Science Center at Houston, One West University Blvd, SPH Bldg, Brownsville, TX, 78520, USA. Blanca.i.restrepo@uth.tmc.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>South Texas Diabetes and Obesity Institute and Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, 78541, USA. Blanca.i.restrepo@uth.tmc.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Population Health and Host Pathogens Interactions Programs and International Center for the Advancement of Research & Education (I•CARE), Texas Biomedical Research Institute, San Antonio, TX, 78229, USA. Blanca.i.restrepo@uth.tmc.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T34GM137854</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T34 GM137854</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30AI168439</GrantID><Agency>National Institute of Allergy and Infectious Diseases</Agency><Country/></Grant><Grant><GrantID>P30 AI168439</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AG051428</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01-AG051428</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Infect Dis</MedlineTA><NlmUniqueID>100968551</NlmUniqueID><ISSNLinking>1471-2334</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="UpdateOf"><RefSource>Res Sq. 2024 Mar 14:rs.3.rs-3989104. doi: 10.21203/rs.3.rs-3989104/v1</RefSource><PMID Version="1">38559235</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014376" MajorTopicYN="Y">Tuberculosis</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013781" MajorTopicYN="N" Type="Geographic">Texas</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008800" MajorTopicYN="N" Type="Geographic">Mexico</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015995" MajorTopicYN="N">Prevalence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">COVID-19</Keyword><Keyword MajorTopicYN="N">Cross-sectional study</Keyword><Keyword MajorTopicYN="N">Mexico</Keyword><Keyword MajorTopicYN="N">Tuberculosis</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: This study was approved by institutional review boards in Mexico (110/2018/CEI) and the US (HSC-SPH-19–0308; HSC-SPH-14–1007) and written informed consent was obtained from participants. 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However, unlike other glucose metrics that are easily defined and have clear targets, GV has a large number of different measures given the complexity involved in assessment. While variabilities in HbA1c, fasting and postprandial glucose have been incorporated under the GV banner, short-term variability in glucose, within day and between days, is more in keeping with the correct definition of GV. This review is focused on short-term GV, as assessed by CGM data, although studies calculating GV from capillary glucose testing are also mentioned as appropriate. The different measures of GV are addressed, and their potential role in microvascular and macrovascular complications, as well as patient-related outcomes, discussed. It should be noted that the independent role of GV in vascular pathology is not always clear, given the inconsistent findings in different populations and the close association between GV and hypoglycaemia, itself an established risk factor for adverse outcomes. Therefore, this review attempts, where possible, to disentangle the contribution of GV to diabetes complications from other glycaemic parameters, particularly hypoglycaemia. Evidence to date strongly suggests an independent role for GV in vascular pathology but future large-scale outcome studies are required to fully understand the exact contribution of this metric to vascular complications. This can be followed by setting appropriate GV measures and targets in different diabetes subgroups, in order to optimise glycaemic management and limit the risk of complications.</AbstractText><CopyrightInformation>© 2024 The Author(s). Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ajjan</LastName><ForeName>R A</ForeName><Initials>RA</Initials><Identifier Source="ORCID">0000-0002-1636-3725</Identifier><AffiliationInfo><Affiliation>LIGHT Laboratories, Leeds Institute for Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Diabetes Obes Metab</MedlineTA><NlmUniqueID>100883645</NlmUniqueID><ISSNLinking>1462-8902</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C517652">hemoglobin A1c protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000085002" MajorTopicYN="Y">Glycemic Control</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015190" MajorTopicYN="Y">Blood Glucose Self-Monitoring</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007003" MajorTopicYN="Y">Hypoglycemia</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003925" MajorTopicYN="N">Diabetic Angiopathies</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="N">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019518" MajorTopicYN="N">Postprandial Period</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000092522" MajorTopicYN="N">Clinical Relevance</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">continuous glucose monitoring</Keyword><Keyword MajorTopicYN="N">glycaemic variability</Keyword><Keyword MajorTopicYN="N">hypoglycaemia</Keyword><Keyword MajorTopicYN="N">macrovascular complications</Keyword><Keyword MajorTopicYN="N">microvascular complications</Keyword><Keyword MajorTopicYN="N">patient‐related outcome measures</Keyword><Keyword MajorTopicYN="N">type 1 diabetes</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>The author reports institutional research grants, honoraria, education support or consulting fees from the Abbott Diabetes Care, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol‐Myers Squibb, Eli Lilly, GlaxoSmithKline, Menarini Pharmaceuticals, Merck Sharp & Dohme and Novo Nordisk.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>10</Month><Day>10</Day></PubMedPubDate><PubMedPubDate 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Lancet. 2016;388(10057):2254‐2263.</Citation><ArticleIdList><ArticleId IdType="pubmed">27634581</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39632534</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>31</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1744-7666</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Expert opinion on pharmacotherapy</Title><ISOAbbreviation>Expert Opin Pharmacother</ISOAbbreviation></Journal><ArticleTitle>Tirzepatide for overweight and obesity management.</ArticleTitle><Pagination><StartPage>31</StartPage><EndPage>49</EndPage><MedlinePgn>31-49</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/14656566.2024.2436595</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="UNASSIGNED">Tirzepatide is a once-weekly dual agonist, acting on glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptors. It is approved at the same doses (5, 10 and 15 mg) for both type 2 diabetes (T2D) and chronic weight management.</AbstractText><AbstractText Label="AREAS COVERED" NlmCategory="UNASSIGNED">Following a search in PubMed, clinicaltrials.gov, conference abstracts and Lilly website, we review herein the global phase 3 SURMOUNT program on tirzepatide's safety and efficacy for chronic weight management. Additionally, we discuss findings from the regional SURMOUNT-CN and SURMOUNT-J trials (in East-Asian populations) and the phase 2 SYNERGY-NASH, phase 3 SURMOUNT-OSA and SUMMIT studies on tirzepatide's impact on obesity-related complications. We also explore the clinical implications of SURMOUNT program results, considerations for tirzepatide prescribing for overweight/obesity, ongoing research and evidence gaps.</AbstractText><AbstractText Label="EXPERT OPINION" NlmCategory="UNASSIGNED">Tirzepatide marks a new era in overweight/obesity treatment, enabling many to achieve ≥ 20% weight loss. It is well-tolerated with a safety profile similar to GLP-1 receptor agonists. Tirzepatide also results in clinically important improvements in multiple obesity-related complications including sleep apnea, metabolic-dysfunction associated steatohepatitis, heart failure with preserved ejection fraction and diabetes prevention. Ongoing trials will provide further data on tirzepatide's long-term safety, efficacy (including cardiovascular outcomes) and potential cost-effectiveness for managing overweight/obesity and/or T2D.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hamza</LastName><ForeName>Malak</ForeName><Initials>M</Initials><Identifier Source="ORCID">0009-0005-8483-8197</Identifier><AffiliationInfo><Affiliation>Diabetes Research Centre, University of Leicester, Leicester, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Papamargaritis</LastName><ForeName>Dimitris</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Diabetes Research Centre, University of Leicester, Leicester, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Diabetes and Endocrinology, Kettering General Hospital NHS Trust, Kettering, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Davies</LastName><ForeName>Melanie J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Diabetes Research Centre, University of Leicester, Leicester, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Opin Pharmacother</MedlineTA><NlmUniqueID>100897346</NlmUniqueID><ISSNLinking>1465-6566</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019440">Anti-Obesity Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>59392-49-3</RegistryNumber><NameOfSubstance UI="D005749">Gastric Inhibitory Polypeptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000067758">Glucagon-Like Peptide-2 Receptor</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019440" MajorTopicYN="Y">Anti-Obesity Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005749" MajorTopicYN="N">Gastric Inhibitory Polypeptide</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="Y">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000067758" MajorTopicYN="N">Glucagon-Like Peptide-2 Receptor</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="Y">Obesity</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050177" MajorTopicYN="Y">Overweight</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015431" MajorTopicYN="N">Weight Loss</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">GIP</Keyword><Keyword MajorTopicYN="N">GLP-1</Keyword><Keyword MajorTopicYN="N">Glucose-dependent insulinotropic polypeptide</Keyword><Keyword MajorTopicYN="N">SURMOUNT</Keyword><Keyword MajorTopicYN="N">glucagon-like peptide-1</Keyword><Keyword MajorTopicYN="N">obesity pharmacotherapy</Keyword><Keyword MajorTopicYN="N">tirzepatide</Keyword><Keyword MajorTopicYN="N">weight loss</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>1</Day><Hour>12</Hour><Minute>42</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>1</Hour><Minute>43</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39632534</ArticleId><ArticleId IdType="doi">10.1080/14656566.2024.2436595</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39632416</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1463-1326</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>2</Issue><PubDate><Year>2025</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Diabetes, obesity & metabolism</Title><ISOAbbreviation>Diabetes Obes Metab</ISOAbbreviation></Journal><ArticleTitle>A biweekly DPP-4 inhibitor cofrogliptin monotherapy in Chinese patients with impaired glucose tolerance: A phase 2, multicenter, randomized, double-blind, placebo-controlled, parallel-group trial.</ArticleTitle><Pagination><StartPage>965</StartPage><EndPage>975</EndPage><MedlinePgn>965-975</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/dom.16096</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">To assess the efficacy and safety of cofrogliptin for impaired glucose tolerance (IGT).</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">In this multicenter, double-blind, placebo-controlled phase 2 trial, IGT patients were randomized 1:1:1 to receive cofrogliptin 10 mg, cofrogliptin 25 mg or placebo once biweekly. The primary endpoint was the change from baseline in glucose total AUC<sub>0-3 h</sub> during meal tolerance test (MTT) at week 12.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Among 261 subjects screened, 99 were enrolled. At week 12, significant mean reductions from baseline in glucose total AUC<sub>0-3 h</sub> during MTT were observed in cofrogliptin groups (10 mg: -1.75 mmol h/L, p = 0.01; 25 mg: -1.54 mmol h/L, p = 0.02) versus placebo (0.36 mmol h/L). Significant benefits were also seen with cofrogliptin for secondary endpoints of the change from baseline in C<sub>max</sub> of glucose during MTT 0-3 h at week 12, and the change from baseline in glucose total AUC<sub>0-3 h</sub> and C<sub>max</sub> of glucose during OGTT 0-3 h at week 10 versus placebo. Additionally, more cofrogliptin-treated patients achieved normoglycaemia versus placebo at week 10. The incidence of AEs was generally comparable in all groups, and all of AEs were mild or moderate. No serious AEs or severe hypoglycaemia were reported.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">A 12-week treatment with cofrogliptin provided significant glucose-lowering, and was safe, well tolerated.</AbstractText><CopyrightInformation>© 2024 John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>He</LastName><ForeName>Qinghua</ForeName><Initials>Q</Initials><Identifier Source="ORCID">0000-0003-2082-5360</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Zhifeng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yufeng</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Beijing Pinggu Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xing</LastName><ForeName>Xiaoyan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Hebei Yanda Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Liping</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xinsheng</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Cangzhou Central Hospital, Cangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Junqing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Peking university first hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Lingling</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Peking Union Medical College Hospital, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Weihong</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Chenzhou First People's Hospital, Chenzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Fangqiong</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine, Haisco Pharmaceutical Group Co. Ltd, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Zhanhui</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine, Haisco Pharmaceutical Group Co. Ltd, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Lixin</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0001-6863-1798</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Haisco Pharmaceutical Group Co. Ltd</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D017427">Clinical Trial, Phase II</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Diabetes Obes Metab</MedlineTA><NlmUniqueID>100883645</NlmUniqueID><ISSNLinking>1462-8902</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054873">Dipeptidyl-Peptidase IV Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002681" MajorTopicYN="N" Type="Geographic">China</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054873" MajorTopicYN="Y">Dipeptidyl-Peptidase IV Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004311" MajorTopicYN="N">Double-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004334" MajorTopicYN="N">Drug Administration Schedule</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000095225" MajorTopicYN="N">East Asian People</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018149" MajorTopicYN="Y">Glucose Intolerance</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005951" MajorTopicYN="N">Glucose Tolerance Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">biweekly</Keyword><Keyword MajorTopicYN="N">cofrogliptin</Keyword><Keyword MajorTopicYN="N">dipeptidyl peptidase‐4 inhibitors</Keyword><Keyword MajorTopicYN="N">glucose intolerance</Keyword><Keyword MajorTopicYN="N">impaired glucose tolerance</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>7</Day><Hour>0</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>0</Hour><Minute>42</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39632416</ArticleId><ArticleId IdType="doi">10.1111/dom.16096</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Rezki A, Fysekidis M, Chiheb S, Vicaut E, Cosson E, Valensi P. 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Curr Med Res Opin. 2019;35:2071‐2078.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39632119</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>14</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2044-6055</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>BMJ open</Title><ISOAbbreviation>BMJ Open</ISOAbbreviation></Journal><ArticleTitle>Effect of communicating genetic risk of type 2 diabetes and wearable technologies on wearable device-measured behavioural outcomes in East Asians: protocol of a randomised controlled trial.</ArticleTitle><Pagination><StartPage>e082635</StartPage><MedlinePgn>e082635</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e082635</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjopen-2023-082635</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">The communication of information about the risk of type 2 diabetes (T2D) alone has not been associated with changes in habitual behaviours among individuals of European ancestry. In contrast, the use of wearable devices that monitor physical activity (PA) has been associated with behavioural changes in some studies. It is uncertain whether risk communication might enhance the effects of wearable devices. We aim to assess the effects of communicating genetic risk for T2D alone or in combination with wearable device functions on wearable device-measured PA among overweight or obese East Asians.</AbstractText><AbstractText Label="METHODS AND ANALYSIS" NlmCategory="METHODS">In a parallel group, randomised controlled trial, 355 overweight or obese East Asian individuals aged 40-60 years are allocated into one of three groups: one control and two intervention groups. Blood samples will be used for estimation of T2D genetic risk and analysis of metabolic risk markers. Genetic risk of T2D will be estimated based on 113 single-nucleotide polymorphisms associated with T2D among East Asians. All three groups receive a Fitbit device. Both intervention groups will receive T2D genetic risk estimates along with lifestyle advice, but one of the intervention groups additionally uses Fitbit's step goal setting and prompt functions. Questionnaires and physical measurements are administered at baseline, immediately after intervention delivery, and 6 and 12 months post intervention. The primary outcome is time spent in moderate-to-vigorous PA from the Fitbit, which will be assessed at baseline, immediately post intervention, 12 months post intervention and at 6-month follow-up. Secondary outcomes include other wearable device-measured parameters, sedentary time, and sleep, blood pressure, metabolic risk markers, hand grip strength, self-reported PA, fruit and vegetable consumption, smoking, and psychological variables. Between-group differences in the continuous and categorical variables collected at baseline will be examined using Analysis of Variance (ANOVA) and χ<sup>2</sup> tests, respectively. A series of linear mixed effects models with fixed effects of time, group and interaction between time and group will be performed, with adjustment for potential confounders.</AbstractText><AbstractText Label="ETHICS AND DISSEMINATION" NlmCategory="BACKGROUND">The study protocol has undergone review and received approval from the ethics committee of the University of Hong Kong. Findings from our trial will be disseminated through publication in peer-reviewed research journals and presented at international academic conferences.</AbstractText><AbstractText Label="TRIAL REGISTRATION NUMBER" NlmCategory="BACKGROUND">ClinicalTrials.gov, NCT05524909. https://register.</AbstractText><AbstractText Label="CLINICALTRIALS" NlmCategory="RESULTS">gov/ (11 November 2024).</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Youngwon</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong youngwon.kim@hku.hk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Godino</LastName><ForeName>Job G</ForeName><Initials>JG</Initials><AffiliationInfo><Affiliation>Exercise and Physical Activity Resource Center, Herbert Wertheim School of Public Health, University of California San Diego, La Jolla, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheung</LastName><ForeName>Flora Lai Tung</ForeName><Initials>FLT</Initials><AffiliationInfo><Affiliation>School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Multhaup</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Guardant Health, Redwood City, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Derwin King Chung K C</ForeName><Initials>DKCKC</Initials><Identifier Source="ORCID">0000-0001-8200-0263</Identifier><AffiliationInfo><Affiliation>The Education University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Ziyuan</ForeName><Initials>Z</Initials><Identifier Source="ORCID">0009-0000-0176-8685</Identifier><AffiliationInfo><Affiliation>School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Harrison Hin Sheung</ForeName><Initials>HHS</Initials><AffiliationInfo><Affiliation>School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tse</LastName><ForeName>Tsz Him Timothy</ForeName><Initials>THT</Initials><AffiliationInfo><Affiliation>School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Au Yeung</LastName><ForeName>Shiu Lun Ryan</ForeName><Initials>SLR</Initials><AffiliationInfo><Affiliation>Division of Epidemiology and Biostatistics, University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lou</LastName><ForeName>Shan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Epidemiology and Biostatistics, University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Joni H</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Mengyao</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chung</LastName><ForeName>Brian</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, The University of Hong Kong, HKSAR, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Griffin</LastName><ForeName>Simon</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>The Primary Care Unit, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>MRC Epidemiology Unit, Cambridge, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName><AccessionNumberList><AccessionNumber>NCT05524909</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D000078325">Clinical Trial Protocol</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open</MedlineTA><NlmUniqueID>101552874</NlmUniqueID><ISSNLinking>2044-6055</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" 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Annu Rev Genomics Hum Genet. 2013;14:491–513. doi: 10.1146/annurev-genom-092010-110722.</Citation><ArticleIdList><ArticleId IdType="doi">10.1146/annurev-genom-092010-110722</ArticleId><ArticleId IdType="pmc">PMC3862080</ArticleId><ArticleId IdType="pubmed">24003856</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39631943</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1756-1833</ISSN><JournalIssue CitedMedium="Internet"><Volume>387</Volume><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>BMJ (Clinical research ed.)</Title><ISOAbbreviation>BMJ</ISOAbbreviation></Journal><ArticleTitle>Chocolate intake and risk of type 2 diabetes: prospective cohort studies.</ArticleTitle><Pagination><StartPage>e078386</StartPage><MedlinePgn>e078386</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e078386</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmj-2023-078386</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To prospectively investigate the associations between dark, milk, and total chocolate consumption and risk of type 2 diabetes (T2D) in three US cohorts.</AbstractText><AbstractText Label="DESIGN" NlmCategory="METHODS">Prospective cohort studies.</AbstractText><AbstractText Label="SETTING" NlmCategory="METHODS">Nurses' Health Study (NHS; 1986-2018), Nurses' Health Study II (NHSII; 1991-2021), and Health Professionals Follow-Up Study (HPFS; 1986-2020).</AbstractText><AbstractText Label="PARTICIPANTS" NlmCategory="METHODS">At study baseline for total chocolate analyses (1986 for NHS and HPFS; 1991 for NHSII), 192 208 participants without T2D, cardiovascular disease, or cancer were included. 111 654 participants were included in the analysis for risk of T2D by intake of chocolate subtypes, assessed from 2006 in NHS and HPFS and from 2007 in NHSII.</AbstractText><AbstractText Label="MAIN OUTCOME MEASURE" NlmCategory="METHODS">Self-reported incident T2D, with patients identified by follow-up questionnaires and confirmed through a validated supplementary questionnaire. Cox proportional hazards regression was used to estimate hazard ratios and 95% confidence intervals (CIs) for T2D according to chocolate consumption.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">In the primary analyses for total chocolate, 18 862 people with incident T2D were identified during 4 829 175 person years of follow-up. After adjusting for personal, lifestyle, and dietary risk factors, participants consuming ≥5 servings/week of any chocolate showed a significant 10% (95% CI 2% to 17%; P trend=0.07) lower rate of T2D compared with those who never or rarely consumed chocolate. In analyses by chocolate subtypes, 4771 people with incident T2D were identified. Participants who consumed ≥5 servings/week of dark chocolate showed a significant 21% (5% to 34%; P trend=0.006) lower risk of T2D. No significant associations were found for milk chocolate intake. Spline regression showed a linear dose-response association between dark chocolate intake and risk of T2D (P for linearity=0.003), with a significant risk reduction of 3% (1% to 5%) observed for each serving/week of dark chocolate consumption. Intake of milk, but not dark, chocolate was positively associated with weight gain.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Increased consumption of dark, but not milk, chocolate was associated with lower risk of T2D. Increased consumption of milk, but not dark, chocolate was associated with long term weight gain. Further randomized controlled trials are needed to replicate these findings and further explore the mechanisms.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Binkai</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zong</LastName><ForeName>Geng</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Lu</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manson</LastName><ForeName>JoAnn E</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Molin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rimm</LastName><ForeName>Eric B</ForeName><Initials>EB</Initials><AffiliationInfo><Affiliation>Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Frank B</ForeName><Initials>FB</Initials><AffiliationInfo><Affiliation>Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Qi</ForeName><Initials>Q</Initials><Identifier Source="ORCID">0000-0002-8480-1563</Identifier><AffiliationInfo><Affiliation>Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA qisun@hsph.harvard.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ</MedlineTA><NlmUniqueID>8900488</NlmUniqueID><ISSNLinking>0959-8138</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069956" MajorTopicYN="Y">Chocolate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014481" MajorTopicYN="N" Type="Geographic">United States</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016016" MajorTopicYN="N">Proportional Hazards Models</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Competing interests: All authors have completed the ICMJE uniform disclosure form at https://www.icmje.org/disclosure-of-interest/ and declare: support from the National Institutes of Health for the submitted work. 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Am J Clin Nutr 1994;60(Suppl):1060S-4S.</Citation><ArticleIdList><ArticleId IdType="pubmed">7977152</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39631844</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2052-4897</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>BMJ open diabetes research & care</Title><ISOAbbreviation>BMJ Open Diabetes Res Care</ISOAbbreviation></Journal><ArticleTitle>Effect of flexor tendon tenotomy of the diabetic hammertoe on plantar pressure: a randomized controlled trial.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e004398</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjdrc-2024-004398</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">The aim of this study was to evaluate the effects of flexor tendon tenotomy treatment of the diabetic hammertoe deformity on plantar pressure.</AbstractText><AbstractText Label="RESEARCH DESIGN AND METHODS" NlmCategory="METHODS">The study was a substudy including participants from a randomized study on tenotomy treatment of diabetic hammertoes. This study was conducted between December 20, 2019 and June 22, 2021. Participants were randomized to tenotomy and standard non-surgical treatment <i>or</i> standard non-surgical treatment alone. Barefoot plantar pressure measurement was performed pre-intervention and 3 months post-intervention. Primary outcome was change in peak plantar pressure post tenotomy treatment.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Of the 95 participants screened in the original study, 45 (57.8% male) were included andcompleted this substudy. Of the 45 participants, 22 were randomized to intervention. The average age of participants was 65.6 ((SD±) 9.5) years and 30 (66.7%) had type 2 diabetes.The average peak plantar pressure (PPP) in toe regions of the participants in the intervention group was significantly (p<0.0001) reduced from 205.6 kPa ((Q1-Q3) 152.0-289.1) pre-intervention to 61.3 kPa (39.1-100.5) post-intervention. The average reduction in PPP of toe regions for participants in the intervention group (-145.3 kPa (-225.9 to -56.2)) was significantly (p=0.00017) higher than what was observed for participants in the control group (-1.6 kPa (-30.2 to 27.9)).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">This study found that tenotomies of the diabetic hammertoe reduces plantar pressure affecting the treated toes. This likely explains the positive effects of tenotomy treatment on diabetic foot ulcers.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Askø Andersen</LastName><ForeName>Jonas</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-5213-5888</Identifier><AffiliationInfo><Affiliation>Orthopedic Department, Nordsjaellands Hospital, Hillerød, Denmark jonas.hedegaard.andersen@regionh.dk.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Steno Diabetes Center Copenhagen, Herlev, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rasmussen</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Copenhagen, Herlev, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Engberg</LastName><ForeName>Susanne</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Copenhagen, Herlev, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Novo Nordisk A/S, Bagsvaerd, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bencke</LastName><ForeName>Jesper</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Orthopedic Surgery, Copenhagen University Hospital at Amager-Hvidovre, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frimodt-Møller</LastName><ForeName>Marie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Copenhagen, Herlev, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kirketerp-Møller</LastName><ForeName>Klaus</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Copenhagen, Herlev, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Copenhagen Wound Healing Center Bispebjerg Hospital, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rossing</LastName><ForeName>Peter</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0002-1531-4294</Identifier><AffiliationInfo><Affiliation>Steno Diabetes Center Copenhagen, Herlev, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open Diabetes Res Care</MedlineTA><NlmUniqueID>101641391</NlmUniqueID><ISSNLinking>2052-4897</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058971" MajorTopicYN="Y">Tenotomy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D037801" MajorTopicYN="Y">Hammer Toe Syndrome</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011312" MajorTopicYN="Y">Pressure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017719" MajorTopicYN="Y">Diabetic Foot</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013710" MajorTopicYN="N">Tendons</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetic Foot</Keyword><Keyword MajorTopicYN="N">Foot Ulcer</Keyword><Keyword MajorTopicYN="N">Plantar Pressure</Keyword></KeywordList><CoiStatement>Competing interests: None of the authors have any competing interests related to this work. Outside of this work: PR has received consultancy and/or speaking fees (to SDCC) from AbbVie, Astellas, AstraZeneca, Bayer, Boehringer Ingelheim, Gilead, Eli Lilly, MSD, Novo Nordisk and Sanofi Aventis, and research grants from Novo Nordisk and AstraZeneca. MF-M has received speaking fees from Boehringer Ingelheim, Novartis, Baxter and Sanofi. KK-M has received consultancy and/or speaking fees from Coloplast, Mölnlycke, SoftOx A/S and Bayer Pharmaceuticals AG. SE is employed in Novo Nordisk A/S.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>5</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>5</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>20</Hour><Minute>43</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39631844</ArticleId><ArticleId IdType="pmc">PMC11624764</ArticleId><ArticleId IdType="doi">10.1136/bmjdrc-2024-004398</ArticleId><ArticleId IdType="pii">12/6/e004398</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Edmonds M, Manu C, Vas P. 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Plantar pressure as a risk assessment tool for diabetic foot ulceration in egyptian patients with diabetes. Clin Med Insights Endocrinol Diabetes. 2014;7:31–9. doi: 10.4137/CMED.S17088.</Citation><ArticleIdList><ArticleId IdType="doi">10.4137/CMED.S17088</ArticleId><ArticleId IdType="pmc">PMC4257475</ArticleId><ArticleId IdType="pubmed">25520564</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39631843</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2052-4897</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>BMJ open diabetes research & care</Title><ISOAbbreviation>BMJ Open Diabetes Res Care</ISOAbbreviation></Journal><ArticleTitle>Comparative risk of type 2 diabetes development between women with gestational diabetes and women with impaired glucose tolerance over two decades: a multiethnic prospective cohort in New Zealand.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e004210</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjdrc-2024-004210</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">To evaluate the long-term risk of developing type 2 diabetes (T2D) among women with a history of gestational diabetes mellitus (GDM) compared with those with impaired glucose tolerance (IGT).</AbstractText><AbstractText Label="RESEARCH DESIGN AND METHODS" NlmCategory="METHODS">Using data from a primary care dataset linked with multiple health registries, this longitudinal study analyzed demographics, clinical data, and lifestyle factors of women diagnosed with GDM or IGT, assessing T2D incidence over 25 years, using Cox regression models.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Women with GDM, especially those over 35 years of Māori ethnicity, or socioeconomic deprivation, exhibited an elevated risk of T2D compared with those with IGT. The first 5 years post partum emerged as a critical window for intervention.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">This study underscores the importance of early, targeted post-GDM interventions to mitigate T2D risk. It highlights the necessity of personalized post-GDM interventions to reduce T2D incidence which consider age, ethnicity, and socioeconomic status to maximize effectiveness.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Dahai</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-8449-7725</Identifier><AffiliationInfo><Affiliation>Henan Key Laboratory of Chronic Disease Prevention and Therapy & Intelligent Health Management, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China d.yu@keele.ac.uk Da.Simmons@westernsydney.edu.au czw202112@zzu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzholu, Henan, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Medicine, Keele University, Keele, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fu</LastName><ForeName>Hang</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Henan Key Laboratory of Chronic Disease Prevention and Therapy & Intelligent Health Management, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Hospital Management of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Zhanzheng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzholu, Henan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pickering</LastName><ForeName>Karen</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Diabetes Foundation Aotearoa, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baker</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Counties Manukau District Health Board, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cutfield</LastName><ForeName>Richard</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Diabetes Foundation Aotearoa, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Orr-Walker</LastName><ForeName>Brandon J</ForeName><Initials>BJ</Initials><AffiliationInfo><Affiliation>Counties Manukau District Health Board, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sundborn</LastName><ForeName>Gerhard</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cai</LastName><ForeName>Yamei</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzholu, Henan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Zheng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzholu, Henan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Chengzeng</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Henan Key Laboratory of Chronic Disease Prevention and Therapy & Intelligent Health Management, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China d.yu@keele.ac.uk Da.Simmons@westernsydney.edu.au czw202112@zzu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Hospital Management of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simmons</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Henan Key Laboratory of Chronic Disease Prevention and Therapy & Intelligent Health Management, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China d.yu@keele.ac.uk Da.Simmons@westernsydney.edu.au czw202112@zzu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Translational Health Research Institute, Western Sydney University, Sydney, New South Wales, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Medicine, Western Sydney University, Sydney, New South Wales, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open Diabetes Res Care</MedlineTA><NlmUniqueID>101641391</NlmUniqueID><ISSNLinking>2052-4897</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016640" MajorTopicYN="Y">Diabetes, Gestational</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009520" MajorTopicYN="N" Type="Geographic">New Zealand</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018149" MajorTopicYN="Y">Glucose Intolerance</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005006" MajorTopicYN="N">Ethnicity</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005951" MajorTopicYN="N">Glucose Tolerance Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes Mellitus, Type 2</Keyword><Keyword MajorTopicYN="N">Diabetes, Gestational</Keyword><Keyword MajorTopicYN="N">Healthcare Disparities</Keyword><Keyword MajorTopicYN="N">Prediabetic State</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>3</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>9</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>5</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>5</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>20</Hour><Minute>43</Minute></PubMedPubDate><PubMedPubDate 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-<PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39631243</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-460X</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of diabetes and its complications</Title><ISOAbbreviation>J Diabetes Complications</ISOAbbreviation></Journal><ArticleTitle>Impact of visit-to-visit glycated hemoglobin variability on diabetes distress and its subscales.</ArticleTitle><Pagination><StartPage>108924</StartPage><MedlinePgn>108924</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jdiacomp.2024.108924</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1056-8727(24)00250-2</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">This study aimed to investigate the correlations between glycated hemoglobin (HbA1C) variability and diabetes distress (DD) and its subscales in older patients with type 2 diabetes mellitus.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The cross-sectional study analyzed 175 patients with type 2 diabetes mellitus, aged ≥60 years, and underwent HbA1C testing at least three times within a 2-year. HbA1C variability was assessed using the coefficient of variation (CV), standard deviation (SD), variability independent of the mean (VIM), and variability score. DD was assessed using a diabetes distress scale (DDS) questionnaire. We analyzed four DDS subscales, including emotional burden (EB), regimen distress (RD), interpersonal distress (ID), and physician distress (PD). Significant DD was defined as a total score ≥ 34.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">All four indices of HbA1C variability were positively correlated with DDS (r = 0.19, P = 0.01 in CV; r = 0.19, P = 0.01 in SD; r = 0.19, P = 0.02 in VIM; and r = 0.18, P = 0.02 in variability score). For the DD subscales, only EB showed a significant correlation with HbA1C variability (β = 0.72, SE = 0.35 in CV; β = 0.70, SE = 0.35 in SD; β = 0.66, SE = 0.31 in VIM; and β = 0.77, SE = 0.35 in variability score).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">HbA1C variability was independently linked to DD, particularly the EB subscale in older type 2 diabetes patients. This underscores the need for DD screening and intervention in patients with high HbA1C variability, irrespective of their HbA1C levels or depressive symptoms.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hong</LastName><ForeName>So-Hyeon</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jee</LastName><ForeName>Yongho</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Advanced Biomedical Research Institute, Ewha Womans University Seoul Hospital, Seoul, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sung</LastName><ForeName>Yeon-Ah</ForeName><Initials>YA</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hong</LastName><ForeName>Young Sun</ForeName><Initials>YS</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Do Kyeong</ForeName><Initials>DK</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jung</LastName><ForeName>Hyein</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Hyejin</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, South Korea. Electronic address: hyejinlee@ewha.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Diabetes Complications</MedlineTA><NlmUniqueID>9204583</NlmUniqueID><ISSNLinking>1056-8727</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C517652">hemoglobin A1c protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000079225" MajorTopicYN="N">Psychological Distress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013315" MajorTopicYN="N">Stress, Psychological</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011795" MajorTopicYN="N">Surveys and Questionnaires</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009819" MajorTopicYN="N">Office Visits</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes distress</Keyword><Keyword MajorTopicYN="N">Emotional burden</Keyword><Keyword MajorTopicYN="N">HbA1C variability</Keyword><Keyword MajorTopicYN="N">Long-term variability</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>5</Day><Hour>5</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>18</Hour><Minute>7</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39631243</ArticleId><ArticleId IdType="doi">10.1016/j.jdiacomp.2024.108924</ArticleId><ArticleId IdType="pii">S1056-8727(24)00250-2</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39631068</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>04</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2561-326X</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>JMIR formative research</Title><ISOAbbreviation>JMIR Form Res</ISOAbbreviation></Journal><ArticleTitle>A 360° Approach to Personalize Lifestyle Treatment in Primary Care for People With Type 2 Diabetes: Feasibility Study.</ArticleTitle><Pagination><StartPage>e57312</StartPage><MedlinePgn>e57312</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e57312</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.2196/57312</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Given the multifactorial nature of type 2 diabetes (T2D), health care for this condition would benefit from a holistic approach and multidisciplinary consultation. To address this, we developed the web-based 360-degree (360°) diagnostic tool, which assesses 4 key domains: "body" (physical health parameters), "thinking and feeling" (eg, mental health and stress), "behavior" (lifestyle factors), and "environment" (eg, work and housing conditions).</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">This work examines the acceptability, implementation, and potential effects of the 360° diagnostic tool and subsequent tailored treatment (360° approach) in a 6-month intervention and feasibility study conducted in standard primary health care settings in the Netherlands.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A single-group design with baseline, 3-month, and 6-month follow-ups was used. A total of 15 people with T2D and their health care providers from 2 practices participated in a 6-month intervention, which included the 360° diagnosis, tailored treatment, and both individual and group consultations. The 360° diagnosis involved clinical measurements for the "body" domain and self-reports for the "thinking and feeling," "behavior," and "environment" domains. After multidisciplinary consultations involving the general practitioner, pharmacist, nurse practitioner (NP), and dietitian, the NP and dietitian provided tailored advice, lifestyle treatment, and ongoing support. At the end of the intervention, face-to-face semistructured interviews were conducted with health care professionals (n=6) and participants (n=13) to assess the acceptability and implementation of the 360° approach in primary health care. Additionally, data from 14 participants on the "thinking and feeling" and "behavior" domains at baseline, 3 months, and 6 months were analyzed to assess changes over time.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The semistructured interviews revealed that both participants with T2D and health care professionals were generally positive about various aspects of the 360° approach, including onboarding, data collection with the 360° diagnosis, consultations and advice from the NP and dietitian, the visual representation of parameters in the profile wheel, counseling during the intervention (including professional collaboration), and the group meetings. The interviews also identified factors that promoted or hindered the implementation of the 360° approach. Promoting factors included (1) the care, attention, support, and experience of professionals; (2) the multidisciplinary team; (3) social support; and (4) the experience of positive health effects. Hindering factors included (1) too much information, (2) survey-related issues, and (3) time-consuming counseling. In terms of effects over time, improvements were observed at 3 months in mental health, diabetes-related problems, and fast-food consumption. At 6 months, there was a reduction in perceived stress and fast-food consumption. Additionally, fruit intake decreased at both 3 and 6 months.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our findings suggest that the 360° approach is acceptable to both people with T2D and health care professionals, implementable, and potentially effective in fostering positive health changes. Overall, it appears feasible to implement the 360° approach in standard primary health care.</AbstractText><AbstractText Label="TRIAL REGISTRATION" NlmCategory="BACKGROUND">Netherlands Trial Register NL-7509/NL-OMON45788; https://onderzoekmetmensen.nl/nl/trial/45788.</AbstractText><CopyrightInformation>©Zeena Harakeh, Iris de Hoogh, Anne-Margreeth Krijger-Dijkema, Susanne Berbée, Gino Kalkman, Pepijn van Empelen, Wilma Otten. Originally published in JMIR Formative Research (https://formative.jmir.org), 04.12.2024.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Harakeh</LastName><ForeName>Zeena</ForeName><Initials>Z</Initials><Identifier Source="ORCID">0000-0002-6571-4894</Identifier><AffiliationInfo><Affiliation>Department of Child Health, TNO, Netherlands Organization for Applied Scientific Research, Leiden, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Hoogh</LastName><ForeName>Iris</ForeName><Initials>I</Initials><Identifier Source="ORCID">0000-0002-1952-4774</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Systems Biology, TNO, Netherlands Organization for Applied Scientific Research, Leiden, Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Internal Medicine, Leiden University Medical Center, Leiden, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krijger-Dijkema</LastName><ForeName>Anne-Margreeth</ForeName><Initials>AM</Initials><Identifier Source="ORCID">0009-0008-0736-2369</Identifier><AffiliationInfo><Affiliation>Academic Pharmacy Stevenshof, Leiden, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Berbée</LastName><ForeName>Susanne</ForeName><Initials>S</Initials><Identifier Source="ORCID">0009-0001-3149-4475</Identifier><AffiliationInfo><Affiliation>Health Center Stevenshof, Leiden, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kalkman</LastName><ForeName>Gino</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0001-8533-5384</Identifier><AffiliationInfo><Affiliation>Department of Risk Analysis for Products in Development, TNO, Netherlands Organization for Applied Scientific Research, Utrecht, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Empelen</LastName><ForeName>Pepijn</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0002-9809-7650</Identifier><AffiliationInfo><Affiliation>Department of Child Health, TNO, Netherlands Organization for Applied Scientific Research, Leiden, Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Otten</LastName><ForeName>Wilma</ForeName><Initials>W</Initials><Identifier Source="ORCID">0000-0001-8613-7638</Identifier><AffiliationInfo><Affiliation>Department of Sustainable Productivity and Employability, TNO, Netherlands Organization for Applied Scientific Research, Leiden, Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>Canada</Country><MedlineTA>JMIR Form Res</MedlineTA><NlmUniqueID>101726394</NlmUniqueID><ISSNLinking>2561-326X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011320" MajorTopicYN="Y">Primary Health Care</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005240" MajorTopicYN="Y">Feasibility Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009426" MajorTopicYN="N" Type="Geographic">Netherlands</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008019" MajorTopicYN="N">Life Style</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057285" MajorTopicYN="N">Precision Medicine</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">diagnostic tool</Keyword><Keyword MajorTopicYN="N">feasibility study</Keyword><Keyword MajorTopicYN="N">health professionals</Keyword><Keyword MajorTopicYN="N">holistic approach</Keyword><Keyword MajorTopicYN="N">intervention</Keyword><Keyword MajorTopicYN="N">personalized treatment</Keyword><Keyword MajorTopicYN="N">primary care</Keyword><Keyword MajorTopicYN="N">shared decision-making</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>Conflicts of Interest: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>2</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>8</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>7</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>18</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>18</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>16</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate 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Curr Diab Rep. 2015 Dec;15(12):112. doi: 10.1007/s11892-015-0688-0.10.1007/s11892-015-0688-0</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s11892-015-0688-0</ArticleId><ArticleId IdType="pubmed">26458383</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39630807</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>04</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1414-431X</ISSN><JournalIssue CitedMedium="Internet"><Volume>57</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas</Title><ISOAbbreviation>Braz J Med Biol Res</ISOAbbreviation></Journal><ArticleTitle>Machine learning approaches and genetic determinants that influence the development of type 2 diabetes mellitus: a genetic association study in Brazilian patients.</ArticleTitle><Pagination><StartPage>e13957</StartPage><MedlinePgn>e13957</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e13957</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1590/1414-431X2024e13957</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0100-879X2024000100689</ELocationID><Abstract><AbstractText>This genetic association study including 120 patients with type 2 diabetes mellitus (T2DM) and 166 non-diabetic individuals aimed to investigate the association of polymorphisms in the genes GSTM1 and GSTT1 (gene deletion), GSTP1 (rs1695), ACE (rs4646994), ACE2 (rs2285666), VEGF-A (rs28357093), and MTHFR (rs1801133) with the development of T2DM in the population of Goiás, Brazil. Additionally, the combined effects of these polymorphisms and the possible differences between sexes in susceptibility to the disease were evaluated. Finally, machine learning models were integrated to select the main risk characteristics for the T2DM diagnosis. Risk associations were found for the GSTT1-null genotype in the non-stratified sample and females, and for mutant C allele of the VEGF-A rs28357093 polymorphism in the non-stratified sample. Furthermore, an association of heterozygous (AG) and mutant (GG) GSTP1 genotypes was observed when combined with GSTT1-null. Machine learning approaches corroborated the results found. Therefore, these results suggested that GSTT1 and GSTP1 polymorphisms may contribute to T2DM susceptibility in a Brazilian sample.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Santos</LastName><ForeName>K F</ForeName><Initials>KF</Initials><Identifier Source="ORCID">0000-0002-0555-3072</Identifier><AffiliationInfo><Affiliation>Laboratório de Patologia Molecular, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Assunção</LastName><ForeName>L P</ForeName><Initials>LP</Initials><Identifier Source="ORCID">0000-0002-1743-8151</Identifier><AffiliationInfo><Affiliation>Laboratório de Patologia Molecular, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Santos</LastName><ForeName>R S</ForeName><Initials>RS</Initials><Identifier Source="ORCID">0000-0002-9480-4362</Identifier><AffiliationInfo><Affiliation>Laboratório de Patologia Molecular, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Departamento de Bioquímica e Biologia Molecular, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reis</LastName><ForeName>A A S</ForeName><Initials>AAS</Initials><Identifier Source="ORCID">0000-0002-8281-7334</Identifier><AffiliationInfo><Affiliation>Laboratório de Patologia Molecular, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Departamento de Bioquímica e Biologia Molecular, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Brazil</Country><MedlineTA>Braz J Med Biol Res</MedlineTA><NlmUniqueID>8112917</NlmUniqueID><ISSNLinking>0100-879X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.5.1.18</RegistryNumber><NameOfSubstance UI="D005982">Glutathione Transferase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.5.1.-</RegistryNumber><NameOfSubstance UI="C413545">glutathione S-transferase T1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.5.1.18</RegistryNumber><NameOfSubstance UI="D051549">Glutathione S-Transferase pi</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069550" MajorTopicYN="Y">Machine Learning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001938" MajorTopicYN="N" Type="Geographic">Brazil</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="Y">Genetic Predisposition to Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="Y">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056726" MajorTopicYN="N">Genetic Association Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005982" MajorTopicYN="N">Glutathione Transferase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011110" MajorTopicYN="N">Polymorphism, Genetic</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051549" MajorTopicYN="N">Glutathione S-Transferase pi</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>3</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>9</Month><Day>26</Day></PubMedPubDate><PubMedPubDate 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Therefore, the current study was conducted to determine the pooled prevalence and its determinants of non-adherence to physical exercise among type two diabetes adult patients in Ethiopia.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Studies were searched systematically using International databases from PubMed, Google Scholar, Cochrane Library, Embase, and CINAHL. The quality of articles that were searched was assessed using the New Castle Ottawa scale for a cross-sectional study design. Statistical analysis was performed using STATA version 14 and a meta-analysis was carried out using a random effect model method. Assessment of the certainty evidence's was done by applying the GRADE method. The Preferred Reporting Item for Systematic Review and Meta-analyses (PRISMA) guideline was followed for reporting results. The title and the protocol of this meta-analysis were registered at the online database PROSPERO registration number CRD42023430579.</AbstractText><AbstractText Label="RESULT" NlmCategory="RESULTS">From the total 1711 records screened, 7 studies with 3437 participants who fulfilled the inclusion criteria were included in this systematic review. The estimated pooled prevalence of exercise non-adherence in Ethiopia was 50.59%. Being female (OR = 1.27, 95% CI (1.82, 1.97)), primary level education (OR = 1.19, 95% CI (1.01, 1.39)) and rural residency (OR = 4.87, 95% CI (2.80, 8.48)) were significantly associated with exercise non-adherence.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">According to papers evaluated by the GRADE assessment the certainty of evidence's was poor. More than half of the diabetes patients had physical exercise non-adherence. Strategies such as emotional support, health education, and emphasis on rural diabetic patients can improve the problem of non-adherence.</AbstractText><CopyrightInformation>Copyright: © 2024 Abate et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Abate</LastName><ForeName>Hailemicahel Kindie</ForeName><Initials>HK</Initials><Identifier Source="ORCID">0000-0002-6252-3574</Identifier><AffiliationInfo><Affiliation>Department Medical Nursing, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Azage</LastName><ForeName>Abere Woretaw</ForeName><Initials>AW</Initials><AffiliationInfo><Affiliation>Department Medical Nursing, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zegeye</LastName><ForeName>Alebachew Ferede</ForeName><Initials>AF</Initials><AffiliationInfo><Affiliation>Department Medical Nursing, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsega</LastName><ForeName>Sintayehu Sime</ForeName><Initials>SS</Initials><AffiliationInfo><Affiliation>Department Medical Nursing, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Agimas</LastName><ForeName>Muluken Chanie</ForeName><Initials>MC</Initials><AffiliationInfo><Affiliation>Institute of Public Health Department of Epidemiology and Biostatistics, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mekonnen</LastName><ForeName>Habtamu Sewunet</ForeName><Initials>HS</Initials><AffiliationInfo><Affiliation>Department Medical Nursing, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nega</LastName><ForeName>Gashaw Adane</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Department of Immunology and Molecular Biology, School of Biomedical and Laboratory Science, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Beko</LastName><ForeName>Zarko Wako</ForeName><Initials>ZW</Initials><AffiliationInfo><Affiliation>Department Medical Nursing, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mekonnen</LastName><ForeName>Chilot Kassa</ForeName><Initials>CK</Initials><AffiliationInfo><Affiliation>Department Medical Nursing, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005002" MajorTopicYN="N" Type="Geographic">Ethiopia</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="Y">Exercise</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010349" MajorTopicYN="N">Patient Compliance</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015995" 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This scoping review evaluates recent literature on text-messaging interventions focused on diabetes prevention, highlighting their development, associated outcomes, reach, and potential sustainability.</AbstractText><AbstractText Label="RECENT FINDINGS" NlmCategory="RESULTS">A total of 28 studies met eligibility criteria and were included in this review. Text-messaging was often used as a primary intervention method, focusing on promoting weight loss through physical activity and dietary changes. Studies also explored hybrid approaches integrating text-messaging with in-person sessions or other digital platforms. Intervention development involved multi-phase content creation, often leveraging established diabetes prevention curricula. Studies generally reported high feasibility and acceptability, although effectiveness was mixed. Cost-effectiveness comparisons favored text-messaging over traditional in-person programs. Implementation strategies aligned interventions with existing healthcare workflows, facilitating scalability and integration into routine care practices. Text-messaging interventions demonstrate considerable promise but require further refinement to ensure their effectiveness, particularly in enhancing participant engagement to ensure effectiveness and sustainability. Future research should focus on refining intervention content, integrating interactive features, and expanding cost-effectiveness evaluations to support broader implementation in real-world settings.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Formagini</LastName><ForeName>Taynara</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Family Medicine, University of California San Diego, 9500 Gilman Dr., La Jolla, San Diego, CA, 92093, USA. tformagini@health.ucsd.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gonzalez</LastName><ForeName>Christopher J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Division of General Internal Medicine, Weill Cornell Medicine, New York, NY, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dias</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, University of Central Florida, Orlando, FL, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arredondo</LastName><ForeName>Elva M</ForeName><Initials>EM</Initials><AffiliationInfo><Affiliation>Psychology Department, San Diego State University, San Diego, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hekler</LastName><ForeName>Eric</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Herbert Wertheim School of Public Health & Human Longevity Science, University of California San Diego, San Diego, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>O'Brien</LastName><ForeName>Matthew J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Department of Medicine, Division of General Internal Medicine and Geriatrics, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K24HL173681</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HL079891</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K24 HL173681</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32HL079891</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 DK092949</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30DK092949</GrantID><Agency>Chicago Center for Diabetes Translation Research</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Curr Diab Rep</MedlineTA><NlmUniqueID>101093791</NlmUniqueID><ISSNLinking>1534-4827</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="N">Exercise</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006293" MajorTopicYN="N">Health Promotion</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060145" MajorTopicYN="Y">Text Messaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000094703" MajorTopicYN="N">Cost-Effectiveness Analysis</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetes Prevention Program (DPP)</Keyword><Keyword MajorTopicYN="N">Narrative review</Keyword><Keyword MajorTopicYN="N">Text messaging</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes prevention</Keyword></KeywordList><CoiStatement>Declarations. Human/Animal Studies Informed Consent Statement: This article does not contain any studies with human or animal subjects performed by any of the authors. 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Technol Forecast Soc Chang. 2022;175:121359.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39630236</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>04</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1470-8728</ISSN><JournalIssue CitedMedium="Internet"><Volume>481</Volume><Issue>23</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>04</Day></PubDate></JournalIssue><Title>The Biochemical journal</Title><ISOAbbreviation>Biochem J</ISOAbbreviation></Journal><ArticleTitle>Biochemical basis and therapeutic potential of mitochondrial uncoupling in cardiometabolic syndrome.</ArticleTitle><Pagination><StartPage>1831</StartPage><EndPage>1854</EndPage><MedlinePgn>1831-1854</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1042/BCJ20240005</ELocationID><Abstract><AbstractText>Mild uncoupling of oxidative phosphorylation is an intrinsic property of all mitochondria, allowing for adjustments in cellular energy metabolism to maintain metabolic homeostasis. Small molecule uncouplers have been extensively studied for their potential to increase metabolic rate, and recent research has focused on developing safe and effective mitochondrial uncoupling agents for the treatment of obesity and cardiometabolic syndrome (CMS). Here, we provide a brief overview of CMS and cover the recent mechanisms by which chemical uncouplers regulate CMS-associated risk-factors and comorbidities, including dyslipidemia, insulin resistance, steatotic liver disease, type 2 diabetes, and atherosclerosis. Additionally, we review the current landscape of uncoupling agents, focusing on repurposed FDA-approved drugs and compounds in advanced preclinical or early-stage clinical development. Lastly, we discuss recent molecular insights by which chemical uncouplers enhance cellular energy expenditure, highlighting their potential as a new addition to the current CMS drug landscape, and outline several limitations that need to be addressed before these agents can successfully be introduced into clinical practice.</AbstractText><CopyrightInformation>© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Dos Santos</LastName><ForeName>Bernardo Gindri</ForeName><Initials>BG</Initials><AffiliationInfo><Affiliation>Department of Medicine (Cardiology), The Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, NY, U.S.A.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Brisnovali</LastName><ForeName>Niki F</ForeName><Initials>NF</Initials><AffiliationInfo><Affiliation>Department of Medicine (Cardiology), The Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, NY, U.S.A.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goedeke</LastName><ForeName>Leigh</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Medicine (Cardiology), The Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, NY, U.S.A.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine (Endocrinology), The Diabetes, Obesity and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York, NY, U.S.A.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Biochem J</MedlineTA><NlmUniqueID>2984726R</NlmUniqueID><ISSNLinking>0264-6021</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014475">Uncoupling Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D024821" MajorTopicYN="Y">Metabolic Syndrome</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="Y">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014475" MajorTopicYN="Y">Uncoupling Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004734" MajorTopicYN="N">Energy Metabolism</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010085" MajorTopicYN="N">Oxidative Phosphorylation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">insulin resistance</Keyword><Keyword MajorTopicYN="N">metabolic syndromes</Keyword><Keyword MajorTopicYN="N">mitochondria</Keyword><Keyword MajorTopicYN="N">mitochondrial respiration</Keyword><Keyword MajorTopicYN="N">oxidative phosphorylation</Keyword><Keyword MajorTopicYN="N">uncoupling proteins</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>12</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>12</Hour><Minute>28</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>11</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39630236</ArticleId><ArticleId IdType="doi">10.1042/BCJ20240005</ArticleId><ArticleId IdType="pii">235328</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39629799</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>31</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1744-7666</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Expert opinion on pharmacotherapy</Title><ISOAbbreviation>Expert Opin Pharmacother</ISOAbbreviation></Journal><ArticleTitle>Evaluating semaglutide + LAI-287 (IcoSema) for the treatment of diabetes mellitus type II.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>7</EndPage><MedlinePgn>1-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/14656566.2024.2436593</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="UNASSIGNED">A stepwise coordinated multiple therapeutic targeted approach to the treatment of type 2 diabetes includes starting with lifestyle modification, oral antihyperglycemic agents, non-insulin injectables (Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), and both short and long-acting insulins. Ultra-long-acting insulins offer more convenient administration. As in any chronic disease, the introduction of a novel medication must balance safety, efficacy, financial cost, as well as improved patient convenience and adherence.</AbstractText><AbstractText Label="AREAS COVERED" NlmCategory="UNASSIGNED">This manuscript describes IcoSema - a new investigational fixed-ratio combination of basal insulin icodec and the GLP-1 RA semaglutide. The key trials from the clinical development process of insulin icodec, semaglutide, and IcoSema are reviewed with important endpoints highlighted.</AbstractText><AbstractText Label="EXPERT OPINION" NlmCategory="UNASSIGNED">Once-weekly IcoSema offers glycemic efficacy that is non-inferior to glargine+aspart, similar risk of hypoglycemia, significant reduction in body weight, the convenience of use, and favorable safety profile with most adverse events being gastrointestinal.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Siamashvili</LastName><ForeName>Maka</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Davis</LastName><ForeName>Stephen N</ForeName><Initials>SN</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Opin Pharmacother</MedlineTA><NlmUniqueID>100897346</NlmUniqueID><ISSNLinking>1465-6566</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>53AXN4NNHX</RegistryNumber><NameOfSubstance UI="C000591245">semaglutide</NameOfSubstance></Chemical><Chemical><RegistryNumber>62340-29-8</RegistryNumber><NameOfSubstance UI="D004763">Glucagon-Like Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004338">Drug Combinations</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000097789">Glucagon-Like Peptide-1 Receptor Agonists</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004763" MajorTopicYN="Y">Glucagon-Like Peptides</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004338" MajorTopicYN="Y">Drug Combinations</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000097789" MajorTopicYN="N">Glucagon-Like Peptide-1 Receptor Agonists</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">IcoSema</Keyword><Keyword MajorTopicYN="N">diabetes</Keyword><Keyword MajorTopicYN="N">icodec</Keyword><Keyword MajorTopicYN="N">insulin</Keyword><Keyword MajorTopicYN="N">semaglutide</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>1</Day><Hour>12</Hour><Minute>41</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>12</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>7</Hour><Minute>53</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39629799</ArticleId><ArticleId IdType="doi">10.1080/14656566.2024.2436593</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39629644</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>04</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-9248</ISSN><JournalIssue CitedMedium="Print"><Volume>125</Volume><Issue>12</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Bratislavske lekarske listy</Title><ISOAbbreviation>Bratisl Lek Listy</ISOAbbreviation></Journal><ArticleTitle>The sodium-glucose cotransporter-2 inhibitors in patients with chronic kidney disease with or without kidney transplantation - a single centre study.</ArticleTitle><Pagination><StartPage>759</StartPage><EndPage>765</EndPage><MedlinePgn>759-765</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4149/BLL_2024_116</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND"> The sodium-glucose cotransporter-2 inhibitors (SGLT2i) represent the first-line treatment for chronic kidney disease. The question remains of their benefit and safety for patients after kidney transplantation. The study aimed to show the renoprotective effect and safety of use in patients with chronic kidney disease with or without kidney transplantation.</AbstractText><AbstractText Label="MATERIAL" NlmCategory="METHODS"> This is a prospective monocentric study of the Transplant-Nephrology Department in Martin in which patients with chronic kidney disease with or without kidney transplant in therapy with dapagliflozin were included (n=79). The changes in glomerular filtration rate, albuminuria and side effects associated with SGLT2i were studied in patients with chronic kidney disease with or without kidney transplantation and in patients with or without diabetes mellitus.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS"> Patients without diabetes mellitus achieved a significantly higher decrease in albuminuria at the time of the third month of follow-up (p=0.0396), with the continuation of the decrease until the average follow-up (10.9 months) (p=0.7866) than patients with diabetes mellitus. During the observed period, we recorded the cessation of the primary decrease in glomerular filtration with a return to the baseline values. In our group, we did not confirm a significant occurrence of adverse effects associated with dapagliflozin.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS"> SGLT2i significantly reduces albuminuria and stabilizes glomerular filtration in patients with chronic kidney disease. Based on our analysis, treatment with gliflozins is effective and safe for patients after kidney transplantation (Tab. 4, Fig. 6, Ref. 16).</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kleinova</LastName><ForeName>Patricia</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Granak</LastName><ForeName>Karol</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Vnucak</LastName><ForeName>Matej</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Beliancinova</LastName><ForeName>Monika</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Blichova</LastName><ForeName>Timea</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Dedinska</LastName><ForeName>Ivana</ForeName><Initials>I</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Slovakia</Country><MedlineTA>Bratisl Lek Listy</MedlineTA><NlmUniqueID>0065324</NlmUniqueID><ISSNLinking>0006-9248</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001559">Benzhydryl Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>1ULL0QJ8UC</RegistryNumber><NameOfSubstance UI="C529054">dapagliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016030" MajorTopicYN="Y">Kidney Transplantation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001559" MajorTopicYN="Y">Benzhydryl Compounds</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="Y">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005919" MajorTopicYN="Y">Glomerular Filtration Rate</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="Y">Glucosides</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000419" MajorTopicYN="Y">Albuminuria</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">chronic kidney disease</Keyword><Keyword MajorTopicYN="N">kidney transplant recipients</Keyword><Keyword MajorTopicYN="N">side effects SGLT2i.</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>12</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>5</Hour><Minute>53</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39629644</ArticleId><ArticleId IdType="doi">10.4149/BLL_2024_116</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39629047</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>04</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>12</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>Efficacy and safety of once-weekly insulin versus once-daily insulin in patients with type 1 and type 2 diabetes mellitus: an updated meta-analysis of randomized controlled trials.</ArticleTitle><Pagination><StartPage>1459127</StartPage><MedlinePgn>1459127</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">1459127</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2024.1459127</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">This meta-analysis was performed to obtain a comprehensive overview of the differences between once-weekly basal insulin (including icodec and basal insulin Fc) and once-daily basal insulin (including glargine and degludec) in patients with type 1 and type 2 diabetes mellitus.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">PubMed, EMBASE, and Cochrane Library were systematically searched for eligible studies up to 2 January 2024.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 12 studies were included, comprising 5,895 patients, with 3,104 (52.7%) using once-weekly insulin and 2,791 (47.3%) using once-daily insulin. In the pooled data, glycated hemoglobin (HbA1c) change from baseline [mean difference (MD) -0.11%; 95% confidence interval (CI) -0.20 to -0.01%] and the odds of achieving an end-of-trial HbA1c <7% (OR 1.41, 95% CI 1.13, 1.77) demonstrated a significantly good glycemic control in the once-weekly insulin group, especially in insulin-naïve type 2 diabetics or patients using icodec. Body weight increase for once-weekly insulin was 0.43 kg compared to controls (95% CI 0.09 to 0.76 kg). In addition, once-weekly insulin was correlated with a higher risk of level 1 hypoglycemia (OR 1.42, 95% CI 1.26 to 1.6). There was no significant difference in fasting plasma glucose (MD 2.46 mg/dL; 95% CI -2.60 to 7.52 mg/dL), time in range (MD 2.03%; 95% CI -0.50 to 4.56%), and level 2 or 3 hypoglycemic events (OR 1.19; 95% CI 0.93 to 1.53).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">Once-weekly basal insulin is safe and effective in modestly reducing HbA1c with similar level 2 or 3 hypoglycemic events compared to once-daily insulin, although the risk of level 1 hypoglycemia and weight gain was slightly increased.</AbstractText><AbstractText Label="SYSTEMATIC REVIEW REGISTRATION" NlmCategory="UNASSIGNED">https://www.crd.york.ac.uk/PROSPERO, Identifier CRD42024496812.</AbstractText><CopyrightInformation>Copyright © 2024 Xue, Shen, Tang, Deng and Dai.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Xue</LastName><ForeName>Mei</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Shen</LastName><ForeName>Pan</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Xuan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dai</LastName><ForeName>Zhe</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D049528">Insulin, Long-Acting</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="Y">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004334" MajorTopicYN="Y">Drug Administration Schedule</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007003" MajorTopicYN="N">Hypoglycemia</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="Y">Insulin</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049528" MajorTopicYN="N">Insulin, Long-Acting</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016032" MajorTopicYN="Y">Randomized Controlled Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">diabetes mellitus</Keyword><Keyword MajorTopicYN="N">glycosylated hemoglobin (HbA1c)</Keyword><Keyword MajorTopicYN="N">hypoglycemia</Keyword><Keyword MajorTopicYN="N">once-daily insulin</Keyword><Keyword MajorTopicYN="N">once-weekly insulin</Keyword></KeywordList><CoiStatement>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>4</Hour><Minute>44</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>1</Month><Day>1</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39629047</ArticleId><ArticleId IdType="pmc">PMC11611561</ArticleId><ArticleId IdType="doi">10.3389/fendo.2024.1459127</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Lewis GF, Brubaker PL. 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However, the changes in the cellular composition and function of PVAT, including the specific cell subsets and mechanisms implicated in type 2 diabetes mellitus (T2DM) vasculopathy, remain unclear.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">To address the above issues, we performed single-cell RNA sequencing on the stromal vascular fraction (SVF) of PVAT from normal and T2DM rats. Then, various bioinformatics tools and functional experiments were used to investigate the characteristic changes in the cellular profile of diabetic PVAT SVF, their implications, and the underlying mechanisms.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Our study reveals the single-cell landscape of the SVF of PVAT, demonstrating its considerable heterogeneity and significant alterations in T2DM, including an enhanced inflammatory response and elevated proportions of macrophages and natural killer (NK) cells. Moreover, macrophages are critical hubs for cross-talk among various cell populations. Notably, we identified a decreased Pdpn<sup>+</sup> macrophage subpopulation in the PVAT of T2DM rats and confirmed this in mice and humans. In vitro and in vivo studies demonstrated that Pdpn<sup>+</sup> macrophages alleviated insulin resistance and modulated adipokine/cytokine expression in adipocytes via the Pla2g2d-DHA/EPA-GPR120 pathway. This subset also enhances the function of vascular endothelial and smooth muscle cells, inhibits vascular inflammation and oxidative stress, and improves vasodilatory function, thereby protecting blood vessels.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Pdpn<sup>+</sup> macrophages exhibit significant vascular protective effects by alleviating insulin resistance and modulating adipokine/cytokine expression in PVAT adipocytes. This macrophage subtype may therefore play pivotal roles in mitigating vascular complications in T2DM. Our findings also underscore the critical role of immune-metabolic cross-talk in maintaining tissue homeostasis.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Li</LastName><ForeName>Jiaxuan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shandong Provincial Hospital, Shandong Laboratory Animal Center, Science and Technology Innovation Center, Shandong First Medical University and Shandong Academy of Medical Science, Jinan, 250021, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Key Laboratory of Endocrine Glucose and Lipids Metabolism and Brain Aging, Chinese Ministry of Education, Shandong First Medical University, Jinan, 250021, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Tian</LastName><ForeName>Zhenyu</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Tongxue</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Jiajia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xinjie</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Biology, University College London, London, NW1 2HE, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Panpan</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Breast and Thyroid Surgery, 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University, Jinan, 250021, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Yingjie</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Shandong Provincial Hospital, Shandong Laboratory Animal Center, Science and Technology Innovation Center, Shandong First Medical University and Shandong Academy of Medical Science, Jinan, 250021, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Key Laboratory of Endocrine Glucose and Lipids Metabolism and Brain Aging, Chinese Ministry of Education, Shandong First Medical University, Jinan, 250021, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xiaowei</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Shucui</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Xuefang</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Dong</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Neurology, Liaocheng People's Hospital, Liaocheng, 252000, China. guodonglc@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Zhe</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Geriatrics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China. wangzhe.zqy@email.sdu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China. wangzhe.zqy@email.sdu.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Qunye</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Cardiology, State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, 250012, China. wz.zhangqy@sdu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2021YFA1301102</GrantID><Agency>National Key R&D Program of China</Agency><Country/></Grant><Grant><GrantID>82070820</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>82170495</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>82100449</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>2018CXGC1218</GrantID><Agency>Major Science and Technology Innovation Project of Shandong Province</Agency><Country/></Grant><Grant><GrantID>202225044</GrantID><Agency>Clinical Medical Science and Technology Innovation Plan of Jinan</Agency><Country/></Grant><Grant><GrantID>ZR2021QH027</GrantID><Agency>Shandong Provincial Natural Science Foundation</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell Mol Biol Lett</MedlineTA><NlmUniqueID>9607427</NlmUniqueID><ISSNLinking>1425-8153</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000273" MajorTopicYN="Y">Adipose Tissue</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="Y">Macrophages</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059010" MajorTopicYN="Y">Single-Cell Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017667" MajorTopicYN="N">Adipocytes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Pdpn + macrophage</Keyword><Keyword MajorTopicYN="N">Diabetes</Keyword><Keyword MajorTopicYN="N">PVAT</Keyword><Keyword MajorTopicYN="N">SVF</Keyword><Keyword MajorTopicYN="N">Single-cell</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: This study was performed in accordance with the principles of the Helsinki Declaration and Basel Declaration. The collection of human samples was approved by the Ethics Committee of Liaocheng People’s Hospital (no. 2024263; date: 30 January 2024), and informed consent was obtained from all participants. All animal experiments were approved by the Animal Ethics Committee of Shandong Provincial Hospital (No. 2022-127; Date: 18 February 2022). Consent for publication: All authors have gave their consent for publication. Competing interests: All authors declare that they have no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>4</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>23</Hour><Minute>50</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39627688</ArticleId><ArticleId IdType="pmc">PMC11616190</ArticleId><ArticleId IdType="doi">10.1186/s11658-024-00668-5</ArticleId><ArticleId IdType="pii">10.1186/s11658-024-00668-5</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Cole JB, Florez JC. 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The multiple linear regression model and the multiple binary logistic regression were used to evaluate the relationships between mVOCs and glucose homeostasis/T2D, respectively. Among the 19 mVOCs, the higher levels of urinary N-acetyl-S-(2-hydroxypropyl)-L-cysteine (2HPMA, compound CID:44146439) and N-acetyl-S-(2-hydroxypropyl)-L-cysteine (HPMMA, compound CID:107774684) were significantly associated with higher odds of T2D (OR = 1.16, 95% confidence interval [CI]:1.01-1.34 for 2HPMA; and OR = 1.27, 95% CI:1.04-1.54 for HPMMA). In addition, higher concentrations of multiple mVOCs in urine were significantly correlated with glucose homeostasis biomarkers, including 2HPMA and 2-thioxothiazolidine-4-carboxylic acid (TTCA, compound CID:3034757) with fasting glucose, HPMMA and mandelic acid (MA, compound CID:1292) with HbA1c, phenylglyoxylic acid (PGA, compound CID:11915) with serum insulin, HbA1c and HOMA-IR. Our findings suggested that exposure to VOCs were associated with increased odds of T2D in older adults, which might be mediated by impaired glucose homeostasis. Mitigating VOCs should be a necessary component of public health strategies aimed at reducing the burden of type 2 diabetes.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chenyang</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>College of Geography and Environmental Science, Henan University, Kaifeng, 475004, Henan, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Henan Urban Plan and Design Institute Co., Ltd, Zhengzhou, 450044, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jinjun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Henan Urban Plan and Design Institute Co., Ltd, Zhengzhou, 450044, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Lingling</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Nutrition and Food Hygiene, School of Public Health of Zhengzhou University, Zhengzhou, 450001, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Kinesiology, School of Physical Education (Main Campus), Zhengzhou University, Zhengzhou, 450001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jinjie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Centre for Nutritional Ecology and Centre for Sport Nutrition and Health, Zhengzhou University, Zhengzhou, 450001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xinxin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Nutrition and Food Hygiene, School of Public Health of Zhengzhou University, Zhengzhou, 450001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Lifeng</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Junxi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>NHC Key Laboratory of Birth Defects Prevention, Henan Key Laboratory of Population Defects Prevention, No. 26, Jingwu Road, Zhengzhou, 450002, Henan, China. zhangjunxi0378@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suo</LastName><ForeName>Xiangying</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Epidemiology and Health Statistics, School of Public Health of Zhengzhou University, No.100, Science Avenue, Zhengzhou, 450001, Henan, China. xy_suo123@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D055549">Volatile Organic Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055549" MajorTopicYN="Y">Volatile Organic Compounds</DescriptorName><QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006706" MajorTopicYN="Y">Homeostasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009749" MajorTopicYN="Y">Nutrition Surveys</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Environmental pollutant</Keyword><Keyword MajorTopicYN="N">Glucose homeostasis</Keyword><Keyword MajorTopicYN="N">NHANES</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword><Keyword MajorTopicYN="N">Volatile organic compounds</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: Not applicable. The data in this study was obtained from NHANES website. This study did not include personal information. 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Pharmacol.54, 62–73 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">28688303</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39627353</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>27</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>A retrospective study of seasonal variation in sodium-glucose co-transporter 2 inhibitor-related adverse events using the Japanese adverse drug event report database.</ArticleTitle><Pagination><StartPage>30072</StartPage><MedlinePgn>30072</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">30072</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-024-81698-z</ELocationID><Abstract><AbstractText>Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a class of drugs used in the clinical management of patients with type 2 diabetes, and their prescriptions have been increasing in recent years. Herein, we performed a retrospective analysis of seasonal variation in SGLT2 inhibitor-associated adverse events recorded in the Japanese Adverse Drug Event Report (JADER) database, an adverse event reporting database which reflects real-world clinical practice. To this end, seasonal variations in SGLT2 inhibitor-related dehydration, cerebral infarction, urinary tract infection, and ketoacidosis were analyzed. Six SGLT2 inhibitors prescribed in Japan (ipragliflozin, empagliflozin, luseogliflozin, canagliflozin, dapagliflozin, and tofogliflozin) were included. The reporting ratio (RR) for SGLT2 inhibitor adverse events per month in the JADER database from April 2014 to December 2023 was determined. The RR for dehydration-related adverse events was highest in the summer months of July and August, as well as in the winter months of December, January, and February. The highest RR for cerebral infarction was in February. No association with seasonal variations in the occurrence of ketoacidosis related to dehydration was observed. Healthcare providers should take adequate precautions against dehydration caused by SGLT2 inhibitors, not only in summer but also in winter. These findings are instructive and informational for health care professionals involved in diabetes care.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Matsumoto</LastName><ForeName>Kiyoka</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goto</LastName><ForeName>Fumiya</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maezawa</LastName><ForeName>Mika</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakao</LastName><ForeName>Satoshi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pharmacy, Kyushu University Hospital, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miyasaka</LastName><ForeName>Koumi</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirofuji</LastName><ForeName>Sakiko</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shiota</LastName><ForeName>Kohei</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ichihara</LastName><ForeName>Nanaka</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamashita</LastName><ForeName>Moe</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nokura</LastName><ForeName>Yuka</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamazaki</LastName><ForeName>Tomofumi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sugishita</LastName><ForeName>Kana</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tanaka</LastName><ForeName>Hideyuki</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tamaki</LastName><ForeName>Hirofumi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Community Pharmacy, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501- 1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ishiguro</LastName><ForeName>Motoyuki</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Ishiguro Clinic, 6-37, Masaki-kita, Gifu, 502-0881, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Iguchi</LastName><ForeName>Kazuhiro</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Laboratory of Community Pharmacy, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501- 1196, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakamura</LastName><ForeName>Mitsuhiro</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratory of Drug Informatics, Gifu Pharmaceutical University, 1-25-4, Daigaku-nishi, Gifu, 501-1196, Japan. mnakamura@gifu-pu.ac.jp.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>21K11100</GrantID><Agency>Japan Society for the Promotion of Science</Agency><Country/></Grant><Grant><GrantID>21K11100</GrantID><Agency>Japan Society for the Promotion of Science</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>1ULL0QJ8UC</RegistryNumber><NameOfSubstance UI="C529054">dapagliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0SAC974Z85</RegistryNumber><NameOfSubstance UI="D000068896">Canagliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>HDC1R2M35U</RegistryNumber><NameOfSubstance UI="C570240">empagliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>3N2N8OOR7X</RegistryNumber><NameOfSubstance UI="C572941">ipragliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001559">Benzhydryl Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>P8DD8KX4O4</RegistryNumber><NameOfSubstance UI="C575086">6-((4-ethylphenyl)methyl)-3',4',5',6'-tetrahydro-6'-(hydroxymethyl)spiro(isobenzofuran-1(3H),2'-(2H)pyran)-3',4',5'-triol</NameOfSubstance></Chemical><Chemical><RegistryNumber>506T60A25R</RegistryNumber><NameOfSubstance UI="D013012">Sorbitol</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013876">Thiophenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>C596HWF74Z</RegistryNumber><NameOfSubstance UI="C549343">1,5-anhydro-1-(5-(4-ethoxybenzyl)-2-methoxy-4-methylphenyl)-1-thioglucitol</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012621" MajorTopicYN="Y">Seasons</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007564" MajorTopicYN="N" Type="Geographic">Japan</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="N">Glucosides</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000068896" MajorTopicYN="N">Canagliflozin</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016907" MajorTopicYN="N">Adverse Drug Reaction Reporting Systems</DescriptorName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001559" MajorTopicYN="N">Benzhydryl Compounds</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016208" MajorTopicYN="N">Databases, Factual</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003681" MajorTopicYN="N">Dehydration</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013012" MajorTopicYN="N">Sorbitol</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013876" MajorTopicYN="N">Thiophenes</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064420" MajorTopicYN="N">Drug-Related Side Effects and Adverse Reactions</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014552" MajorTopicYN="N">Urinary Tract Infections</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000095225" MajorTopicYN="N">East Asian People</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adverse events</Keyword><Keyword MajorTopicYN="N">Dehydration</Keyword><Keyword MajorTopicYN="N">Seasonal variation</Keyword><Keyword MajorTopicYN="N">Sodium-glucose co-transporter 2 inhibitors</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes mellitus</Keyword></KeywordList><CoiStatement>Declarations. Competing interests: The authors declare no competing interests. Ethical approval: Ethical approval was not sought for this study because the study was a database-related observational study which did not directly involve any research subjects. All results were obtained from data openly available online from the PMDA website ( www.pmda.go.jp ). All data from the JADER database were fully anonymized by the relevant regulatory authority before we accessed them. Our research does not fall within the purview of any of the following laws and guidelines: “Clinical Trials Act (Act No. 16 of April 14, 2017),” “Act on Securing Quality, Efficacy and Safety of Products Including Pharmaceuticals and Medical Devices (Law number: Act No. 145 of 1960, Last Version: Amendment of Act No. 50 of 2015),” “Guideline for good clinical practice E6 (R1), https://www.pmda.go.jp/int-activities/int-harmony/ich/0076.html ,” “Ethical guidelines for human genome and gene analysis research, https://www.mhlw.go.jp/general/seido/kousei/i-kenkyu/genome/0504sisin.html ,” and “Ethical Guidelines for Medical and Health Research Involving Human Subjects, https://www.mhlw.go.jp/stf/seisakunitsuite/bunya/hokabunya/kenkyujigyou/i-kenkyu/index.html .” Therefore, it is not subject to ethical examination. The study was an observational study without any research subjects. 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Sci.455, 122789 (2023).</Citation><ArticleIdList><ArticleId IdType="pubmed">37984106</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39627335</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Association of systemic immunity-inflammation index with type 2 diabetes and insulin resistance in NHANES 2005-2018.</ArticleTitle><Pagination><StartPage>30133</StartPage><MedlinePgn>30133</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">30133</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-024-79763-8</ELocationID><Abstract><AbstractText>Although the interplay between inflammation and diabetes is increasingly recognized, it is unclear whether the systemic immunity-inflammation index (SII), as a biomarker of systemic inflammatory response, is associated with type 2 diabetes (T2D) and insulin resistance (IR). This cross-sectional study was performed in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2018, and finally enrolled 17,017 participants. To explore the relationship between SII and T2D and IR, a series of statistical analyses were conducted including weighted multivariate linear regression, logistic regression, and subgroup analysis. The fully adjusted multivariate linear regression revealed a positive correlation between SII and fasting plasma glucose (β = 0.13, 95% CI: 0.01, 0.24), fasting serum insulin (β = 12.90, 95% CI: 6.77, 19.04), and homeostasis model assessment of insulin resistance (β = 0.68, 95% CI: 0.25, 1.10). A per-SD increase in SII was found to be associated with a 4% increase in the odds of T2D, and a 5% increase in the odds of IR. The trend was significant across all SII quartile groups. Subgroup analysis revealed a stronger positive association existed between SII and T2D and IR in female, younger, and obese populations. SII was positively associated with the risk of T2D and IR, indicating that reducing SII levels may help prevent these conditions in the general population.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Qinying</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin, 300052, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xuan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin, 300052, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Jialu</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin, 300052, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rao</LastName><ForeName>Xiaojuan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin, 300052, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ming</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin, 300052, China. mingliu@tmu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2022YFE0131400</GrantID><Agency>National Key R&amp;D Program</Agency><Country/></Grant><Grant><GrantID>82220108014</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>TJYXZDXK-030A</GrantID><Agency>Tianjin Key Medical Discipline (Specialty) Construction Project</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="Y">Inflammation</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009749" MajorTopicYN="Y">Nutrition Surveys</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Insulin resistance</Keyword><Keyword MajorTopicYN="N">NHANES</Keyword><Keyword MajorTopicYN="N">Systemic immunity-inflammation index</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declarations. Competing interests: The authors declare no competing interests. Informed consent: Consent to participate was obtained and the National Center for Health Statistics ethics committee approved the protocol of the NHANES study. 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The cohort was predominantly male (66%) with an average age of 64.7 years.</AbstractText><AbstractText Label="PRIMARY AND SECONDARY OUTCOME MEASURES" NlmCategory="METHODS">The primary outcomes of DIALECT were all-cause mortality, microvascular and macrovascular diseases. The secondary outcomes are blood pressure levels, kidney function indicators and albuminuria levels RESULTS: Principal component analysis (PCA) was applied to 53 accelerometer-derived PA measures. Principal components were identified using a scree plot, key measures determining the principal components were derived and <i>k-</i>mean cluster analysis was applied to the components. The main PA measures were steps/day, active time, zero steps, total sedentary behaviour (SB) bout duration and total moderate to vigorous physical activity (MVPA) bout duration. Based on three PCA components, three clusters were identified. The inactive cluster had a higher BMI, diabetes duration, age and SB bout duration, and lower steps/day and MVPA bout duration compared with the other clusters (p<0.05). The active cluster still scores low on MVPA bout duration (18 min/week) and high on SB bout duration (5.0 hours/day).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">PA behaviour in patients can be categorised into three distinct clusters. The identified PA measures and behaviour clusters offer promising opportunities for tailored lifestyle treatment. However, further studies are needed to determine which PA measures are clinically most relevant, validate the usefulness of this classification and evaluate whether tailoring lifestyle advice according to these clusters adds clinical value.</AbstractText><AbstractText Label="TRIAL REGISTRATION NUMBER" NlmCategory="BACKGROUND">NTR5855.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>den Braber</LastName><ForeName>Niala</ForeName><Initials>N</Initials><Identifier Source="ORCID">0000-0002-9098-3439</Identifier><AffiliationInfo><Affiliation>Biomedical Signal and Systems, University of Twente, Enschede, The Netherlands nialadb@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Internal Medicine, Ziekenhuisgroep Twente, Almelo, Overijssel, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vollenbroek-Hutten</LastName><ForeName>Miriam M</ForeName><Initials>MM</Initials><Identifier Source="ORCID">0000-0001-8730-1487</Identifier><AffiliationInfo><Affiliation>Biomedical Signal and Systems, University of Twente, Enschede, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kappert</LastName><ForeName>Kilian D R</ForeName><Initials>KDR</Initials><Identifier Source="ORCID">0000-0002-1278-205X</Identifier><AffiliationInfo><Affiliation>Biomedical Signal and Systems, University of Twente, Enschede, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Internal Medicine, Ziekenhuisgroep Twente, Almelo, Overijssel, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laverman</LastName><ForeName>Gozewijn D</ForeName><Initials>GD</Initials><Identifier Source="ORCID">0000-0002-8716-7115</Identifier><AffiliationInfo><Affiliation>Biomedical Signal and Systems, University of Twente, Enschede, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Internal Medicine, Ziekenhuisgroep Twente, Almelo, Overijssel, The Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open</MedlineTA><NlmUniqueID>101552874</NlmUniqueID><ISSNLinking>2044-6055</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="Y">Exercise</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009426" MajorTopicYN="N" Type="Geographic">Netherlands</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016000" MajorTopicYN="N">Cluster Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D061725" MajorTopicYN="Y">Accelerometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057185" MajorTopicYN="N">Sedentary Behavior</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D063127" MajorTopicYN="N">Secondary Care</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D025341" MajorTopicYN="N">Principal Component Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008019" MajorTopicYN="N">Life Style</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Clinical Decision-Making</Keyword><Keyword MajorTopicYN="N">General diabetes</Keyword><Keyword MajorTopicYN="N">Information technology</Keyword><Keyword MajorTopicYN="N">eHealth</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>22</Hour><Minute>3</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>3</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId 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Int J Behav Nutr Phys Act. 2015;12:159. doi: 10.1186/s12966-015-0314-1.</Citation><ArticleIdList><ArticleId IdType="doi">10.1186/s12966-015-0314-1</ArticleId><ArticleId IdType="pmc">PMC4683756</ArticleId><ArticleId IdType="pubmed">26684758</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39626843</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>06</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-8600</ISSN><JournalIssue CitedMedium="Internet"><Volume>163</Volume><PubDate><Year>2025</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Metabolism: clinical and experimental</Title><ISOAbbreviation>Metabolism</ISOAbbreviation></Journal><ArticleTitle>Human subjects with impaired beta-cell function and glucose tolerance have higher levels of intra-islet intact GLP-1.</ArticleTitle><Pagination><StartPage>156087</StartPage><MedlinePgn>156087</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.metabol.2024.156087</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0026-0495(24)00315-9</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">A number of studies have suggested that pancreatic α cells produce intact GLP-1, thereby constituting a gut-independent paracrine incretin system. However, the debate on whether human α cells contain intact GLP-1 and whether this relates to the presence of diabetes is still ongoing. This study aimed to determine the presence of proglucagon-derived peptides, including GLP-1 isoforms, in pancreas biopsies obtained during partial pancreatectomy from metabolically profiled human donors, stratified according to pre-surgery glucose tolerance.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We enrolled 61 individuals with no known history of type 2 diabetes (31F/30M, age 64.6 ± 10.6 yrs., BMI 24.2 ± 3.68 kg/m<sup>2</sup>) scheduled for partial pancreatectomy for periampullary neoplasm. Differences in glucose tolerance and insulin secretion/sensitivity were assessed using preoperative 2 h OGTT, 4 h-Mixed Meal Test and Hyperinsulinemic Euglycemic Clamp. Subjects were subsequently classified as normal glucose tolerant (NGT, n = 19), impaired glucose tolerant (IGT, n = 20) or newly diagnosed diabetes (DM) (n = 22). We measured total GLP-1, intact GLP-1, glucagon, insulin, and C-peptide in pancreas biopsies and plasma from these subjects and correlated the results with their secretory and metabolic parameters.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Extractable levels of total GLP-1 were 23.9 ± 2.66 pmol/g, while intact GLP-1 levels were 1.15 ± 0.18 pmol/g. When we examined proglucagon derived peptides (adjusted for glucagon levels), in subjects classified according to glucose tolerance, we observed similar levels of total GLP-1, however, intact GLP-1 was significantly increased in IGT and DM groups and inversely associated with beta cell glucose sensitivity and insulin secretion in vivo.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our data show that development of glucose intolerance and beta cell dysfunction are significantly associated with increased levels of intra-islet intact GLP-1, a potentially beneficial adaptation of the paracrine regulation of insulin secretion in type 2 diabetes.</AbstractText><CopyrightInformation>Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mezza</LastName><ForeName>Teresa</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Pancreas Unit, CEMAD Centro Malattie dell'Apparato Digerente, Medicina Interna e Gastroenterologia, Fondazione Policlinico Universitario Gemelli IRCCS, Roma, Italy; Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wewer Albrechtsen</LastName><ForeName>Nicolai J</ForeName><Initials>NJ</Initials><AffiliationInfo><Affiliation>Department of Clinical Biochemistry, Copenhagen University Hospital - Bispebjerg, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Di Giuseppe</LastName><ForeName>Gianfranco</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Endocrinologia e Diabetologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferraro</LastName><ForeName>Pietro Manuel</ForeName><Initials>PM</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Sezione di Nefrologia, Dipartimento di Medicina, Università degli Studi di Verona, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soldovieri</LastName><ForeName>Laura</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Endocrinologia e Diabetologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ciccarelli</LastName><ForeName>Gea</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Endocrinologia e Diabetologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brunetti</LastName><ForeName>Michela</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Endocrinologia e Diabetologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Quero</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Chirurgia Digestiva, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alfieri</LastName><ForeName>Sergio</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Chirurgia Digestiva, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nista</LastName><ForeName>Enrico Celestino</ForeName><Initials>EC</Initials><AffiliationInfo><Affiliation>Pancreas Unit, CEMAD Centro Malattie dell'Apparato Digerente, Medicina Interna e Gastroenterologia, Fondazione Policlinico Universitario Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gasbarrini</LastName><ForeName>Antonio</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Pancreas Unit, CEMAD Centro Malattie dell'Apparato Digerente, Medicina Interna e Gastroenterologia, Fondazione Policlinico Universitario Gemelli IRCCS, Roma, Italy; Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tondolo</LastName><ForeName>Vincenzo</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Digestive Surgery Unit, Ospedale Isola Tiberina - Gemelli Isola, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mari</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute of Neuroscience, National Council of Research - Padua (IT), Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pontecorvi</LastName><ForeName>Alfredo</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Endocrinologia e Diabetologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Giaccari</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; Endocrinologia e Diabetologia, Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy. Electronic address: andrea.giaccari@unicatt.it.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Holst</LastName><ForeName>Jens J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Novo Nordisk Foundation Center for Basic Metabolic Research and Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address: jjholst@sund.ku.dk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Metabolism</MedlineTA><NlmUniqueID>0375267</NlmUniqueID><ISSNLinking>0026-0495</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>89750-14-1</RegistryNumber><NameOfSubstance UI="D052216">Glucagon-Like Peptide 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052216" MajorTopicYN="Y">Glucagon-Like Peptide 1</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018149" MajorTopicYN="Y">Glucose Intolerance</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050417" MajorTopicYN="Y">Insulin-Secreting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005951" MajorTopicYN="Y">Glucose Tolerance Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007515" MajorTopicYN="N">Islets of Langerhans</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015309" MajorTopicYN="N">Glucose Clamp Technique</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010180" MajorTopicYN="N">Pancreatectomy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alpha-cells</Keyword><Keyword MajorTopicYN="N">Glucagon-like peptide 1</Keyword><Keyword MajorTopicYN="N">Islets biology</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest Authors have no conflicts to declare.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>7</Day><Hour>0</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>4</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>19</Hour><Minute>28</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39626843</ArticleId><ArticleId IdType="doi">10.1016/j.metabol.2024.156087</ArticleId><ArticleId IdType="pii">S0026-0495(24)00315-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39626773</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1752-8984</ISSN><JournalIssue CitedMedium="Internet"><Volume>21</Volume><Issue>6</Issue><PubDate><Year>2024</Year><Season>Nov-Dec</Season></PubDate></JournalIssue><Title>Diabetes & vascular disease research</Title><ISOAbbreviation>Diab Vasc Dis Res</ISOAbbreviation></Journal><ArticleTitle>The association between osteoprotegerin and arterial stiffness in a 10-year longitudinal study of patients with type 2 diabetes.</ArticleTitle><Pagination><StartPage>14791641241304435</StartPage><MedlinePgn>14791641241304435</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">14791641241304435</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1177/14791641241304435</ELocationID><Abstract><AbstractText><b>Introduction</b>: Osteoprotegerin (OPG) inhibits vascular calcification which is central to pathogenesis of arterial stiffness. However, it promotes inflammation by upregulating expression of vascular cell adhesion molecule-1(VCAM-1), thereby contributing to arterial stiffness. We investigated longitudinal association between OPG and arterial stiffness in type 2 diabetes (T2D), causality of the association and mediation by VCAM-1. <b>Methods</b>: This was a prospective cohort study of T2D patients (<i>N</i> = 1877, mean age 57.0 ± 10.8) with 10 years' follow-up. Baseline plasma OPG was measured using immunoassay. Pulse wave velocity (PWV) was assessed using applanation tonometry. We examined association between OPG and follow-up PWV using linear mixed model. One-sample Mendelian Randomization (MR) was conducted with rs1385492 as OPG-associated single nucleotide polymorphism (SNP). <b>Results</b>: Baseline natural log (Ln)-transformed OPG was positively associated with baseline and follow-up PWV with adjusted coefficients 0.43 (95%CI 0.05, 0.80; <i>p</i> = .026) and 0.51 (95%CI 0.06 to 0.97; <i>p</i> = .028) respectively. Genetically-predicted higher levels of plasma OPG was associated with higher last follow-up PWV with coefficient 10.81 (95%CI 2.97, 18.65; <i>p</i> = .007) per unit increase in LnOPG. Higher VCAM-1 accounted for 10.2% of association between LnOPG and follow-up PWV. <b>Discussion</b>: Baseline plasma OPG was associated with higher follow-up PWV in patients with T2D, with genetic evidence from MR. This association may be mediated, at least in part, by VCAM-1.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Low</LastName><ForeName>Serena</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">150819</Identifier></AffiliationInfo><AffiliationInfo><Affiliation>Diabetes Centre, Admiralty Medical Centre, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">609710</Identifier></AffiliationInfo><AffiliationInfo><Affiliation>Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pek</LastName><ForeName>Sharon</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">150819</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moh</LastName><ForeName>Angela</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">150819</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jian-Jun</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">150819</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pandian</LastName><ForeName>Bhuvaneswari</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">150819</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ang</LastName><ForeName>Keven</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">150819</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Wern Ee</ForeName><Initials>WE</Initials><AffiliationInfo><Affiliation>National Healthcare Group Polyclinics, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">63707</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lim</LastName><ForeName>Ziliang</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>National Healthcare Group Polyclinics, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">63707</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Subramaniam</LastName><ForeName>Tavintharan</ForeName><Initials>T</Initials><Identifier Source="ORCID">0000-0002-5365-8899</Identifier><AffiliationInfo><Affiliation>Diabetes Centre, Admiralty Medical Centre, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">609710</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sum</LastName><ForeName>Chee Fang</ForeName><Initials>CF</Initials><AffiliationInfo><Affiliation>Diabetes Centre, Admiralty Medical Centre, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">609710</Identifier></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lim</LastName><ForeName>Su Chi</ForeName><Initials>SC</Initials><Identifier Source="ORCID">0000-0003-1742-5817</Identifier><AffiliationInfo><Affiliation>Clinical Research Unit, Khoo Teck Puat Hospital, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">150819</Identifier></AffiliationInfo><AffiliationInfo><Affiliation>Diabetes Centre, Admiralty Medical Centre, Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">609710</Identifier></AffiliationInfo><AffiliationInfo><Affiliation>Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Saw Swee Hock School of Public Health, National University of Singapore, Singapore.</Affiliation><Identifier Source="RINGGOLD">203377</Identifier></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Diab Vasc Dis Res</MedlineTA><NlmUniqueID>101234011</NlmUniqueID><ISSNLinking>1479-1641</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053244">Osteoprotegerin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C506030">TNFRSF11B protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019010">Vascular Cell Adhesion Molecule-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053244" MajorTopicYN="Y">Osteoprotegerin</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059289" MajorTopicYN="Y">Vascular Stiffness</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019010" MajorTopicYN="Y">Vascular Cell Adhesion Molecule-1</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="Y">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="Y">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D063177" MajorTopicYN="Y">Pulse Wave Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057182" MajorTopicYN="N">Mendelian Randomization Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003925" MajorTopicYN="N">Diabetic Angiopathies</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">arterial stiffness</Keyword><Keyword MajorTopicYN="N">osteoprotegerin</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this 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Stroke 2021; 52: 2992–3003.</Citation><ArticleIdList><ArticleId IdType="pubmed">34399585</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39626509</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2352-3964</ISSN><JournalIssue CitedMedium="Internet"><Volume>110</Volume><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>EBioMedicine</Title><ISOAbbreviation>EBioMedicine</ISOAbbreviation></Journal><ArticleTitle>The role of exosomes for sustained specific cardiorespiratory and metabolic improvements in males with type 2 diabetes after detraining.</ArticleTitle><Pagination><StartPage>105471</StartPage><MedlinePgn>105471</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">105471</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ebiom.2024.105471</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S2352-3964(24)00507-3</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">High-intensity interval training (HIIT) has been shown to improve cardiorespiratory fitness (V˙O<sub>2</sub> max) but may ameliorate insulin sensitivity only in insulin-resistant humans. It is yet unclear whether these benefits persist after detraining and to which extent duration and effectiveness of metabolic improvements differ between individuals without and with prediabetes or type 2 diabetes (T2D). Understanding these differences is relevant for developing targeted exercise training modes for individuals with different stages of dysglycemia.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Men with (20 T2D) and without T2D (12 insulin-sensitive, IS-NDM; 10 insulin-resistant, IR-NDM) underwent hyperinsulinemic-euglycemic clamps, spiroergometry, ectopic lipid quantification and muscle biopsies at baseline, after 12-week HIIT and after 4-week detraining.</AbstractText><AbstractText Label="FINDINGS" NlmCategory="RESULTS">After detraining, the HIIT-stimulated V˙O<sub>2</sub> max declined in T2D and IR-NDM, but remained higher compared to baseline in all groups. The HIIT-induced changes in hepatic insulin sensitivity and ectopic lipid content were sustained after detraining in T2D and IR-NDM, whereas improvements of whole-body insulin sensitivity were abolished in T2D. T2D and IR-NDM showed persistent increases in the number of small extracellular vesicles, which carry among others antioxidant proteins. The ratio of reduced-to-oxidized glutathione further decreased after detraining in all groups, whereas changes in proteins involved in mitochondrial turnover were dependent on insulin sensitivity, with some evidence for upregulation of fusion and mitophagy in T2D and IR-NDM and upregulation of fission in IS-NDM. Levels of different lipolytic proteins were reduced in all participants after detraining.</AbstractText><AbstractText Label="INTERPRETATION" NlmCategory="CONCLUSIONS">HIIT offers sustained improvement of energy metabolism and hepatic insulin sensitivity in insulin-resistant humans, but long-term adherence is required to maintain these benefits.</AbstractText><AbstractText Label="FUNDING" NlmCategory="BACKGROUND">Funding bodies that contributed to this study are listed in the Acknowledgements section.</AbstractText><CopyrightInformation>Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mastrototaro</LastName><ForeName>Lucia</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Apostolopoulou</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Department of Endocrinology and Diabetology, Medical Faculty and University Hospital, Heinrich-Heine-University, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hartwig</LastName><ForeName>Sonja</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Institute for Clinical Biochemistry and Pathobiochemistry German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Strassburger</LastName><ForeName>Klaus</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Institute for Biometrics and Epidemiology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lipaeva</LastName><ForeName>Polina</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Department of Endocrinology and Diabetology, Medical Faculty and University Hospital, Heinrich-Heine-University, Düsseldorf, Germany; Institute for Medical Biometry and Bioinformatics, Medical Faculty and University Hospital, Heinrich Heine University, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Trinks</LastName><ForeName>Nina</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karusheva</LastName><ForeName>Yanislava</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gancheva</LastName><ForeName>Sofiya</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Department of Endocrinology and Diabetology, Medical Faculty and University Hospital, Heinrich-Heine-University, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Trenkamp</LastName><ForeName>Sandra</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lehr</LastName><ForeName>Stefan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Institute for Clinical Biochemistry and Pathobiochemistry German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Hasani</LastName><ForeName>Hadi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Institute for Clinical Biochemistry and Pathobiochemistry German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Szendroedi</LastName><ForeName>Julia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, Heidelberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roden</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany; Department of Endocrinology and Diabetology, Medical Faculty and University Hospital, Heinrich-Heine-University, Düsseldorf, Germany. Electronic address: michael.roden@ddz.de.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>EBioMedicine</MedlineTA><NlmUniqueID>101647039</NlmUniqueID><ISSNLinking>2352-3964</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055354" MajorTopicYN="Y">Exosomes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000072696" MajorTopicYN="N">High-Intensity Interval Training</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000072599" MajorTopicYN="N">Cardiorespiratory Fitness</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Detraining</Keyword><Keyword MajorTopicYN="N">Exercise</Keyword><Keyword MajorTopicYN="N">Insulin sensitivity</Keyword><Keyword MajorTopicYN="N">Inter-organ crosstalk</Keyword><Keyword MajorTopicYN="N">Small extracellular vesicles</Keyword></KeywordList><CoiStatement>Declaration of interests MR is currently on scientific advisory boards of Boehringer Ingelheim, Lilly, Novo Nordisk and has received personal fees from Echosens, Novo Nordisk and Target RWE, honoraria for lectures from Astra-Zeneca, Boehringer-Ingelheim, Novo Nordisk, Kenes Group, Madrigal, MSD and investigator-initiated research support from Boehringer-Ingelheim and Novo Nordisk. The research of MR is supported by grants from the European Community (HORIZON-HLTH-2022-STAYHLTH-02-01: Panel A) to the INTERCEPT-T2D consortium and German Research Foundation (DFG, GRK2576 Vivid). 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In this study, we investigate the interplay between genetics, metabolomics, and T2D risk in the UK Biobank dataset using the Nightingale panel composed of 249 metabolites, 92% of which correspond to lipids (HDL, IDL, LDL, VLDL) and lipoproteins. By integrating these data with large-scale T2D GWAS from the DIAMANTE meta-analysis through Mendelian randomization analyses, we find 79 metabolites with a causal association to T2D, all spanning lipid-related classes except for Glucose and Tyrosine. Twice as many metabolites are causally affected by T2D liability, spanning almost all tested classes, including branched-chain amino acids. Secondly, using an interaction quantitative trait locus (QTL) analysis, we describe four metabolites consistently replicated in an independent dataset from the Estonian Biobank, for which genetic loci in two different genomic regions show attenuated regulation in T2D cases compared to controls. The significant variants from the interaction QTL analysis are significant QTLs for the corresponding metabolites in the general population but are not associated with T2D risk, pointing towards consequences of T2D on the genetic regulation of metabolite levels. Finally, through differential level analyses, we find 165 metabolites associated with microvascular, macrovascular, or both types of T2D complications, with only a few discriminating between complication classes. Of the 165 metabolites, 40 are not causally linked to T2D in either direction, suggesting biological mechanisms specific to the occurrence of complications. Overall, this work provides a map of the consequences of T2D on Nightingale targeted metabolite levels and on their genetic regulation, enabling a better understanding of the T2D trajectory leading to complications.</AbstractText><CopyrightInformation>Copyright: © 2024 Bocher et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bocher</LastName><ForeName>Ozvan</ForeName><Initials>O</Initials><Identifier Source="ORCID">0000-0002-2467-9236</Identifier><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Singh</LastName><ForeName>Archit</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-3983-6126</Identifier><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Munich School for Data Science (MUDS), Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Technical University of Munich (TUM), TUM School of Medicine and Health, Graduate School of Experimental Medicine, Munich, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Yue</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0000-0003-1671-7017</Identifier><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Technical University of Munich (TUM), TUM School of Medicine and Health, Graduate School of Experimental Medicine, Munich, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Võsa</LastName><ForeName>Urmo</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Estonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reimann</LastName><ForeName>Ene</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Estonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arruda</LastName><ForeName>Ana</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-6550-9794</Identifier><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Munich School for Data Science (MUDS), Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Technical University of Munich (TUM), TUM School of Medicine and Health, Graduate School of Experimental Medicine, Munich, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barysenska</LastName><ForeName>Andrei</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-9571-6292</Identifier><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kolde</LastName><ForeName>Anastassia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Estonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Mathematics and Statistics, University of Tartu, Tartu, Estonia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rayner</LastName><ForeName>Nigel W</ForeName><Initials>NW</Initials><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>Estonian Biobank research team</CollectiveName></Author><Author ValidYN="Y"><LastName>Esko</LastName><ForeName>Tõnu</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Estonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mägi</LastName><ForeName>Reedik</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Estonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zeggini</LastName><ForeName>Eleftheria</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institute of Translational Genomics, Helmholtz Zentrum München- German Research Center for Environmental Health, Neuherberg, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>TUM school of medicine and health, Technical University Munich and Klinikum Rechts der Isar, Munich, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Genet</MedlineTA><NlmUniqueID>101239074</NlmUniqueID><ISSNLinking>1553-7390</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008074">Lipoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008055">Lipids</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040641" MajorTopicYN="Y">Quantitative Trait Loci</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055106" MajorTopicYN="Y">Genome-Wide Association Study</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055432" MajorTopicYN="N">Metabolomics</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057182" MajorTopicYN="N">Mendelian Randomization Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055442" MajorTopicYN="N">Metabolome</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008074" MajorTopicYN="N">Lipoproteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008055" MajorTopicYN="N">Lipids</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006113" MajorTopicYN="N" Type="Geographic">United Kingdom</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>12</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>13</Day><Hour>20</Hour><Minute>6</Minute></PubMedPubDate><PubMedPubDate 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Nov 10;40(25):5434–52. doi: 10.1002/sim.9133</Citation><ArticleIdList><ArticleId IdType="doi">10.1002/sim.9133</ArticleId><ArticleId IdType="pmc">PMC9479726</ArticleId><ArticleId IdType="pubmed">34338327</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39625868</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>12</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2291-5222</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><PubDate><Year>2024</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>JMIR mHealth and uHealth</Title><ISOAbbreviation>JMIR Mhealth Uhealth</ISOAbbreviation></Journal><ArticleTitle>The Role of Smartwatch Technology in the Provision of Care for Type 1 or 2 Diabetes Mellitus or Gestational Diabetes: Systematic Review.</ArticleTitle><Pagination><StartPage>e54826</StartPage><MedlinePgn>e54826</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e54826</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.2196/54826</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="UNASSIGNED">The use of smart technology in the management of all forms of diabetes mellitus has grown significantly in the past 10 years. Technologies such as the smartwatch have been proposed as a method of assisting in the monitoring of blood glucose levels as well as other alert prompts such as medication adherence and daily physical activity targets. These important outcomes reach across all forms of diabetes and have the potential to increase compliance of self-monitoring with the aim of improving long-term outcomes such as hemoglobin A1c (HbA1c).</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">This systematic review aims to explore the literature for evidence of smartwatch technology in type 1, 2, and gestational diabetes.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">A systematic review was undertaken by searching Ovid MEDLINE and CINAHL databases. A second search using all identified keywords and index terms was performed on Ovid MEDLINE (January 1966 to August 2023), Embase (January 1980 to August 2023), Cochrane Central Register of Controlled Trials (CENTRAL, the Cochrane Library, latest issue), CINAHL (from 1982), IEEE Xplore, ACM Digital Libraries, and Web of Science databases. Type 1, type 2, and gestational diabetes were eligible for inclusion. Quantitative studies such as prospective cohort or randomized clinical trials that explored the feasibility, usability, or effect of smartwatch technology in people with diabetes were eligible. Outcomes of interest were changes in blood glucose or HbA1c, physical activity levels, medication adherence, and feasibility or usability scores.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Of the 8558 titles and abstracts screened, 5 studies were included for qualitative synthesis in this review. A total of 322 participants with either type 1 or type 2 diabetes mellitus were included in the review. A total of 4 studies focused on the feasibility and usability of smartwatch technology in diabetes management. One study conducted a proof-of-concept randomized clinical trial including smartwatch technology for exercise time prescriptions for participants with type 2 diabetes mellitus. Adherence of participants to smartwatch technology varied between included studies, with one reporting input submissions of 58% and another reporting that participants logged 50% more entries than they were required to. One study reported significantly improved glycemic control with integrated smartwatch technology, with increased exercise prescriptions; however, this study was not powered and required a longer observational period.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="UNASSIGNED">This systematic review has highlighted the lack of robust randomized clinical trials that explore the efficacy of smartwatch technology in the management of patients with type 1, type 2, and gestational diabetes. Further research is required to establish the role of integrated smartwatch technology in important outcomes such as glycemic control, exercise participation, drug adherence, and diet monitoring in people with all forms of diabetes mellitus.</AbstractText><CopyrightInformation>© Sergio Diez Alvarez, Antoni Fellas, Katie Wynne, Derek Santos, Dean Sculley, Shamasunder Acharya, Pooshan Navathe, Xavier Gironès, Andrea Coda. Originally published in JMIR mHealth and uHealth (https://mhealth.jmir.org).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Diez Alvarez</LastName><ForeName>Sergio</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0002-3393-5764</Identifier><AffiliationInfo><Affiliation>School of Medicine and Public Health, College of Health Medicine and Wellbeing, University of Newcastle, University Drive, Callaghan, Newcastle, 2308, Australia, 61409916949.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fellas</LastName><ForeName>Antoni</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-1557-6232</Identifier><AffiliationInfo><Affiliation>School of Health Sciences, College of Health, Medicine and Wellbeing, University of Newcastle, Newcastle, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Equity in Health and Wellbeing Research Program, Hunter Medical Research Institute, Newcastle, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wynne</LastName><ForeName>Katie</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0002-7980-3337</Identifier><AffiliationInfo><Affiliation>School of Medicine and Public Health, College of Health Medicine and Wellbeing, University of Newcastle, University Drive, Callaghan, Newcastle, 2308, Australia, 61409916949.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Equity in Health and Wellbeing Research Program, Hunter Medical Research Institute, Newcastle, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Endocrinology, John Hunter Hospital, Newcastle, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Santos</LastName><ForeName>Derek</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0001-9936-715X</Identifier><AffiliationInfo><Affiliation>Queen Margaret University, School of Health Sciences, Edinburgh, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University of Gibraltar, Gibraltar, Gibraltar.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sculley</LastName><ForeName>Dean</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0003-3972-8309</Identifier><AffiliationInfo><Affiliation>School of Biomedical Sciences and Pharmacy, College of Health Medicine and Wellbeing, University of Newcastle, Newcastle, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Acharya</LastName><ForeName>Shamasunder</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-4565-1571</Identifier><AffiliationInfo><Affiliation>School of Medicine and Public Health, College of Health Medicine and Wellbeing, University of Newcastle, University Drive, Callaghan, Newcastle, 2308, Australia, 61409916949.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Endocrinology, John Hunter Hospital, Newcastle, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Navathe</LastName><ForeName>Pooshan</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0003-1768-355X</Identifier><AffiliationInfo><Affiliation>Central Queensland Health, Rockhampton, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gironès</LastName><ForeName>Xavier</ForeName><Initials>X</Initials><Identifier Source="ORCID">0000-0002-2329-5927</Identifier><AffiliationInfo><Affiliation>Department of Research and Universities, Government of Catalonia-Generalitat de Catalunya, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Coda</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0003-0427-6672</Identifier><AffiliationInfo><Affiliation>School of Health Sciences, College of Health, Medicine and Wellbeing, University of Newcastle, Newcastle, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Equity in Health and Wellbeing Research Program, Hunter Medical Research Institute, Newcastle, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D000078182">Systematic Review</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Canada</Country><MedlineTA>JMIR Mhealth Uhealth</MedlineTA><NlmUniqueID>101624439</NlmUniqueID><ISSNLinking>2291-5222</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016640" MajorTopicYN="Y">Diabetes, Gestational</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="Y">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015190" MajorTopicYN="N">Blood Glucose Self-Monitoring</DescriptorName><QualifierName UI="Q000295" MajorTopicYN="N">instrumentation</QualifierName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076251" MajorTopicYN="N">Wearable Electronic Devices</DescriptorName><QualifierName UI="Q000592" MajorTopicYN="N">standards</QualifierName><QualifierName UI="Q000706" MajorTopicYN="N">statistics & numerical data</QualifierName><QualifierName UI="Q000639" MajorTopicYN="N">trends</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">blood glucose</Keyword><Keyword MajorTopicYN="N">diabetes</Keyword><Keyword MajorTopicYN="N">diabetes mellitus</Keyword><Keyword MajorTopicYN="N">digital health</Keyword><Keyword MajorTopicYN="N">feasibility</Keyword><Keyword MajorTopicYN="N">flash glucose monitoring</Keyword><Keyword MajorTopicYN="N">gestational diabetes</Keyword><Keyword MajorTopicYN="N">glucose monitoring</Keyword><Keyword MajorTopicYN="N">mHealth</Keyword><Keyword MajorTopicYN="N">medication adherence</Keyword><Keyword MajorTopicYN="N">mobile health</Keyword><Keyword MajorTopicYN="N">mobile phone</Keyword><Keyword MajorTopicYN="N">self-monitoring</Keyword><Keyword MajorTopicYN="N">smartphones</Keyword><Keyword MajorTopicYN="N">smartwatch</Keyword><Keyword MajorTopicYN="N">smartwatch technology</Keyword><Keyword MajorTopicYN="N">systematic review</Keyword><Keyword MajorTopicYN="N">usability</Keyword></KeywordList><CoiStatement>None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>11</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>7</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>8</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>18</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate 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Medline.</Citation><ArticleIdList><ArticleId IdType="doi">10.1111/jgh.14451</ArticleId><ArticleId IdType="pubmed">30151918</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39625861</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>05</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1752-8062</ISSN><JournalIssue CitedMedium="Internet"><Volume>17</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Clinical and translational science</Title><ISOAbbreviation>Clin Transl Sci</ISOAbbreviation></Journal><ArticleTitle>Effect of carrot intake on glucose tolerance, microbiota, and gene expression in a type 2 diabetes mouse model.</ArticleTitle><Pagination><StartPage>e70090</StartPage><MedlinePgn>e70090</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e70090</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1111/cts.70090</ELocationID><Abstract><AbstractText>Type 2 diabetes (T2D) pathophysiology involves insulin resistance (IR) and inadequate insulin secretion. Current T2D management includes dietary adjustments and/or oral medications such as thiazolidinediones (TZDs). Carrots have shown to contain bioactive acetylenic oxylipins that are partial agonists of the peroxisome proliferator-activated receptor γ (Pparg) that mimic the antidiabetic effect of TZDs without any adverse effects. TZDs exert hypoglycemic effects through activation of Pparg and through the regulation of the gut microbiota (GM) producing short-chain fatty acids (SCFAs), which impact glucose and energy homeostasis, promote intestinal gluconeogenesis, and influence insulin signaling pathways. This study investigated the metabolic effects of carrot intake in a T2D mouse model, elucidating underlying mechanisms. Mice were fed a low-fat diet (LFD), high-fat diet (HFD), or adjusted HFD supplemented with 10% carrot powder for 16 weeks. Oral glucose tolerance tests were conducted at weeks 0 and 16. Fecal, cecum, and colon samples, as well as tissue samples, were collected at week 16 during the autopsy. Results showed improved oral glucose tolerance in the HFD carrot group compared to HFD alone after 16 weeks. GM analysis demonstrated increased diversity and compositional changes in the cecum of mice fed HFD with carrot relative to HFD. These findings suggest the potential effect of carrots in T2D management, possibly through modulation of GM. Gene expression analysis revealed no significant alterations in adipose or muscle tissue between diet groups. Further research into carrot-derived bioactive compounds and their mechanisms of action is warranted for developing effective dietary strategies against T2D.</AbstractText><CopyrightInformation>© 2024 The Author(s). Clinical and Translational Science published by Wiley Periodicals LLC on behalf of American Society for Clinical Pharmacology and Therapeutics.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kobaek-Larsen</LastName><ForeName>Morten</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-5097-9283</Identifier><AffiliationInfo><Affiliation>Department of Clinical Research, University of Southern Denmark, Odense M, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maschek</LastName><ForeName>Sina</ForeName><Initials>S</Initials><Identifier Source="ORCID">0009-0001-2408-729X</Identifier><AffiliationInfo><Affiliation>Department of Food Science, University of Copenhagen, Frederiksberg C, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kolstrup</LastName><ForeName>Stefanie Hansborg</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Institute for Molecular Medicine, University of Southern Denmark, Odense M, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Højlund</LastName><ForeName>Kurt</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0002-0891-4224</Identifier><AffiliationInfo><Affiliation>Department of Clinical Research, University of Southern Denmark, Odense M, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Steno Diabetes Center Odense, Odense University Hospital, Odense C, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nielsen</LastName><ForeName>Dennis Sandris</ForeName><Initials>DS</Initials><Identifier Source="ORCID">0000-0001-8121-1114</Identifier><AffiliationInfo><Affiliation>Department of Food Science, University of Copenhagen, Frederiksberg C, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hansen</LastName><ForeName>Axel Kornerup</ForeName><Initials>AK</Initials><Identifier Source="ORCID">0000-0003-1575-2507</Identifier><AffiliationInfo><Affiliation>Department of Veterinary and Animal Science, University of Copenhagen, Frederiksberg C, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Christensen</LastName><ForeName>Lars Porskjær</ForeName><Initials>LP</Initials><Identifier Source="ORCID">0000-0002-5035-9201</Identifier><AffiliationInfo><Affiliation>Department of Physics, Chemistry and Pharmacy, University of Southern Denmark, Odense M, Denmark.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>122-A5125</GrantID><Agency>Odense University Hospital Fund for Free Research</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Transl Sci</MedlineTA><NlmUniqueID>101474067</NlmUniqueID><ISSNLinking>1752-8054</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047495">PPAR gamma</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018552" MajorTopicYN="Y">Daucus carota</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000178" MajorTopicYN="N">diet therapy</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069196" MajorTopicYN="Y">Gastrointestinal Microbiome</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005951" MajorTopicYN="N">Glucose Tolerance Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018752" MajorTopicYN="N">Diet, Fat-Restricted</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D047495" MajorTopicYN="N">PPAR gamma</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000178" MajorTopicYN="N">diet therapy</QualifierName><QualifierName UI="Q000097" 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Adv Med Sci. 2021;66:284‐292. doi:10.1016/j.advms.2021.05.003</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.advms.2021.05.003</ArticleId><ArticleId IdType="pubmed">34098509</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39625456</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>12</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>12</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1948-7185</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>49</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>12</Day></PubDate></JournalIssue><Title>The journal of physical chemistry letters</Title><ISOAbbreviation>J Phys Chem Lett</ISOAbbreviation></Journal><ArticleTitle>Heterotypic Interactions of Amyloid β and the Islet Amyloid Polypeptide Produce Mixed Aggregates with Non-Native Fibril Structure.</ArticleTitle><Pagination><StartPage>12197</StartPage><EndPage>12205</EndPage><MedlinePgn>12197-12205</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1021/acs.jpclett.4c02827</ELocationID><Abstract><AbstractText>Amyloid aggregates are hallmarks of the pathology of a wide range of diseases, including type 2 diabetes (T2D) and Alzheimer's disease (AD). Much epidemiological and pathological evidence points to significant overlap between AD and T2D. Individuals with T2D have a higher likelihood of developing AD; moreover, colocalized aggregates of amyloid β (Aβ) and the islet amyloid polypeptide (IAPP), the two main peptides implicated in the formation of toxic amyloid aggregates in AD and T2D, have also been identified in the brain. However, how these peptides interact with each other is not well understood, and the structural facets of heterotypic mixed fibrils formed via such interactions remain elusive. Here we use atomic force microscopy augmented with infrared spectroscopy to probe the secondary structure of individual aggregates formed via heterotypic interactions of Aβ and IAPP and provide unequivocal direct evidence of mixed aggregates. Furthermore, we show that co-aggregation of the peptides from the monomeric stage leads to the formation of unique polymorphs, in which both peptides undergo structural deviation from their native states, whereas seeding with preformed IAPP fibrils leads to aggregates similar to native Aβ. These findings highlight how heterotypic interactions between amyloidogenic peptides can lead to polymorphic diversity proteinopathies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baghel</LastName><ForeName>Divya</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Chemistry and Biochemistry, The University of Alabama, 1007E Shelby Hall, Tuscaloosa, Alabama 35487, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghosh</LastName><ForeName>Ayanjeet</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0001-9458-3910</Identifier><AffiliationInfo><Affiliation>Department of Chemistry and Biochemistry, The University of Alabama, 1007E Shelby Hall, Tuscaloosa, Alabama 35487, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Phys Chem Lett</MedlineTA><NlmUniqueID>101526034</NlmUniqueID><ISSNLinking>1948-7185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058228">Islet Amyloid Polypeptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016229">Amyloid beta-Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D066329">Protein Aggregates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000682">Amyloid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D058228" MajorTopicYN="Y">Islet Amyloid Polypeptide</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016229" MajorTopicYN="Y">Amyloid beta-Peptides</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018625" MajorTopicYN="Y">Microscopy, Atomic Force</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066329" MajorTopicYN="Y">Protein Aggregates</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017433" MajorTopicYN="N">Protein Structure, Secondary</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000682" MajorTopicYN="N">Amyloid</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>12</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>12</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>10</Hour><Minute>43</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39625456</ArticleId><ArticleId IdType="doi">10.1021/acs.jpclett.4c02827</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39625348</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>03</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1757-9996</ISSN><JournalIssue CitedMedium="Internet"><Volume>22</Volume><PubDate><Year>2024</Year><Month>Dec</Month><Day>03</Day></PubDate></JournalIssue><Title>Oral health & preventive dentistry</Title><ISOAbbreviation>Oral Health Prev Dent</ISOAbbreviation></Journal><ArticleTitle>Clinical Outcomes and Cytokine Profile of Standard and Short Implant-supported Prostheses in Diabetics Treated for Periodontal Disease: A 5-year Study.</ArticleTitle><Pagination><StartPage>623</StartPage><EndPage>630</EndPage><MedlinePgn>623-630</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3290/j.ohpd.b5866861</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">The present cross-sectional study aimed to assess the clinico-radiographic parameters as well as salivary levels of receptor activator of nuclear factor kappa-Β ligand (RANKL), osteoprotegerin (OPG), interleukin (IL)-6, and tumor necrosis factor-alpha (TNF-α) around standard and short dental implants (SDIs)-supported fixed partial denture in partially dentate type-II diabetes mellitus (T2DM) patients treated for periodontitis.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">The study comprised 4 groups: group 1 included T2DM patients with standard implants (n = 20); group II included non-T2DM patients with standard implants (n = 20); group III included T2DM patients with SDIs (n = 20); and group IV included non-T2DM patients with SDIs (n = 20). Participants eligible for the study included medically diagnosed T2DM patients with glycated hemoglobin (HbA1c) levels ≥ 6.5%, and non-T2DM participants with HbA1c levels between 4.0% and 5.0%. All had undergone previous periodontal therapy and had at least one standard implant and one SDI in the posterior maxillary or mandibular region. Exclusions were subjects with systemic conditions other than T2DM, recent use of steroids or antimicrobials, pregnancy or lactation, edentulism, misaligned dentition, or alcohol/tobacco use. Treatment involved non-surgical periodontal therapy, implant placement, and prosthetic procedures, with assessments including clinical (plaque index [PI], bleeding on probing [BOP], probing depth [PD]), radiographic (crestal bone loss [CBL]) parameters, and salivary cytokine levels including RANKL, OPG, IL-6, and TNF-α.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The study groups, each comprising 20 participants, showed no significant differences in demographics, restoration type, T2DM duration, family history, body mass index, or brushing routine (p>0.05). At baseline and 5-year follow-up, T2DM participants exhibited poorer periodontal parameters compared to non-T2DM, with higher PI (baseline: 62.2 ± 5.8% vs 29.6 ± 3.7%; 5-year follow-up: 69.2 ± 6.1% vs 32.8 ± 3.8%), BOP (baseline: 30.5 ± 3.2% vs 18.2 ± 2.6%; 5-year follow-up: 35.5 ± 3.9% vs 20.5 ± 2.5%), PD (baseline: 5.5 ± 1.1 mm vs 3.1 ± 0.9 mm; 5-year follow-up: 4.2 ± 0.8 mm vs 2.4 ± 0.7 mm), and CBL (baseline: 4.4 ± 0.4 mm vs 2.0 ± 0.2 mm; 5-yearfollow-up: 4.9 ± 0.5 mm vs 2.3 ± 0.3 mm), regardless of implant type. Salivary cytokine levels (RANKL, OPG, IL-6, TNF-α) were consistently higher in T2DM groups than non-T2DM across both implant types. Participants with SDIs showed comparable clinico-radiographic outcomes and salivary levels of cytokines to standard implants.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The application of SDI-supported rehabilitation in T2DM and non-diabetics showed comparable clinico-radiographic outcomes and salivary levels of cytokines to standard dental implants. Furthermore, T2DM patients exhibit poorer periodontal health and elevated inflammatory markers in patients with standard implants and SDIs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>AlHelal</LastName><ForeName>Abdulaziz A</ForeName><Initials>AA</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Oral Health Prev Dent</MedlineTA><NlmUniqueID>101167768</NlmUniqueID><ISSNLinking>1602-1622</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015921">Dental Implants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053245">RANK Ligand</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053244">Osteoprotegerin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019094" MajorTopicYN="Y">Dental Prosthesis, Implant-Supported</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="Y">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="Y">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015921" MajorTopicYN="N">Dental Implants</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053245" MajorTopicYN="N">RANK Ligand</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012463" MajorTopicYN="N">Saliva</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053244" MajorTopicYN="N">Osteoprotegerin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003830" MajorTopicYN="N">Denture, Partial, Fixed</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010518" MajorTopicYN="N">Periodontitis</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">RANKL</Keyword><Keyword MajorTopicYN="N">bone loss</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">short implant</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>12</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>12</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>9</Hour><Minute>33</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39625348</ArticleId><ArticleId IdType="doi">10.3290/j.ohpd.b5866861</ArticleId><ArticleId IdType="pii">5866861</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39623849</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1819-2718</ISSN><JournalIssue CitedMedium="Internet"><Volume>36</Volume><Issue>3</Issue><PubDate><Year>2024</Year><Season>Jul-Sep</Season></PubDate></JournalIssue><Title>Journal of Ayub Medical College, Abbottabad : JAMC</Title><ISOAbbreviation>J Ayub Med Coll Abbottabad</ISOAbbreviation></Journal><ArticleTitle>IRISIN AS A NOVEL DIAGNOSTIC BIOMARKER FOR INFLAMMATORY DISEASES: A REVIEW.</ArticleTitle><Pagination><StartPage>636</StartPage><EndPage>641</EndPage><MedlinePgn>636-641</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.55519/JAMC-03-12344</ELocationID><Abstract><AbstractText>Inflammatory biomarkers are molecules that can offer vital information on the intricate chain of happenings and molecular processes underpinning the pathophysiology of any inflammatory disease. They can be measured in various biological samples such as blood, urine, or saliva, and are used as indicators of the presence and severity of inflammation. Measuring salivary inflammatory biomarkers is a non-invasive and relatively easy way to monitor inflammation, and it has been shown to be a useful tool in the diagnosis and management of various oral and systemic inflammatory diseases. Irisin is a novel anti-inflammatory protein and its implication and diagnostic role in inflammation have been widely studied; however, not much have been studied in oral inflammation per se. Irisin is predominantly downregulated in several inflammatory conditions, including obesity, type 2 diabetes, periodontitis, and cardiovascular diseases. This suggests that irisin may be involved in the inflammatory process, but more research is needed, especially of salivary irisin to understand its precise role. Overall, the role of irisin as an inflammatory biomarker is still an area of active research, and more studies are needed to determine its diagnostic and therapeutic potential. This review highlights the diagnostic and therapeutic potential of irisin in various systemic and oral inflammatory conditions.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rana</LastName><ForeName>Sadia</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>School of Dental Sciences, Universiti Sains Malaysia Health Campus, 16150 Kubang Kerian, Kota Bharu, Kelantan-Malaysia, Sharif Medical and Dental College Lahore-Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wahab</LastName><ForeName>Norsila Abdul</ForeName><Initials>NA</Initials><AffiliationInfo><Affiliation>School of Dental Sciences, Universiti Sains Malaysia Health Campus, 16150 Kubang Kerian, Kota Bharu, Kelantan-Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shima Shahidan</LastName><ForeName>Wan Nazatul</ForeName><Initials>WN</Initials><AffiliationInfo><Affiliation>School of Dental Sciences, Universiti Sains Malaysia Health Campus, 16150 Kubang Kerian, Kota Bharu, Kelantan-Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Atif</LastName><ForeName>Saira</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>CMH Lahore Medical College & Institute of Dentistry, National University of Medical Sciences-Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fahim</LastName><ForeName>Ayesha</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Islamic International Dental College, Riphah International University Islamabad-Pakistan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Pakistan</Country><MedlineTA>J Ayub Med Coll Abbottabad</MedlineTA><NlmUniqueID>8910750</NlmUniqueID><ISSNLinking>1025-9589</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005353">Fibronectins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C577593">FNDC5 protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005353" MajorTopicYN="Y">Fibronectins</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="Y">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="Y">Inflammation</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012463" MajorTopicYN="N">Saliva</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010518" MajorTopicYN="N">Periodontitis</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diagnostic biomarkers; Inflammatory diseases; Salivary irisin; Serum irisin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>25</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>2</Hour><Minute>33</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39623849</ArticleId><ArticleId IdType="doi">10.55519/JAMC-03-12344</ArticleId><ArticleId IdType="pii">11586/3581</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39623445</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>06</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1741-7015</ISSN><JournalIssue CitedMedium="Internet"><Volume>22</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>02</Day></PubDate></JournalIssue><Title>BMC medicine</Title><ISOAbbreviation>BMC Med</ISOAbbreviation></Journal><ArticleTitle>Multiomics profiling of DNA methylation, microRNA, and mRNA in skeletal muscle from monozygotic twin pairs discordant for type 2 diabetes identifies dysregulated genes controlling metabolism.</ArticleTitle><Pagination><StartPage>572</StartPage><MedlinePgn>572</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">572</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12916-024-03789-y</ELocationID><Abstract><AbstractText Label="BACKGROUND">A large proportion of skeletal muscle insulin resistance in type 2 diabetes (T2D) is caused by environmental factors.</AbstractText><AbstractText Label="METHODS">By applying multiomics mRNA, microRNA (miRNA), and DNA methylation platforms in biopsies from 20 monozygotic twin pairs discordant for T2D, we aimed to delineate the epigenetic and transcriptional machinery underlying non-genetic muscle insulin resistance in T2D.</AbstractText><AbstractText Label="RESULTS">Using gene set enrichment analysis (GSEA), we found decreased mRNA expression of genes involved in extracellular matrix organization, branched-chain amino acid catabolism, metabolism of vitamins and cofactors, lipid metabolism, muscle contraction, signaling by receptor tyrosine kinases pathways, and translocation of glucose transporter 4 (GLUT4) to the plasma membrane in muscle from twins with T2D. Differential expression levels of one or more predicted target relevant miRNA(s) were identified for approximately 35% of the dysregulated GSEA pathways. These include miRNAs with a significant overrepresentation of targets involved in GLUT4 translocation (miR-4643 and miR-548z), signaling by receptor tyrosine kinases pathways (miR-607), and muscle contraction (miR-4658). Acquired DNA methylation changes in skeletal muscle were quantitatively small in twins with T2D compared with the co-twins without T2D. Key methylation and expression results were validated in muscle, myotubes, and/or myoblasts from unrelated subjects with T2D and controls. Finally, mimicking T2D-associated changes by overexpressing miR-548 and miR-607 in cultured myotubes decreased expression of target genes, GLUT4 and FGFR4, respectively, and impaired insulin-stimulated phosphorylation of Akt (Ser473) and TBC1D4.</AbstractText><AbstractText Label="CONCLUSIONS">Together, we show that T2D is associated with non- and epigenetically determined differential transcriptional regulation of pathways regulating skeletal muscle metabolism and contraction.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ling</LastName><ForeName>Charlotte</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, 205 02, Sweden. charlotte.ling@med.lu.se.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vavakova</LastName><ForeName>Magdalena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahmad Mir</LastName><ForeName>Bilal</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Genomics, Diabetes and Endocrinology Unit, Department of Clinical Sciences, Lund University Diabetes Center, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Säll</LastName><ForeName>Johanna</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perfilyev</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>Melina</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jansson</LastName><ForeName>Per-Anders</ForeName><Initials>PA</Initials><AffiliationInfo><Affiliation>Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska University Hospital, Bruna Straket 16, Level 2/3, Gothenburg, 413 45, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Davegårdh</LastName><ForeName>Cajsa</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Asplund</LastName><ForeName>Olof</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Genomics, Diabetes and Endocrinology Unit, Department of Clinical Sciences, Lund University Diabetes Center, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hansson</LastName><ForeName>Ola</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Genomics, Diabetes and Endocrinology Unit, Department of Clinical Sciences, Lund University Diabetes Center, Lund University, Malmö, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute for Molecular Medicine Finland (FIMM), Helsinki University, Helsinki, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vaag</LastName><ForeName>Allan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Copenhagen, Herlev, Denmark.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Lund University Diabetes Centre, Lund University, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Endocrinology, Scania University Hospital, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nilsson</LastName><ForeName>Emma</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Epigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2016-02486</GrantID><Agency>Vetenskapsrådet</Agency><Country/></Grant><Grant><GrantID>2018-02567</GrantID><Agency>Vetenskapsrådet</Agency><Country/></Grant><Grant><GrantID>2021-00628</GrantID><Agency>Vetenskapsrådet</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D018486">Twin Study</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Med</MedlineTA><NlmUniqueID>101190723</NlmUniqueID><ISSNLinking>1741-7015</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D035683">MicroRNAs</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="Y">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D035683" MajorTopicYN="Y">MicroRNAs</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014430" MajorTopicYN="Y">Twins, Monozygotic</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019175" MajorTopicYN="Y">DNA Methylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="Y">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000095028" MajorTopicYN="N">Multiomics</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DNA methylation</Keyword><Keyword MajorTopicYN="N">Discordant monozygotic twins</Keyword><Keyword MajorTopicYN="N">Epigenetics</Keyword><Keyword MajorTopicYN="N">Gene expression</Keyword><Keyword MajorTopicYN="N">MicroRNA (miRNA)</Keyword><Keyword MajorTopicYN="N">Skeletal muscle</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes (T2D)</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: All study participants provided informed written consent and the study was approved by the local ethics committees (461/2006 and 520/2008) and conducted in accordance with the principles of the Helsinki Declaration. Consent for publication: Not applicable. 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Diabetes. 2021;70(10):2402–18.</Citation><ArticleIdList><ArticleId IdType="pubmed">34315727</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39623437</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1475-2840</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>02</Day></PubDate></JournalIssue><Title>Cardiovascular diabetology</Title><ISOAbbreviation>Cardiovasc Diabetol</ISOAbbreviation></Journal><ArticleTitle>Adipsin improves diabetic hindlimb ischemia through SERPINE1 dependent angiogenesis.</ArticleTitle><Pagination><StartPage>429</StartPage><MedlinePgn>429</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">429</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12933-024-02526-2</ELocationID><Abstract><AbstractText Label="BACKGROUND">Adipsin (complement factor D, CFD), as the first described adipokine, is well-known for its regulatory effects in diabetic cardiovascular complications. However, its role in diabetic hind-limb ischemia was not clarified. This study aimed to evaluate the possible therapeutic effect of Adipsin in hind-limb ischemia in type 2 diabetic mice and to elucidate the molecular mechanisms involved.</AbstractText><AbstractText Label="METHODS">A high-fat diet and streptozotocin (HFD/STZ)-induced diabetic mouse model, and a transgenic mouse model with adipose tissue-specific overexpression of Adipsin (Adipsin-Tg) were employed. Hindlimb ischemia was established by femoral artery ligation, and blood flow recovery was monitored using Laser Doppler perfusion imaging. Molecular mechanisms underlying Adipsin-potentiated angiogenesis were examined using RNA sequencing and co-immunoprecipitation/mass spectrometry (Co-IP/MS) analyses.</AbstractText><AbstractText Label="RESULTS">Adipsin expression was upregulated in non-diabetic mice following HLI, while suppressed in diabetic mice, indicating its potential role in ischemic recovery which is impaired in diabetes. Adipsin-Tg mice exhibited significantly improved blood flow recovery, increased capillary density, and enhanced muscle regeneration in comparison with non-transgenic (NTg) diabetic mice. Adipsin facilitated proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs) under hyperglycemic and hypoxic conditions. Additionally, it enhanced phosphorylation of AKT, ERK, and eNOS pathways both in vivo and in vitro. RNA sequencing and co-immunoprecipitation/mass spectrometry (Co-IP/MS) analyses identified that Adipsin promoted angiogenesis by interacting with SERBP1, which disrupted the binding of SERBP1 to SERPINE1 mRNA, resulting in reduced SERPINE1 expression and the subsequent activation of the VEGFR2 signaling cascade.</AbstractText><AbstractText Label="CONCLUSIONS">Adipsin promotes angiogenesis and facilitates blood perfusion recovery in diabetic mice with HLI by downregulating SERPINE1 through interaction with SERBP1. These findings elucidate a novel therapeutic potential for Adipsin in the management of PAD in diabetic patients, highlighting its role in enhancing angiogenesis and tissue repair.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Zhang</LastName><ForeName>Xiaohua</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Jiang</LastName><ForeName>Mengyuan</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Zhang</LastName><ForeName>Xuebin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zuo</LastName><ForeName>Yixuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Huanle</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Tingting</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Xijing 986 Hospital Department, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Liyu</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dai</LastName><ForeName>Xinchun</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ge</LastName><ForeName>Wen</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Chuang</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Fang</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Basic Medical Teaching Experiment Center, Basic Medical College, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jiye</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yue</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yangyang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qiang</LastName><ForeName>Huanhuan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xiaojie</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Dongdong</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China. wintersun3@fmmu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>82470358</GrantID><Agency>National Natural Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>2024RS-CXTD-78</GrantID><Agency>Shaanxi Provincial Science and Technology Innovation Team</Agency><Country/></Grant><Grant><GrantID>BKJWS221J004</GrantID><Agency>Key logistic research projects</Agency><Country/></Grant><Grant><GrantID>2020</GrantID><Agency>Top Young Talents Special Support Program in Shaanxi Province</Agency><Country/></Grant><Grant><GrantID>XJZT24CZ13</GrantID><Agency>Xijing Hospital Research Promotion Program</Agency><Country/></Grant><Grant><GrantID>2024SF2-GJHX-27</GrantID><Agency>Shaanxi Province Key Technology Research Project</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cardiovasc Diabetol</MedlineTA><NlmUniqueID>101147637</NlmUniqueID><ISSNLinking>1475-2840</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 3.4.21.46</RegistryNumber><NameOfSubstance UI="D011416">Complement Factor D</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.46</RegistryNumber><NameOfSubstance UI="C493488">CFD protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D043925">Angiogenesis Inducing Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="Y">Ischemia</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006614" MajorTopicYN="Y">Hindlimb</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018919" MajorTopicYN="Y">Neovascularization, Physiologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="Y">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="Y">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012039" MajorTopicYN="Y">Regional Blood Flow</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D061307" MajorTopicYN="Y">Human Umbilical Vein Endothelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011416" MajorTopicYN="Y">Complement Factor D</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="Y">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="N">blood supply</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="Y">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003925" MajorTopicYN="N">Diabetic Angiopathies</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020127" MajorTopicYN="N">Recovery of Function</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D043925" MajorTopicYN="N">Angiogenesis Inducing Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000082644" MajorTopicYN="N">Microvascular Density</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000096482" MajorTopicYN="N">Angiogenesis</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adipsin</Keyword><Keyword MajorTopicYN="N">Angiogenesis</Keyword><Keyword MajorTopicYN="N">Diabetes</Keyword><Keyword MajorTopicYN="N">Endothelial cells</Keyword><Keyword MajorTopicYN="N">Hindlimb ischemia</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: All experimental animal procedures were approved by the Animal Care and Use Committee of the Air Force Medical University and followed the Animal Research Advisory Committee of the National Institutes of Health guidelines (Approval ID: 20201017). Consent for publication: Not applicable. 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However, islet β-cell control of Proinsulin translation remains incompletely understood. Here, we identify OSGEP, an enzyme responsible for t<sup>6</sup>A<sub>37</sub> modification of tRNA<sup>NNU</sup> that tunes glucose metabolism in β-cells. Global Osgep deletion causes glucose intolerance, while β-cell-specific deletion induces hyperglycemia and glucose intolerance due to impaired insulin activity. Transcriptomics and proteomics reveal activation of the unfolded protein response (UPR) and apoptosis signaling pathways in Osgep-deficient islets, linked to an increase in misfolded Proinsulin from reduced t<sup>6</sup>A<sub>37</sub> modification. Osgep overexpression in pancreas rescues insulin secretion and mitigates diabetes in high-fat diet mice. Osgep enhances translational fidelity and alleviates UPR signaling, highlighting its potential as a therapeutic target for diabetes. Individuals carrying the C allele at rs74512655, which promotes OSGEP transcription, may show reduced susceptibility to T2DM. These findings show OSGEP is essential for islet β-cells and a potential diabetes therapy target.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yujie</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pharmacy, Xiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xuechun</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Haijun</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ruimeng</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Peng</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Rong</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Tianyuan</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, 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Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Rong</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0003-3435-7289</Identifier><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Wei</ForeName><Initials>W</Initials><Identifier Source="ORCID">0000-0002-6190-3129</Identifier><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Honghao</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, 410078, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Clinical Research Center for Geriatric Disorders, Changsha, 410008, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qing</ForeName><Initials>Q</Initials><Identifier 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metabolism].</ArticleTitle><Pagination><StartPage>1170</StartPage><EndPage>1174</EndPage><MedlinePgn>1170-1174</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3760/cma.j.cn112138-20240713-00448</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Y</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinolgy, First Medical Center of Chinese PLA General Hospital, Beijing100039, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Y J</ForeName><Initials>YJ</Initials><AffiliationInfo><Affiliation>Department of Endocrinolgy, First Medical Center of Chinese PLA General Hospital, Beijing100039, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mu</LastName><ForeName>Y M</ForeName><Initials>YM</Initials><AffiliationInfo><Affiliation>Department of Endocrinolgy, First Medical Center of Chinese PLA General Hospital, Beijing100039, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Nei Ke Za Zhi</MedlineTA><NlmUniqueID>16210490R</NlmUniqueID><ISSNLinking>0578-1426</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.1.2</RegistryNumber><NameOfSubstance UI="D005941">Glucokinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005941" MajorTopicYN="Y">Glucokinase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="Y">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><AbstractText>在2型糖尿病（T2DM）病理生理机制探索中发现，作为人体葡萄糖传感器的葡萄糖激酶（GK）对于血糖稳态调节具有重要作用。GK的激活是启动葡萄糖代谢的首个步骤，GK可在胰脏、肝脏、肠道和下丘脑等器官/系统中通过多种途径调控血糖水平。以GK为靶点的葡萄糖激酶激活剂（GKA）历经数十年的研发，于近年取得了重大突破。GKA能够修复GK的功能，显著降低血糖并改善血糖稳态，是治疗T2DM患者的新一类降糖药物靶点。本文简要阐述了GK在葡萄糖代谢中的关键作用，并总结了GKA的作用机制及其应用现状。.</AbstractText></OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>21</Hour><Minute>50</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39622719</ArticleId><ArticleId IdType="doi">10.3760/cma.j.cn112138-20240713-00448</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39622714</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0578-1426</ISSN><JournalIssue CitedMedium="Print"><Volume>63</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>01</Day></PubDate></JournalIssue><Title>Zhonghua nei ke za zhi</Title><ISOAbbreviation>Zhonghua Nei Ke Za Zhi</ISOAbbreviation></Journal><ArticleTitle>[Progress of type 2 diabetes in the past decade].</ArticleTitle><Pagination><StartPage>1137</StartPage><EndPage>1143</EndPage><MedlinePgn>1137-1143</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3760/cma.j.cn112138-20240904-00552</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Y P</ForeName><Initials>YP</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, the First Medical Center of Chinese PLA General Hospital, Beijing100039, China School of Medicine, Nankai University, Tianjin300071, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mu</LastName><ForeName>Y M</ForeName><Initials>YM</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, the First Medical Center of Chinese PLA General Hospital, Beijing100039, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Nei Ke Za Zhi</MedlineTA><NlmUniqueID>16210490R</NlmUniqueID><ISSNLinking>0578-1426</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><AbstractText>糖尿病是最常见的内分泌系统疾病。糖尿病患病率近十年仍处于上升趋势，且2型糖尿病趋于年轻化，糖尿病的疾病负担正在逐渐加重。餐后1 h血糖≥8.6 mmol/L成为中间高血糖的诊断标准。糖尿病的管理理念朝着减重降脂、心肾获益的综合性目标发展。胰高血糖素样肽-1受体激动剂及钠-葡萄糖共转运蛋白2抑制剂在合并心肾疾病或风险的糖尿病患者中的治疗地位显著提高。本文对近十年来2型糖尿病流行病学趋势、发病机制、治疗策略，以及药物和器械等相关领域的进展进行回顾。.</AbstractText></OtherAbstract></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>21</Hour><Minute>50</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39622714</ArticleId><ArticleId IdType="doi">10.3760/cma.j.cn112138-20240904-00552</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39622567</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>14</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2044-6055</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>02</Day></PubDate></JournalIssue><Title>BMJ open</Title><ISOAbbreviation>BMJ Open</ISOAbbreviation></Journal><ArticleTitle>Home self-management of type 2 diabetes with diabetes technologies in northern France: a focused ethnographic study protocol.</ArticleTitle><Pagination><StartPage>e084475</StartPage><MedlinePgn>e084475</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e084475</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjopen-2024-084475</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Type 2 diabetes is a chronic condition associated with impaired glucose tolerance and a high prevalence of comorbidity, polypharmacy and medication safety incidents. Little is known about the patient work associated with using diabetes management technologies by patients and their informal caregivers at home. This study aims to apply a systems engineering approach to better understand this work.</AbstractText><AbstractText Label="METHODS AND ANALYSIS" NlmCategory="METHODS">This is a qualitative focused ethnographic study using interview and photography. Adults, living independently at home, with type 2 diabetes who have been using insulin as part of their treatment regimen for a minimum of 6 months and who are using at least one diabetes management technology without support of a professional at home are eligible for inclusion. Participants will be recruited through advertisements on social media, in diabetes clinics and by contacting associations of persons living with diabetes and diabetes specialists. Participant consent will be taken, interviews will be undertaken in the participant's home, audio-recorded and photographs securely saved. The Systems Engineering Initiative for Patient Safety (SEIPS) model will frame the data coding and we will develop new codes to accommodate data outside the SEIPS model. Results will be interpreted to produce a description of work processes, work system elements and interactions that support or jeopardise the achievement of safety. This protocol will follow the consolidated criteria for reporting qualitative research checklist for the reporting of qualitative research interviews.</AbstractText><AbstractText Label="ETHICAL CONSIDERATIONS AND DISSEMINATION" NlmCategory="UNASSIGNED">This protocol was approved by the University of Lille's Behavioural Sciences Ethics Committee. The study will comply with data protection legislation: the protocol has been declared by the Data Protection Officer of the University of Lille to the National Commission on Informatics and Liberty. We plan to disseminate our findings via presentations at relevant patient/public, professional, academic and scientific meetings, and publish in a peer-reviewed journal.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Marcilly</LastName><ForeName>Romaric</ForeName><Initials>R</Initials><Identifier Source="ORCID">0000-0002-7077-7267</Identifier><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, ULR 2694 - METRICS : Évaluation des technologies de santé et des pratiques médicales, F-59000 Lille, France, Lille, France romaric.marcilly@univ-lille.fr.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Inserm, CIC-IT 1403, F-59000 Lille, France, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Quindroit</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, ULR 2694 - METRICS : Évaluation des technologies de santé et des pratiques médicales, F-59000 Lille, France, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lemaitre</LastName><ForeName>Madleen</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, ULR 2694 - METRICS : Évaluation des technologies de santé et des pratiques médicales, F-59000 Lille, France, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CHU Lille, Department of Diabetology, Endocrinology, Metabolism and Nutrition Lille University Hospital, F-59000 Lille, France, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vambergue</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>CHU Lille, Department of Diabetology, Endocrinology, Metabolism and Nutrition Lille University Hospital, F-59000 Lille, France, Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>European Genomic Institute for Diabetes, University School of Medicine, F-59000 Lille, France, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Avez</LastName><ForeName>Eric</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Patient and Public Involvement panel, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bubeck</LastName><ForeName>Arnaud</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Diabète LAB, Fédération Française des Diabétiques, 88 rue de la Roquette, 75011 Paris, France, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hehn</LastName><ForeName>Coline</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Diabète LAB, Fédération Française des Diabétiques, 88 rue de la Roquette, 75011 Paris, France, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Beuscart</LastName><ForeName>Jean-Baptiste</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, ULR 2694 - METRICS : Évaluation des technologies de santé et des pratiques médicales, F-59000 Lille, France, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grimes</LastName><ForeName>Tamasine C</ForeName><Initials>TC</Initials><Identifier Source="ORCID">0000-0002-7154-3243</Identifier><AffiliationInfo><Affiliation>School of Pharmacy, Trinity College Dublin, Dublin, Ireland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open</MedlineTA><NlmUniqueID>101552874</NlmUniqueID><ISSNLinking>2044-6055</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000884" MajorTopicYN="Y">Anthropology, Cultural</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D036301" MajorTopicYN="Y">Qualitative Research</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073278" MajorTopicYN="Y">Self-Management</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005602" MajorTopicYN="N" Type="Geographic">France</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012107" MajorTopicYN="N">Research Design</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017028" MajorTopicYN="N">Caregivers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007407" MajorTopicYN="N">Interviews as Topic</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">BIOTECHNOLOGY & BIOINFORMATICS</Keyword><Keyword MajorTopicYN="N">General diabetes</Keyword><Keyword MajorTopicYN="N">QUALITATIVE RESEARCH</Keyword><Keyword MajorTopicYN="N">Self-Management</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>20</Hour><Minute>43</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>12</Month><Day>2</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39622567</ArticleId><ArticleId IdType="pmc">PMC11624803</ArticleId><ArticleId IdType="doi">10.1136/bmjopen-2024-084475</ArticleId><ArticleId IdType="pii">bmjopen-2024-084475</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Basu S, Yudkin JS, Kehlenbrink S, et al. 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Neurological surgery</Title><ISOAbbreviation>No Shinkei Geka</ISOAbbreviation></Journal><ArticleTitle>[Pharmacological Treatment for Type 2 Diabetes].</ArticleTitle><Pagination><StartPage>1144</StartPage><EndPage>1154</EndPage><MedlinePgn>1144-1154</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.11477/mf.1436205031</ELocationID><Abstract><AbstractText>Diabetes management primarily aims to achieve a life expectancy and quality of life similar to that of people without diabetes. The key to achieving this goal is the effective prevention and management of both the microvascular and macrovascular complications associated with diabetes. Although glycated hemoglobin levels of less than 7% are recommended to minimize complications, individual targets should be set considering variables such as age, duration of diabetes, risk of hypoglycemia, organ function, support system, general health status, and social background. Treatment decisions should be individualized according to each patient's diabetes status and guided by the latest evidence on diabetes pharmacotherapy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Otsuka</LastName><ForeName>Hideaki</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, Metabolism and Nephrology, Graduate School of Medicine, Nippon Medical School.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagamine</LastName><ForeName>Tomoko</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Iwabu</LastName><ForeName>Masato</ForeName><Initials>M</Initials></Author></AuthorList><Language>jpn</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D004740">English Abstract</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>No Shinkei Geka</MedlineTA><NlmUniqueID>0377015</NlmUniqueID><ISSNLinking>0301-2603</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>3</Day><Hour>0</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>19</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39622320</ArticleId><ArticleId IdType="doi">10.11477/mf.1436205031</ArticleId><ArticleId IdType="pii">1436205031</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39622099</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>21</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0534</ISSN><JournalIssue CitedMedium="Internet"><Volume>184</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Computers in biology and medicine</Title><ISOAbbreviation>Comput Biol Med</ISOAbbreviation></Journal><ArticleTitle>Differences in brain spindle density during sleep between patients with and without type 2 diabetes.</ArticleTitle><Pagination><StartPage>109484</StartPage><MedlinePgn>109484</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.compbiomed.2024.109484</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0010-4825(24)01569-5</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Sleep spindles may be implicated in sensing and regulation of peripheral glucose. Whether spindle density in patients with type 2 diabetes mellitus (T2DM) differs from that of healthy subjects is unknown.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Our retrospective analysis of polysomnography (PSG) studies identified 952 patients with T2DM and 952 sex-, age- and BMI-matched control subjects. We extracted spindles from PSG electroencephalograms and used rank-based statistical methods to test for differences between subjects with and without diabetes. We also explored potential modifiers of spindle density differences. We replicated our analysis on independent data from the Sleep Heart Health Study.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We found that patients with T2DM exhibited about half the spindle density during sleep as matched controls (P < 0.0001). The replication dataset showed similar trends. The patient-minus-control paired difference in spindle density for pairs where the patient had major complications were larger than corresponding paired differences in pairs where the patient lacked major complications, despite both patient groups having significantly lower spindle density compared to their respective control subjects. Patients with a prescription for a glucagon-like peptide 1 receptor agonist had significantly higher spindle density than those without one (P ≤ 0.03). Spindle density in patients with T2DM monotonically decreased as their highest recorded HbA1C level increased (P ≤ 0.003).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">T2DM patients had significantly lower spindle density than control subjects; the size of that difference was correlated with markers of disease severity (complications and glycemic control). These findings expand our understanding of the relationships between sleep and glucose regulation.</AbstractText><CopyrightInformation>Published by Elsevier Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yeung</LastName><ForeName>Deryck</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Talukder</LastName><ForeName>Amlan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Min</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Umbach</LastName><ForeName>David M</ForeName><Initials>DM</Initials><AffiliationInfo><Affiliation>Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yuanyuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Motsinger-Reif</LastName><ForeName>Alison</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hwang</LastName><ForeName>Janice J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism and Department of Internal Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Zheng</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Division of Sleep Medicine and Department of Neurology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Leping</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: li3@niehs.nih.gov.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>ZIA ES101765</GrantID><Acronym>ImNIH</Acronym><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Comput Biol Med</MedlineTA><NlmUniqueID>1250250</NlmUniqueID><ISSNLinking>0010-4825</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004569" MajorTopicYN="Y">Electroencephalography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017286" MajorTopicYN="Y">Polysomnography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012890" MajorTopicYN="N">Sleep</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Brain</Keyword><Keyword MajorTopicYN="N">EEG</Keyword><Keyword MajorTopicYN="N">GLP-1RA</Keyword><Keyword MajorTopicYN="N">Hemoglobin A1C</Keyword><Keyword MajorTopicYN="N">Polysomnography</Keyword><Keyword MajorTopicYN="N">Spindle</Keyword><Keyword MajorTopicYN="N">T2DM</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2026</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>21</Day><Hour>16</Hour><Minute>43</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>18</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>18</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39622099</ArticleId><ArticleId IdType="mid">NIHMS2039512</ArticleId><ArticleId IdType="pmc">PMC11663128</ArticleId><ArticleId IdType="doi">10.1016/j.compbiomed.2024.109484</ArticleId><ArticleId IdType="pii">S0010-4825(24)01569-5</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>International-Diabetes-Federation, IDF Diabetes Atlas, 10th edn., (2021).</Citation></Reference><Reference><Citation>Bastaki S. 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ValidYN="Y">10.7326/ANNALS-24-02887-JC</ELocationID><Abstract><AbstractText>Taylor K, Eastwood S, Walker V, et al. <b>Incidence of diabetes after SARS-CoV-2 infection in England and the implications of COVID-19 vaccination: a retrospective cohort study of 16 million people.</b> Lancet Diabetes Endocrinol. 2024;12:558-568. 39054034.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vassilopoulos</LastName><ForeName>Stephanos</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA (S.V.).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mylonakis</LastName><ForeName>Eleftherios</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Houston Methodist Hospital, Houston, Texas, USA (E.M.).</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Ann Intern Med</MedlineTA><NlmUniqueID>0372351</NlmUniqueID><ISSNLinking>0003-4819</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000086663">COVID-19 Vaccines</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="Y">COVID-19</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015994" MajorTopicYN="N">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="Y">SARS-CoV-2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004739" MajorTopicYN="N" Type="Geographic">England</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086663" MajorTopicYN="N">COVID-19 Vaccines</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement><b>Disclosures:</b> Disclosure forms are available with the article online.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>16</Day><Hour>18</Hour><Minute>18</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>18</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>17</Hour><Minute>3</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39622055</ArticleId><ArticleId IdType="doi">10.7326/ANNALS-24-02887-JC</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39621725</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>12</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Activity of glucose-6-phosphate dehydrogenease and its correlation with inflammatory factors in diabetic retinopathy.</ArticleTitle><Pagination><StartPage>e0312452</StartPage><MedlinePgn>e0312452</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e0312452</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0312452</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">This study aims to explore glucose-6-phosphate dehydrogenase (G6PD) activity in diabetic retinopathy (DR) and its correlation with inflammatory factors, elucidating the regulatory role of G6PD in DR pathology.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A total of 151 T2DM patients were divided into three groups: diabetes without retinopathy (DNR, n = 59), non-proliferative retinopathy (NPDR, n = 46) and proliferative retinopathy (PDR, n = 49). Plasma G6PD activity was measured by a Randox G6PD kit and compared between these groups. Then the G6PD activity was correlated with inflammatory cytokines and metabolic parameters in these patients. A STZ-induced diabetic rat model was established, G6PD activity was validated by western blot and immunofluorescence staining in the retina of this model.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Plasma G6PD activity decreased in the order of DNR, NPDR and PDR groups (P<0.01). G6PD activity was negatively correlated with IL-6, IL-8, TNF-α, cholesterol, and LDL (r = -0.1625, -0.1808, -0.1865, -0.1747, r = -0.1807, P<0.05). Multiple regression analysis showed TNF-α, IL-6, and LDL were independent related factors for G6PD. Logistic regression analysis showed G6PD, triglyceride, cholesterol, IL-8, TNF-α, and macular edema were influencing factors for T2DM with DR. Western Blot analysis indicated a significant reduction of G6PD expression in the retina, and immunofluorescence staining showed distribution of G6PD especially in the retinal endothelium cell decreased.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">G6PD may play an important role in DR occurrence and progression, with decreased expression correlating closely with lipid metabolism and inflammatory factors.</AbstractText><CopyrightInformation>Copyright: © 2024 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Dan</ForeName><Initials>D</Initials><Identifier Source="ORCID">0009-0002-2738-5679</Identifier><AffiliationInfo><Affiliation>Department of Ophthalmology, The Second Clinical Medical College, Jinan University, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Chuchu</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, The Second People's Hospital of Futian District, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Lan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Post-doctoral Scientific Research Station of Basic Medicine, Jinan University, Guangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zeng</LastName><ForeName>Qiqiao</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zi</LastName><ForeName>Tao</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Gongyi</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Hongyan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Cunzi</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Endocrinology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ming-Ming</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology, The Shenzhen People's Hospital, Shenzhen, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 1.1.1.49</RegistryNumber><NameOfSubstance UI="D005954">Glucosephosphate Dehydrogenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003930" MajorTopicYN="Y">Diabetic Retinopathy</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005954" MajorTopicYN="Y">Glucosephosphate Dehydrogenase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012160" MajorTopicYN="N">Retina</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017207" 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The connection between SUD and DM stems from rapid cell damage, pancreatic beta-cell dysfunction, and glucose dysregulation due to increased oxidative stress and decreased antioxidant activity. This study aims to reduce the risk of T2DM among individuals undergoing SUD recovery treatments.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">This nurse-led diabetes prevention program, a 1-year-long, peer-based intervention, was implemented among clients at a federally funded, stand-alone drug addictions treatment center based on evidence that lifestyle modifications in dietary control, physical activity, and health behaviors can halt or delay the progression of Type 2 diabetes. Four trained peer educators delivered diabetes prevention interventions to a sample of individuals in drug addiction treatment in Nigeria. The nurse program leader provided weekly mentoring and guidance to the peer educators and collected, reviewed, and analyzed study participants' logs of weights and self-reported lifestyle modifications.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">There were significant differences in participants' behaviors pre- and post-lifestyle interventions, except in dairy product intakes as well as cigarette and cannabis use.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">This diabetes prevention program is innovative and effective with this at-risk population. Interventions were delivered with minor financial resources.</AbstractText><AbstractText Label="IMPLICATIONS FOR NURSING AND PATIENT CARE" NlmCategory="UNASSIGNED">SUD treatment must address physical and psychological health and consider the heightened risks of chronic illness in this population. Preventing somatic diseases, such as T2DM, is vital to long-term health and well-being.</AbstractText><CopyrightInformation>Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Adejumo</LastName><ForeName>Oluremi A</ForeName><Initials>OA</Initials><Identifier Source="ORCID">0000-0001-8563-1079</Identifier></Author><Author ValidYN="Y"><LastName>Ogunbiyi</LastName><ForeName>Elizabeth O</ForeName><Initials>EO</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Ling-Yin</ForeName><Initials>LY</Initials><Identifier Source="ORCID">0009-0003-8112-4899</Identifier></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Addict Nurs</MedlineTA><NlmUniqueID>9616159</NlmUniqueID><ISSNLinking>1088-4602</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019966" MajorTopicYN="Y">Substance-Related Disorders</DescriptorName><QualifierName UI="Q000451" MajorTopicYN="N">nursing</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000451" MajorTopicYN="N">nursing</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040242" MajorTopicYN="Y">Risk Reduction Behavior</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057184" MajorTopicYN="N">Practice Patterns, Nurses'</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors report no conflicts of interest. 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Drug and Alcohol Dependence, 186, 86–93. https://doi.org/10.1016/j.drugalcdep.2018.01.008</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.drugalcdep.2018.01.008</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39621105</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>14</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-0428</ISSN><JournalIssue CitedMedium="Internet"><Volume>68</Volume><Issue>2</Issue><PubDate><Year>2025</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Diabetologia</Title><ISOAbbreviation>Diabetologia</ISOAbbreviation></Journal><ArticleTitle>Evidence on the effectiveness and equity of population-based policies to reduce the burden of type 2 diabetes: a narrative review.</ArticleTitle><Pagination><StartPage>281</StartPage><EndPage>294</EndPage><MedlinePgn>281-294</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00125-024-06330-1</ELocationID><Abstract><AbstractText>There is increasing evidence for the effectiveness of population-based policies to reduce the burden of type 2 diabetes. Yet, there are concerns about the equity effects of some policies, whereby socioeconomically disadvantaged populations are not reached or are adversely affected. There is a lack of knowledge on the effectiveness and equity of policies that are both population based (i.e. targeting both at-risk and low-risk populations) and low agency (i.e. not requiring personal resources to benefit from the policy). In this narrative review, we selected 16 policies that were both population based and low agency and reviewed the evidence on their effectiveness and equity. Substantial evidence suggests that fruit and vegetable subsidies, unhealthy food taxes, mass media campaigns, and school nutrition and physical activity education are effective in promoting healthier lifestyle behaviours. Less evidence was available for mandatory food reformulation, reduced portion sizes, marketing restrictions and restriction of availability and promotion of unhealthy products, although the available evidence suggested that these policies were effective in reducing unhealthy food choices. Effects could rarely be quantified across different studies due to substantial heterogeneity. There is an overall lack of evidence on equity effects of population-based policies, although available studies mostly concluded that the policies had favourable equity effects, with the exception of food-labelling policies. Each of the policies is likely to have a relatively modest effect on population-level diabetes risks, which emphasises the importance of combining different policy measures. Future research should consider the type of evidence needed to demonstrate the real-world effectiveness and equity of population-based diabetes prevention policies.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mackenbach</LastName><ForeName>Joreintje D</ForeName><Initials>JD</Initials><Identifier Source="ORCID">0000-0002-2783-721X</Identifier><AffiliationInfo><Affiliation>Amsterdam UMC location Vrije Universiteit, Epidemiology and Data Science, Amsterdam, the Netherlands. j.mackenbach@amsterdamumc.nl.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Amsterdam Public Health Research Institute, Amsterdam, the Netherlands. j.mackenbach@amsterdamumc.nl.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Upstream Team, Amsterdam, the Netherlands. j.mackenbach@amsterdamumc.nl.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stuber</LastName><ForeName>Josine M</ForeName><Initials>JM</Initials><Identifier Source="ORCID">0000-0001-7825-018X</Identifier><AffiliationInfo><Affiliation>Amsterdam UMC location Vrije Universiteit, Epidemiology and Data Science, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Amsterdam Public Health Research Institute, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Upstream Team, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Beulens</LastName><ForeName>Joline W J</ForeName><Initials>JWJ</Initials><Identifier Source="ORCID">0000-0003-4521-9500</Identifier><AffiliationInfo><Affiliation>Amsterdam UMC location Vrije Universiteit, Epidemiology and Data Science, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Amsterdam Public Health Research Institute, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Upstream Team, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>024.004.017</GrantID><Agency>Dutch Ministry of Education, Culture, and Science and the Netherlands Organization for Scientific Research</Agency><Country/></Grant><Grant><GrantID>874627</GrantID><Agency>Horizon 2020 Framework Programme</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Diabetologia</MedlineTA><NlmUniqueID>0006777</NlmUniqueID><ISSNLinking>0012-186X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006291" MajorTopicYN="N">Health Policy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="N">Exercise</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006293" MajorTopicYN="N">Health Promotion</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Agency</Keyword><Keyword MajorTopicYN="N">Obesity</Keyword><Keyword MajorTopicYN="N">Population-level approaches</Keyword><Keyword MajorTopicYN="N">Prevention</Keyword><Keyword MajorTopicYN="N">Review</Keyword><Keyword MajorTopicYN="N">WHO Best Buys</Keyword></KeywordList><CoiStatement>Funding: This work is part of EXPOSOME-NL which is funded through the Gravitation programme of the Dutch Ministry of Education, Culture, and Science and the Netherlands Organisation for Scientific Research (NWO grant number 024.004.017). This work is also part of the EXPANSE project which is funded by the European Union’s Horizon 2020 research and innovation programme under grant agreement number 874627. The funders were not involved in the design of the study; the collection, analysis, and interpretation of data; writing the report; and did not impose any restrictions regarding the publication of the report. Authors’ relationships and activities: The authors declare that there are no relationships or activities that might bias, or be perceived to bias, their work. Contribution statement: JDM and JWJB contributed to the conceptualisation of the article. All authors contributed to the formal analysis of findings. JDM and JMS wrote the original draft. 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Routledge, New York, NY, pp 155–187. 10.4324/9780429494284-3</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39620343</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1670-4959</ISSN><JournalIssue CitedMedium="Internet"><Volume>110</Volume><Issue>12</Issue><PubDate><Year>2024</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Laeknabladid</Title><ISOAbbreviation>Laeknabladid</ISOAbbreviation></Journal><ArticleTitle>[SGLT2 inhibitors - A novel treatment for congestive heart failure and chronic kidney disease].</ArticleTitle><Pagination><StartPage>558</StartPage><EndPage>563</EndPage><MedlinePgn>558-563</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.17992/lbl.2024.12.817</ELocationID><Abstract><AbstractText>SGLT2 inhibitors increase renal excretion of sodium and glucose by blocking the SGLT2 transporters in the proximal tubule. Not only do they lower blood sugars levels but also have positive effects on blood pressure and weight. They lead to more efficient energy metabolism in the heart and kidneys, increase the production of red blood cells and decrease fibrosis and inflammation in the heart and the kidneys. Large double blind randomized trials have shown both cardiac and renal protective effects. Patient with heart failure, both with reduced and preserved ejection fraction have shown to benefit from treatment with SGLT2 inhibitors. They have lower risk of death due to cardiovascular causes and decreased risk of hospitalization because of heart failure compared to patient treated with placebo both with and without diabetes type 2. SGLT2 inhibitors are shown to decrease risk of chronic kidney disease stage 5 and dialysis, death due of cardiovascular events and doubling of serum creatinine in patients with chronic kidney disease both with and without diabetes type 2. They are now recommended for treatment of heart failure and chronic kidney disease with the highest evidence grade. SGLT2 inhibitors do not increase risk of hypoglycemia or acute kidney injury but do have a serious uncommon adverse effect that are normoglycemic ketoacidosis and Fournier's gangrene that physicians need to be alert to.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Eliasdottir</LastName><ForeName>Sigridur Birna</ForeName><Initials>SB</Initials><AffiliationInfo><Affiliation>MD, MS. Sahlgrenska University Hospital, Gothenburg, Sweden.</Affiliation></AffiliationInfo></Author></AuthorList><Language>ice</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D004740">English Abstract</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Iceland</Country><MedlineTA>Laeknabladid</MedlineTA><NlmUniqueID>7901326</NlmUniqueID><ISSNLinking>0023-7213</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="Y">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007668" MajorTopicYN="N">Kidney</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Chronic kidney disease</Keyword><Keyword MajorTopicYN="N">Congestive heart failur</Keyword><Keyword MajorTopicYN="N">Diabetes type 2</Keyword><Keyword MajorTopicYN="N">Mechanism</Keyword><Keyword MajorTopicYN="N">SGLT2 inhbitors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>12</Hour><Minute>34</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>12</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39620343</ArticleId><ArticleId IdType="doi">10.17992/lbl.2024.12.817</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39620193</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2308-118X</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>2</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Journal of the ASEAN Federation of Endocrine Societies</Title><ISOAbbreviation>J ASEAN Fed Endocr Soc</ISOAbbreviation></Journal><ArticleTitle>Initiating or Switching to Insulin Degludec/Insulin Aspart in Adults With Type 2 Diabetes in the Philippines: Results from a Prospective, Non-interventional, Real-World Study.</ArticleTitle><Pagination><StartPage>61</StartPage><EndPage>69</EndPage><MedlinePgn>61-69</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.15605/jafes.039.02.02</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">Blood glucose levels of the majority of Filipino patients with type 2 diabetes (T2D) remain uncontrolled. Insulin degludec/insulin aspart (IDegAsp) is a fixed-ratio co-formulation of the long-acting basal insulin degludec and the rapidacting prandial insulin aspart. The real-world ARISE (A Ryzodeg<sup>®</sup> Initiation and Switch Effectiveness) study investigated clinical outcomes across six countries in people with T2D who initiated IDegAsp. This publication presents the clinical outcomes of the Filipino cohort from a subgroup analysis of the ARISE study.</AbstractText><AbstractText Label="METHODOLOGY" NlmCategory="UNASSIGNED">This 26-week, open-label, non-interventional study examined outcomes in adults with T2D initiating or switching to IDegAsp (N=185) from other antidiabetic treatments per local clinical guidance.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">Compared with the baseline, there was a significant improvement in glycated hemoglobin at the end of the study (EOS) (estimated difference [ED] -1.4% [95% confidence interval -1.7, -1.1]; <i>P</i> <0.0001). Fasting plasma glucose (ED -46.1 mg/dL [-58.2, -34.0]; <i>P</i> <0.0001) and body weight (ED -1.0 kg [-2.0, -0.1]; <i>P</i> = 0.028) were significantly reduced at EOS compared with baseline. IDegAsp was associated with a decrease in the incidence of self-reported healthcare resource utilization. Adverse events were reported in eight (4.3%) participants.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">Initiating or switching to IDegAsp was associated with improved glycemic control, lower body weight, and lower HRU for people with T2D in the Philippines. No new, unexpected AEs were reported.</AbstractText><CopyrightInformation>© 2024 Journal of the ASEAN Federation of Endocrine Societies.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nicodemus</LastName><ForeName>Nemencio</ForeName><Initials>N</Initials><Suffix>Jr</Suffix><AffiliationInfo><Affiliation>Manila Doctors Hospital, Manila, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ang-Golangco</LastName><ForeName>Nerissa</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Makati Medical Center, Makati, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aquitania</LastName><ForeName>Grace</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Davao Doctors Hospital, Davao, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ardeña</LastName><ForeName>Gregory Joseph Ryan</ForeName><Initials>GJR</Initials><AffiliationInfo><Affiliation>Panay Health Care Multi-Purpose Cooperative Hospital, Kalibo, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dampil</LastName><ForeName>Oliver Allan</ForeName><Initials>OA</Initials><AffiliationInfo><Affiliation>Providence Hospital, Quezon City, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fernando</LastName><ForeName>Richard Elwyn</ForeName><Initials>RE</Initials><AffiliationInfo><Affiliation>Saint Luke's Medical Center, Quezon City, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Flor</LastName><ForeName>Nicole-Therese</ForeName><Initials>NT</Initials><AffiliationInfo><Affiliation>Novo Nordisk Philippines, Taguig City, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kho</LastName><ForeName>Sjoberg</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>University of Santo Tomas Hospital, Manila, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mirasol</LastName><ForeName>Roberto</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Manila Doctors Hospital, Manila, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Panelo</LastName><ForeName>Araceli</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of the East Ramon Magsaysay Memorial Medical Center, Quezon City, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pasaporte</LastName><ForeName>Francis</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Fancom Medical Plaza and Diagnostics, Iloilo City, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Puno-Rocamora</LastName><ForeName>Mercerose</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Novo Nordisk Philippines, Taguig City, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shoeb</LastName><ForeName>Ahsan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Novo Nordisk Philippines, Taguig City, Philippines.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tolentino</LastName><ForeName>Marsha</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Perpetual Succour Hospital, Cebu, Philippines.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>08</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>Philippines</Country><MedlineTA>J ASEAN Fed Endocr Soc</MedlineTA><NlmUniqueID>8608483</NlmUniqueID><ISSNLinking>0857-1074</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D049528">Insulin, Long-Acting</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C578220">insulin degludec, insulin aspart drug combination</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004338">Drug Combinations</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C517652">hemoglobin A1c protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010679" MajorTopicYN="N" Type="Geographic">Philippines</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049528" MajorTopicYN="Y">Insulin, Long-Acting</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004338" MajorTopicYN="Y">Drug Combinations</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="Y">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057915" MajorTopicYN="N">Drug Substitution</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">insulin aspart drug combination;</Keyword><Keyword MajorTopicYN="N">insulin aspart;</Keyword><Keyword MajorTopicYN="N">insulin degludec</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>Nicole-Therese Flor, Mercerose Puno-Rocamora, and Ahsan Shoeb are employees of Novo Nordisk Philippines, Taguig City, Philippines and hold stocks in Novo Nordisk.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>8</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2023</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>12</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>5</Hour><Minute>31</Minute></PubMedPubDate><PubMedPubDate 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Accessed December 2, 2022.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39620180</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2308-118X</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>2</Issue><PubDate><Year>2024</Year></PubDate></JournalIssue><Title>Journal of the ASEAN Federation of Endocrine Societies</Title><ISOAbbreviation>J ASEAN Fed Endocr Soc</ISOAbbreviation></Journal><ArticleTitle>Assessment of Various Insulin Resistance Surrogate Indices in Thai People with Type 2 Diabetes Mellitus.</ArticleTitle><Pagination><StartPage>33</StartPage><EndPage>40</EndPage><MedlinePgn>33-40</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.15605/jafes.039.02.21</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">To compare insulin surrogate indices with the homeostasis model assessment of insulin resistance (HOMA-IR) in Thai people with type 2 diabetes (T2D).</AbstractText><AbstractText Label="METHODOLOGY" NlmCategory="UNASSIGNED">A cross-sectional study of 97 individuals with T2D was done to determine the association between HOMAIR and seven surrogate indices for insulin resistance. IR was defined as HOMA-IR ≥2.0. The indices included Waist Circumference (WC), Waist-to-Hip Ratio (WHR), Waist-to-Height Ratio (WHtR), Triglyceride-Glucose (TyG) index, estimated Glucose Disposal Rate (eGDR) calculated by WC, BMI, and WHR.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 97 subjects with T2D (36.1% female, mean age 61.7 ± 12.0 years, BMI 26.4 ± 3.7 kg/m<sup>2</sup>, A1C 6.9 ± 1.2%) were studied. The TyG index showed a positive association with HOMA-IR, while eGDR exhibited a negative association. TyG index had the strongest correlation with IR (r = 0.49), while various eGDR formulas showed weaker negative correlations (r = 0.12-0.25). However, subgroup analysis in individuals with T2D and coronary artery disease (CAD) showed that only eGDR-WC and eGDR-BMI demonstrated a significant correlation with triple vessel disease.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">The TyG index was a useful and simple marker for identifying the presence of IR in Thai people with T2D. Future longitudinal studies are warranted to demonstrate the prediction value of cardiovascular outcomes.</AbstractText><CopyrightInformation>© 2024 Journal of the ASEAN Federation of Endocrine Societies.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chatchomchuan</LastName><ForeName>Waralee</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Diabetes and Thyroid Center, Theptarin Hospital, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thewjitcharoen</LastName><ForeName>Yotsapon</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Diabetes and Thyroid Center, Theptarin Hospital, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakasatien</LastName><ForeName>Soontaree</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Diabetes and Thyroid Center, Theptarin Hospital, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wanothayaroj</LastName><ForeName>Ekgaluck</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Diabetes and Thyroid Center, Theptarin Hospital, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krittiyawong</LastName><ForeName>Sirinate</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Diabetes and Thyroid Center, Theptarin Hospital, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Himathongkam</LastName><ForeName>Thep</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Diabetes and Thyroid Center, Theptarin Hospital, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>09</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Philippines</Country><MedlineTA>J ASEAN Fed Endocr Soc</MedlineTA><NlmUniqueID>8608483</NlmUniqueID><ISSNLinking>0857-1074</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014280">Triglycerides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013785" MajorTopicYN="N" Type="Geographic">Thailand</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055105" MajorTopicYN="Y">Waist Circumference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014280" MajorTopicYN="N">Triglycerides</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049629" MajorTopicYN="N">Waist-Hip Ratio</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015992" MajorTopicYN="N">Body Mass Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065927" MajorTopicYN="N">Waist-Height Ratio</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000095224" MajorTopicYN="N">Southeast Asian People</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">HOMA-IR</Keyword><Keyword MajorTopicYN="N">Insulin resistance</Keyword><Keyword MajorTopicYN="N">Surrogate Markers</Keyword><Keyword MajorTopicYN="N">Triglyceride-Glucose (TyG) index</Keyword><Keyword MajorTopicYN="N">estimated Glucose Disposal Rate (eGDR)</Keyword></KeywordList><CoiStatement>The authors declared no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>5</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>7</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>12</Hour><Minute>33</Minute></PubMedPubDate><PubMedPubDate 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PMID: 21051585 PMCID: DOI: 10.1210/jc.2010-2167</Citation><ArticleIdList><ArticleId IdType="doi">10.1210/jc.2010-2167</ArticleId><ArticleId IdType="pmc">PMC2968734</ArticleId><ArticleId IdType="pubmed">21051585</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39618225</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1750-8460</ISSN><JournalIssue CitedMedium="Internet"><Volume>85</Volume><Issue>11</Issue><PubDate><Year>2024</Year><Month>Nov</Month><Day>30</Day></PubDate></JournalIssue><Title>British journal of hospital medicine (London, England : 2005)</Title><ISOAbbreviation>Br J Hosp Med (Lond)</ISOAbbreviation></Journal><ArticleTitle>SGLT2 Inhibitors in Cardiovascular Medicine: Panacea or Pandora's Box?</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>10</EndPage><MedlinePgn>1-10</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.12968/hmed.2024.0546</ELocationID><Abstract><AbstractText>Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are antidiabetic agents that effectively lower blood glucose levels in patients with Type 2 Diabetes Mellitus (T2DM). Beyond their glycemic control properties, SGLT2 inhibitors have demonstrated significant cardiovascular benefits, including reductions in major adverse cardiovascular events. However, the limitations of the pivotal trials investigating these outcomes have not been fully explored. This letter aims to critically assess the major randomized clinical trials that evaluated the cardiovascular effects of SGLT2 inhibitors, highlighting both their strengths and limitations.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ferreira</LastName><ForeName>Stella de Aguiar Trigueirinho</ForeName><Initials>SAT</Initials><AffiliationInfo><Affiliation>Department of Emergency, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oliveira</LastName><ForeName>Lucas Lentini Herling de</ForeName><Initials>LLH</Initials><AffiliationInfo><Affiliation>Department of Emergency, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Assis</LastName><ForeName>Arthur Cicupira Rodrigues de</ForeName><Initials>ACR</Initials><AffiliationInfo><Affiliation>Department of Emergency, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soares</LastName><ForeName>Paulo Rogério</ForeName><Initials>PR</Initials><AffiliationInfo><Affiliation>Department of Emergency, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scudeler</LastName><ForeName>Thiago Luis</ForeName><Initials>TL</Initials><AffiliationInfo><Affiliation>Department of Emergency, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016422">Letter</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Br J Hosp Med (Lond)</MedlineTA><NlmUniqueID>101257109</NlmUniqueID><ISSNLinking>1750-8460</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016032" MajorTopicYN="N">Randomized Controlled Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">SGLT2 inhibitors</Keyword><Keyword MajorTopicYN="N">cardiovascular events</Keyword><Keyword MajorTopicYN="N">diabetes mellitus</Keyword><Keyword MajorTopicYN="N">heart failure</Keyword><Keyword MajorTopicYN="N">myocardial infarction</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>28</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>3</Hour><Minute>23</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39618225</ArticleId><ArticleId IdType="doi">10.12968/hmed.2024.0546</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39618173</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1463-1326</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>2</Issue><PubDate><Year>2025</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Diabetes, obesity & metabolism</Title><ISOAbbreviation>Diabetes Obes Metab</ISOAbbreviation></Journal><ArticleTitle>The role of the glucagon-FGF21 axis in improving beta cell function during glucose intolerance and SGLT2 inhibition.</ArticleTitle><Pagination><StartPage>885</StartPage><EndPage>898</EndPage><MedlinePgn>885-898</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/dom.16089</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Although primarily secreted by the liver, Fibroblast Growth Factor 21 (FGF21) is also expressed in the pancreas, where its function remains unclear. This study aims to elucidate the role of the glucagon-FGF21 interaction in the metabolic benefits of SGLT2 inhibition (SGLT2i) and hypothesizes it is key to enhancing glucose and lipid metabolism in individuals with glucose intolerance or type 2 diabetes (T2D).</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">FGF21, FGF1R, and β-klotho expression in human pancreas was analysed by RNAscope, qPCR and immunofluorescent techniques. Glucose-stimulated insulin secretion (GSIS) assay was used to investigate the effects of recombinant FGF21 (rFGF21) on islets from donors with glucose intolerance or T2D. To explore the role of the glucagon-FGF21 axis in the benefits of SGLT2i, we used WT and Sglt2 knockout (KO) mice fed a chow diet (CD) or a high-fat diet (HFD) and chronically treated with vehicle or dapagliflozin.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Chronic rFGF21 treatment enhanced GSIS in islets from donors with glucose intolerance, with increased FGFR1 expression, suggesting FGF21's greater efficacy in the early stages of disease. In diet-induced insulin-resistant mice, dapagliflozin reduced postprandial glycaemia and elevated plasma glucagon and FGF21 levels. Sglt2 KO mice on a CD showed increased fasting plasma glucagon without changes in FGF21. In diet-induced insulin-resistant Sglt2 KO mice, elevated glucagon and FGF21 levels paralleled chronic dapagliflozin treatment, indicating similar metabolic adaptations in both models.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Our findings indicate FGF21 as a crucial mediator in liver-pancreas crosstalk, improving lipid and glucose metabolism, enhancing pancreatic function, and potentiating the therapeutic efficacy of SGLT2i, thereby representing a target for prediabetes treatment.</AbstractText><CopyrightInformation>© 2024 The Author(s). Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moreno-Lopez</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Louvet</LastName><ForeName>Isaline</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delalleau</LastName><ForeName>Nathalie</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Acosta-Montalvo</LastName><ForeName>Ana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thevenet</LastName><ForeName>Julien</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pasquetti</LastName><ForeName>Gianni</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gmyr</LastName><ForeName>Valery</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kerr-Conte</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pattou</LastName><ForeName>Francois</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bonner</LastName><ForeName>Caroline</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-4430-8280</Identifier><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saponaro</LastName><ForeName>Chiara</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0001-7336-7362</Identifier><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, Inserm U1190, EGID, Institut Pasteur de Lille, Lille, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>1-RSC-2014-101-I-X</GrantID><Agency>European Consortium for Islet Transplantation by the Juvenile Diabetes Research Foundation</Agency><Country/></Grant><Grant><GrantID>ANR-10-LABX-0046</GrantID><Agency>European Genomic Institute for Diabetes</Agency><Country/></Grant><Grant><Agency>Société Francophone du Diabète 2015 Award</Agency><Country/></Grant><Grant><Agency>EFSD/Lilly 2016</Agency><Country/></Grant><Grant><Agency>PRECIDIAB Ph.D. thesis stipend</Agency><Country/></Grant><Grant><Agency>EFSD/Lilly Young Investigator Research Award 2021</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Diabetes Obes Metab</MedlineTA><NlmUniqueID>100883645</NlmUniqueID><ISSNLinking>1462-8902</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>62031-54-3</RegistryNumber><NameOfSubstance UI="D005346">Fibroblast Growth Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-92-5</RegistryNumber><NameOfSubstance UI="D005934">Glucagon</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077203">Sodium-Glucose Transporter 2 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C414620">fibroblast growth factor 21</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001559">Benzhydryl Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>1ULL0QJ8UC</RegistryNumber><NameOfSubstance UI="C529054">dapagliflozin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.2.1.31</RegistryNumber><NameOfSubstance UI="D000090265">Klotho Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000706947">FGF21 protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005346" MajorTopicYN="Y">Fibroblast Growth Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005934" MajorTopicYN="Y">Glucagon</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018149" MajorTopicYN="Y">Glucose Intolerance</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050417" MajorTopicYN="Y">Insulin-Secreting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077203" MajorTopicYN="Y">Sodium-Glucose Transporter 2 Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="Y">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="Y">Glucosides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001559" MajorTopicYN="N">Benzhydryl Compounds</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000078790" MajorTopicYN="N">Insulin Secretion</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000090265" MajorTopicYN="N">Klotho Proteins</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">FGF21</Keyword><Keyword MajorTopicYN="N">SGLT2 inhibition</Keyword><Keyword MajorTopicYN="N">glucagon</Keyword><Keyword MajorTopicYN="N">glucose intolerance</Keyword><Keyword MajorTopicYN="N">human islets</Keyword><Keyword MajorTopicYN="N">type 2 diabetes</Keyword></KeywordList><CoiStatement>All authors declare no 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A machine learning approach was performed in order to identify distinctive patterns in three omics (gut microbiome, blood DNA methylome, and visceral adipose tissue-VAT- DNA methylome) according to the different study groups.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Robust distinctive distribution patterns of the three different omics were found between healthy controls and patients with obesity; participants with and without T2DM, and patients with obesity with and without insulin resistance. Importantly, strong correlations between the gut microbiome (including Odoribacteriaceae and Christensenllaceae families) and both blood and VAT DNA methylome were found. Moreover, in the entire study population, three main bacterial genera (Sutterella, Collinsella and Eubacterium) were related to the epigenetic regulation of different genes involved in distinct processes related to cellular metabolism and metabolic diseases, including small ubiquitin-related modifier (SUMO) transferase activity or lipid binding.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">We show that distinctive interactions between the gut microbiome and DNA methylome may occur in subjects with different metabolic characteristics. Further research is needed to elucidate the potential role of these interactions in the pathophysiology of obesity and related comorbidities.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Martínez-Montoro</LastName><ForeName>José Ignacio</ForeName><Initials>JI</Initials><Identifier Source="ORCID">0000-0001-9761-6888</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, 29010, Málaga, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Instituto de Investigación Biomédica de Málaga (IBIMA)- Plataforma BIONAND, Málaga, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of Medicine, University of Málaga, Málaga, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martín-Núñez</LastName><ForeName>Gracia M</ForeName><Initials>GM</Initials><AffiliationInfo><Affiliation>Instituto de Investigación Biomédica de Málaga (IBIMA)- Plataforma BIONAND, Málaga, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>González-Jiménez</LastName><ForeName>Andrés</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Instituto de Investigación Biomédica de Málaga (IBIMA)- Plataforma BIONAND, Málaga, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garrido-Sánchez</LastName><ForeName>Lourdes</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, 29010, Málaga, Spain. lourgarrido@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Instituto de Investigación Biomédica de Málaga (IBIMA)- Plataforma BIONAND, Málaga, Spain. lourgarrido@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain. lourgarrido@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moreno-Indias</LastName><ForeName>Isabel</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, 29010, Málaga, Spain. isabel.moreno@ibima.eu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Instituto de Investigación Biomédica de Málaga (IBIMA)- Plataforma BIONAND, Málaga, Spain. isabel.moreno@ibima.eu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain. isabel.moreno@ibima.eu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tinahones</LastName><ForeName>Francisco J</ForeName><Initials>FJ</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, 29010, Málaga, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Instituto de Investigación Biomédica de Málaga (IBIMA)- Plataforma BIONAND, Málaga, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of Medicine, University of Málaga, Málaga, Spain.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CM22/00217</GrantID><Agency>Instituto de Salud Carlos III</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Transl Med</MedlineTA><NlmUniqueID>101190741</NlmUniqueID><ISSNLinking>1479-5876</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019175" MajorTopicYN="Y">DNA Methylation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069196" MajorTopicYN="Y">Gastrointestinal Microbiome</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050152" MajorTopicYN="Y">Intra-Abdominal Fat</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DNA methylation</Keyword><Keyword MajorTopicYN="N">Epigenetics</Keyword><Keyword MajorTopicYN="N">Gut microbiota</Keyword><Keyword MajorTopicYN="N">Insulin resistance</Keyword><Keyword MajorTopicYN="N">Obesity</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword><Keyword MajorTopicYN="N">Visceral adipose tissue</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: This study was conducted according to the principles of the Declaration of Helsinki, and was reviewed and approved by the Ethics Research Committee of Virgen de la Victoria University Hospital (Málaga, Spain). All participants gave their written informed consent to participate in this study. Consent for publication: Not applicable. 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Biochem Biophys Res Commun. 2021;552:91–7.</Citation><ArticleIdList><ArticleId IdType="pubmed">33744765</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39617888</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>04</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1472-6823</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>02</Day></PubDate></JournalIssue><Title>BMC endocrine disorders</Title><ISOAbbreviation>BMC Endocr Disord</ISOAbbreviation></Journal><ArticleTitle>Safety and efficacy of different basal insulin in type 2 diabetes mellitus with chronic kidney disease in Ramadan: prospective observational study.</ArticleTitle><Pagination><StartPage>260</StartPage><MedlinePgn>260</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">260</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12902-024-01778-z</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Diabetic kidney disease populations are categorized as high risk for fasting in Ramadan due to various potential fasting-related complications. Insulin analogues are recommended to be used in place of human insulin during fasting, as they carry a lower risk of hypoglycaemia and stable glycaemic variability. A paucity of data exits on the safety and efficacy of different basal insulin types during fasting for this population. This study aims to evaluate the safety and efficacy of three basal insulin among patients with Type 2 Diabetes Mellitus and concomitant mild to moderate chronic kidney disease who are keen to fast during Ramadan.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">A single-centered, prospective observational study was conducted among 46 patients with type 2 diabetes mellitus and concomitant chronic kidney disease stage 2 and 3 who were on three different types of basal insulin (Glargine U-100, Levemir, and Insulatard), fasted in Ramadan 2022. All variables were listed as median (IQR). Hypoglycaemia events and glycemic variability obtained from Freestyle Libre continuous glucose monitoring were compared between insulin groups. Changes in glycated haemoglobin, fasting plasma glucose, renal profile, body weight, body mass index, and waist circumference pre and post-Ramadan were evaluated.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The glycaemic variability was found highest in Insulatard with a median (IQR) of 37.2(33)% versus Levemir 34.4(32.4)% versus Glargine U-100 36.8(30.6)%, p = NS. Levemir had reported the lowest median time of below range of 2.5(13)% followed by Glargine 4(25)% and Insulatard 5(8)%; p = NS. The findings of this study indicated that glycated haemoglobin, fasting plasma glucose, renal profile, body weight, body mass index, and waist circumference did not alter statistically between the three groups post-Ramadan. Individually, Insulatard showed a significant reduction in weight and waist circumference (0.9kg, p = 0.026; 0.44 cm, p = 0.008) while Levemir showed a reduction in waist circumference (0.75cm, p = 0.019).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">This study revealed that Insulatard, Levemir, and Glargine demonstrated similar levels of safety and efficacy among those with diabetic kidney disease who observed fasting during Ramadan.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baharum</LastName><ForeName>Nur Haziqah</ForeName><Initials>NH</Initials><AffiliationInfo><Affiliation>Endocrine Unit, Department of Internal Medicine, Faculty of Medicine, University Technology Mara, Sungai Buloh, 47000, Selangor, Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wan Muhammad Hatta</LastName><ForeName>Sharifah Faradila</ForeName><Initials>SF</Initials><AffiliationInfo><Affiliation>Endocrine Unit, KPJ Damansara Specialist Hospital 2, Kuala Lumpur, 60000, Wilayah Persekutuan Kuala Lumpur, Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zainordin</LastName><ForeName>Nur Aisyah</ForeName><Initials>NA</Initials><AffiliationInfo><Affiliation>Endocrine Unit, Department of Internal Medicine, Faculty of Medicine, University Technology Mara, Sungai Buloh, 47000, Selangor, Malaysia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abdul Ghani</LastName><ForeName>Rohana</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Endocrine Unit, Department of Internal Medicine, Faculty of Medicine, University Technology Mara, Sungai Buloh, 47000, Selangor, Malaysia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Endocr Disord</MedlineTA><NlmUniqueID>101088676</NlmUniqueID><ISSNLinking>1472-6823</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>2ZM8CX04RZ</RegistryNumber><NameOfSubstance UI="D000069036">Insulin Glargine</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007514" MajorTopicYN="Y">Islam</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005215" MajorTopicYN="Y">Fasting</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051436" MajorTopicYN="Y">Renal Insufficiency, Chronic</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007003" MajorTopicYN="N">Hypoglycemia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069036" MajorTopicYN="N">Insulin Glargine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diabetic kidney disease</Keyword><Keyword MajorTopicYN="N">Glycaemic variability</Keyword><Keyword MajorTopicYN="N">Time below range</Keyword></KeywordList><CoiStatement>Declarations. Ethics approval and consent to participate: The study was conducted according to the ethical guidelines of the Helsinki Declaration. The study protocol was approved by the Research Ethics Committee of University Technology MARA (REC no: REC/01/2022 (PG/FB/7). Written informed consent was obtained from each participant before data collection. Consent of application: Not applicable. 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Obes Metabolism. 2015;17(10):919–27.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4744774</ArticleId><ArticleId IdType="pubmed">25974283</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39617593</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-3592</ISSN><JournalIssue CitedMedium="Internet"><Volume>900</Volume><PubDate><Year>2024</Year><Season>Nov-Dec</Season></PubDate></JournalIssue><Title>Mutation research. Genetic toxicology and environmental mutagenesis</Title><ISOAbbreviation>Mutat Res Genet Toxicol Environ Mutagen</ISOAbbreviation></Journal><ArticleTitle>Investigation of genetic instability in patients with Diabetes Mellitus type I, II and LADA using buccal micronucleus cytome assay.</ArticleTitle><Pagination><StartPage>503828</StartPage><MedlinePgn>503828</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.mrgentox.2024.503828</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1383-5718(24)00104-9</ELocationID><Abstract><AbstractText>The aim of our pilot study was to investigate the frequency of micronuclei (MN) and other nuclear anomalies in exfoliated cells of the oral mucosa in patients with type I, II, and LADA (Latent Autoimmune Diabetes in Adults, classified as type 1.5 intermediate, slowly progressing diabetes) types of diabetes mellitus (DM) and compare them with healthy individuals of the Armenian population using the MN test. For each participant essential clinical and biochemical parameters were studied, including blood pressure, duration of illness, glycosylated hemoglobin (HbA1c), blood glucose, plasma glucose, urea, total protein, creatinine, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, HOMA-IR (insulin resistance), insulin, and triglycerides, as well as necessary anthropometric, genealogical, and genetic data. All participants were surveyed regarding habits that might affect MN levels, such as smoking, alcohol consumption, drug use, hereditary diseases, and viral infections. Cytogenetic analyses of exfoliated cells showed that the level of MN in exfoliated cells of DM patients was elevated approximately two to three times compared to healthy individuals. However, statistical significance was only reached in type I DM and LADA patients. The levels of other nuclear anomalies in the squamous epithelial cells of DM patients were also analyzed, and a significant increase in their levels was observed in all three DM types, indicating cytotoxic and genotoxic effects. The results of this study also revealed a high correlation between the total number of MN, cells with MN, blood glucose concentration, and glycosylated hemoglobin.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Parsadanyan</LastName><ForeName>G</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Yerevan State Medical University, Yerevan, Armenia. Electronic address: Gohar@Parsadanyan.AM.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zalinyan</LastName><ForeName>G</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Yerevan State University, Yerevan, Armenia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Markosyan</LastName><ForeName>R</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Yerevan State Medical University, Yerevan, Armenia; Center of Endocrinology "Muratsan" MC, Yerevan, Armenia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sarkisyan</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Yerevan State Medical University, Yerevan, Armenia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aghajanova</LastName><ForeName>E</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Yerevan State Medical University, Yerevan, Armenia; Center of Endocrinology "Muratsan" MC, Yerevan, Armenia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sahakyan</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Medline Clinic MC, Yerevan, Armenia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>10</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Mutat Res Genet Toxicol Environ Mutagen</MedlineTA><NlmUniqueID>101632149</NlmUniqueID><ISSNLinking>1383-5718</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015162" MajorTopicYN="Y">Micronucleus Tests</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003922" MajorTopicYN="Y">Diabetes Mellitus, Type 1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009061" MajorTopicYN="Y">Mouth Mucosa</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010865" MajorTopicYN="N">Pilot Projects</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042822" MajorTopicYN="N">Genomic Instability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D048629" MajorTopicYN="N">Micronuclei, Chromosome-Defective</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Buccal mucosa</Keyword><Keyword MajorTopicYN="N">Diabetes mellitus</Keyword><Keyword MajorTopicYN="N">Micronucleus</Keyword><Keyword MajorTopicYN="N">Nuclear anomalies</Keyword></KeywordList><CoiStatement>Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Conflicts of Interest The authors declare that they have no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>10</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>6</Hour><Minute>27</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>5</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>21</Hour><Minute>16</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39617593</ArticleId><ArticleId IdType="doi">10.1016/j.mrgentox.2024.503828</ArticleId><ArticleId IdType="pii">S1383-5718(24)00104-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39617334</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8227</ISSN><JournalIssue CitedMedium="Internet"><Volume>219</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Diabetes research and clinical practice</Title><ISOAbbreviation>Diabetes Res Clin Pract</ISOAbbreviation></Journal><ArticleTitle>High one-hour plasma glucose is an intermediate risk state and an early predictor of type 2 diabetes in a longitudinal Korean cohort.</ArticleTitle><Pagination><StartPage>111938</StartPage><MedlinePgn>111938</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.diabres.2024.111938</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0168-8227(24)00848-9</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">Because one-hour post-load plasma glucose (1h-PG) ≥ 155 mg/dL (8.6 mmol/L) has been proposed as an early marker for future diabetes but lacks sufficient longitudinal confirmation of its risk, we aimed to evaluate the risk of T2D based on 1h-PG and track changes of insulin sensitivity and β-cell function over time by 1h-PG in a longitudinal cohort.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">OGTTs were conducted every 2 years in the 10-year longitudinal Korean Genome Epidemiology study (n = 6144) with three groups characterized at baseline: Low 1h-PG (< 155 mg/dL) with Normal Glucose Tolerance (NGT), High 1h-PG (≥155 mg/dL) with NGT, and prediabetes (PreDM).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">T2D risk was higher in people with High 1h-PG with NGT and PreDM than those with Low 1h-PG with NGT. Baseline insulin sensitivity in Low 1h-PG as measured by the insulin sensitivity and secretion (ISS) model and Matsuda insulin sensitivity index (ISI) was higher than in High 1h-PG, which was comparable to PreDM. β-cell function as assessed by ISS and the insulinogenic index decreased from Low 1h-PG to High 1h-PG to PreDM. Over time, insulin sensitivity decreased in the three groups. Time from High 1h-PG to T2D was 0.9 years shorter than from Low 1h-PG. All participants passed the 1h-PG threshold for T2D (209 mg/dL, 11.6 mmol/L) first, and 74 % passed the 1h-PG threshold for impaired glucose tolerance (IGT; 155 mg/dL) first.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">High 1h-PG NGT is an intermediate risk category between Low 1h-PG NGT and PreDM and may provide an opportunity for early intervention to prese rve ß-cell function.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Im</LastName><ForeName>Myungsoo</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Internal Medicine, Pusan National University School of Medicine, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jinmi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Biostatistics, Clinical Trial Center, Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Internal Medicine, Pusan National University School of Medicine, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ryang</LastName><ForeName>Soree</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Internal Medicine, Pusan National University School of Medicine, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Doohwa</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Internal Medicine, Pusan National University School of Medicine, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yi</LastName><ForeName>Wook</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mi Kim</LastName><ForeName>Jeong</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Minsoo</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jin Kim</LastName><ForeName>Yeong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jin Kim</LastName><ForeName>Young</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Center for Global R&D Data Analysis, Division of Data Analysis, Korea Institute of Science and Technology Information (KISTI), Seoul, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Hyuk</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Division of Fundamental Research On Public Agenda, National Institute for Mathematical Sciences, Daejeon, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Joo Kim</LastName><ForeName>In</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Department of Internal Medicine, Pusan National University School of Medicine, Yangsan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jagannathan</LastName><ForeName>Ram</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Hubert Department of Global Health, Emory University School of Public Health Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chung</LastName><ForeName>Stephanie T</ForeName><Initials>ST</Initials><AffiliationInfo><Affiliation>Section on Pediatric Diabetes, Obesity, and Metabolism, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes, Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bergman</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>NYU Grossman School of Medicine, Holman Division of Endocrinology, Diabetes and Metabolism, VA New York Harbor Healthcare System, New York, NY, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sherman</LastName><ForeName>Arthur S</ForeName><Initials>AS</Initials><AffiliationInfo><Affiliation>Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soo Kim</LastName><ForeName>Sang</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Internal Medicine, Pusan National University School of Medicine, Yangsan, Republic of Korea. Electronic address: drsskim7@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ha</LastName><ForeName>Joon</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Mathematics, Howard University, Washington DC, USA. Electronic address: joon.ha@howard.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Diabetes Res Clin Pract</MedlineTA><NlmUniqueID>8508335</NlmUniqueID><ISSNLinking>0168-8227</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056910" MajorTopicYN="N" Type="Geographic">Republic of Korea</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011236" MajorTopicYN="Y">Prediabetic State</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005951" MajorTopicYN="Y">Glucose Tolerance Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050417" MajorTopicYN="N">Insulin-Secreting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Beta-cell function</Keyword><Keyword MajorTopicYN="N">Insulin sensitivity</Keyword><Keyword MajorTopicYN="N">One-hour plasma glucose</Keyword><Keyword MajorTopicYN="N">Prediabetes</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>12</Day><Hour>15</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>5</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>19</Hour><Minute>30</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39617334</ArticleId><ArticleId IdType="doi">10.1016/j.diabres.2024.111938</ArticleId><ArticleId IdType="pii">S0168-8227(24)00848-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39617333</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8227</ISSN><JournalIssue CitedMedium="Internet"><Volume>219</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Diabetes research and clinical practice</Title><ISOAbbreviation>Diabetes Res Clin Pract</ISOAbbreviation></Journal><ArticleTitle>Differences in target organ damage in individuals with intermediate hyperglycemia and type 2 diabetes identified by 1-hour plasma glucose during an oral glucose tolerance test.</ArticleTitle><Pagination><StartPage>111941</StartPage><MedlinePgn>111941</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.diabres.2024.111941</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0168-8227(24)00851-9</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">The International Diabetes Federation (IDF) has recently recommended determination of 1-hour glucose during an oral glucose tolerance test (OGTT) to diagnose intermediate hyperglycemia (IH) and type 2 diabetes (T2D). Herein, we investigated the implications of IDF recommendation for characterizing the risk of cardiovascular target organ damage including left ventricular mass normalized by body surface area (LVM index [LVMI]), and myocardial mechano-energetic efficiency normalized by LVM (MEEi) in individuals with IH and T2D.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">LVMI, and MEEi were assessed in 1847 adults classified on the basis of fasting, 1-hour and 2- hour glucose during an OGTT according to the IDF recommendation as having normal glucose tolerance (NGT, n = 736), isolated impaired fasting glucose (iIFG, n = 105), IH (n = 676), and newly diagnosed T2D (n = 330).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">As compared with NGT group, individuals with either IH or T2D exhibited significantly higher LVMI (97 ± 26, 109 ± 30, and 116 ± g/m2, P < 0.001, respectively), and a decrease in MEEi (0.42 ± 0.11, 0.37 ± 0.10, and 0.35 ± 0.11 ml/sec*g-1, P < 0.001, respectively). LVMI, and MEEi did not differ between NGT and iIFG groups.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The thresholds of 1-hour post-load glucose proposed by IDF as diagnostic criteria for IH and T2D are capable of detecting individuals at risk of cardiovascular target organ damage.</AbstractText><CopyrightInformation>Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Assunta Cefalo</LastName><ForeName>Chiara Maria</ForeName><Initials>CM</Initials><AffiliationInfo><Affiliation>Department of Clinical and Molecular Medicine, University of Rome-Sapienza, 00189 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riccio</LastName><ForeName>Alessia</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Clinical and Molecular Medicine, University of Rome-Sapienza, 00189 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fiorentino</LastName><ForeName>Teresa Vanessa</ForeName><Initials>TV</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy. Electronic address: vanessa.fiorentino@unicz.it.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Succurro</LastName><ForeName>Elena</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mannino</LastName><ForeName>Gaia Chiara</ForeName><Initials>GC</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perticone</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sciacqua</LastName><ForeName>Angela</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Andreozzi</LastName><ForeName>Francesco</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sesti</LastName><ForeName>Giorgio</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Clinical and Molecular Medicine, University of Rome-Sapienza, 00189 Rome, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Diabetes Res Clin Pract</MedlineTA><NlmUniqueID>8508335</NlmUniqueID><ISSNLinking>0168-8227</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005951" MajorTopicYN="Y">Glucose Tolerance Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006943" MajorTopicYN="Y">Hyperglycemia</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">1-hour post-load glucose</Keyword><Keyword MajorTopicYN="N">Cardiovascular damage</Keyword><Keyword MajorTopicYN="N">Intermediate hyperglycemia</Keyword><Keyword MajorTopicYN="N">Left ventricular mass</Keyword><Keyword MajorTopicYN="N">Myocardial mechano-energetic efficiency</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>9</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>12</Day><Hour>15</Hour><Minute>21</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>5</Hour><Minute>29</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>19</Hour><Minute>30</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39617333</ArticleId><ArticleId IdType="doi">10.1016/j.diabres.2024.111941</ArticleId><ArticleId IdType="pii">S0168-8227(24)00851-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39617207</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-5875</ISSN><JournalIssue CitedMedium="Internet"><Volume>178</Volume><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>The international journal of biochemistry & cell biology</Title><ISOAbbreviation>Int J Biochem Cell Biol</ISOAbbreviation></Journal><ArticleTitle>Adipose tissue macrophages-derived exosomal MiR-500a-5p under high glucose promotes adipocytes inflammation by suppressing Nrf2 expression.</ArticleTitle><Pagination><StartPage>106713</StartPage><MedlinePgn>106713</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biocel.2024.106713</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1357-2725(24)00206-1</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Type 2 diabetes (T2DM) is a chronic metabolic disorder characterized by insulin resistance and chronic inflammation. Adipose tissue macrophages (ATMs), central players in mediating pro-inflammatory responses within adipose tissue, have been shown to influence insulin sensitivity through exosome secretion. While the role of macrophages-derived exosomal miRNA has been studied in various diseases, their pathogenic roles in T2DM, particularly ATMs-derived exosomal miRNA in adipose tissue inflammation, remain underexplored.</AbstractText><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">This study focuses specifically on T2DM, investigating the role of ATM-derived exosomal miRNAs in adipose tissue inflammation, a critical factor in the pathogenesis of T2DM.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">ATM were isolated from visceral adipose tissues in patients with or without diabetes. Differentially expressed miRNAs in ATM-derived exosomes were predicted by high-throughput RNA sequencing. The RAW264.7 macrophages and 3T3-L1 preadipocytes was selected as a model system. Quantitative RT-PCR was used to assess miR-500a-5p expression. The direct binding of miR-500a-5p to Nrf2 mRNA 3' UTR was verified by dual luciferase assay.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">MiR-500a-5p was also enriched in the exosomes of high-glucose-treated macrophages. Furthermore, these exosomes induced high expression of miR-500a-5p and activation of the NLRP3 inflammasome in adipocytes when co-cultured with them. Additionally, the reduction of miR-500a-5p expression in macrophages by using a miR-500a-5p inhibitor ameliorated the pro-inflammatory properties of the exosomes, and co-culturing these exosomes with adipocytes resulted in decreased expression of NLRP3 inflammasome-associated proteins in adipocytes. In contrast, induction of miR-500a-5p expression led to the opposite results. Moreover, the dual-luciferase assay confirmed that miR-500a-5p directly targeted the 3' UTR of Nrf2 mRNA. Unlike miR-500a-5p, Nrf2 exhibited an anti-inflammatory response.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The results indicate that ATM-derived exosomal miR-500a-5p promotes NLRP3 inflammasome activation and adipose tissue inflammation through down-regulation of Nrf2 in adipocytes.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yong-Zhen</ForeName><Initials>YZ</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan province, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, PR China; Department of Pathology, The First People's Hospital of Zigong, Zigong 643099, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tian</LastName><ForeName>Yuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan province, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Chen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan province, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, PR China; Department of Pathology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441021, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yi-Fan</ForeName><Initials>YF</Initials><AffiliationInfo><Affiliation>Research Laboratory of Translational Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qu</LastName><ForeName>Shun-Lin</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan province, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Liang</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Research Laboratory of Translational Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, PR China. Electronic address: huangliang0530@hotmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Chi</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan province, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, PR China. Electronic address: zhangchi9966@hotmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Biochem Cell Biol</MedlineTA><NlmUniqueID>9508482</NlmUniqueID><ISSNLinking>1357-2725</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D035683">MicroRNAs</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495635">NFE2L2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071199">NLR Family, Pyrin Domain-Containing 3 Protein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D035683" MajorTopicYN="Y">MicroRNAs</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051267" MajorTopicYN="Y">NF-E2-Related Factor 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055354" MajorTopicYN="Y">Exosomes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="Y">Macrophages</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017667" MajorTopicYN="Y">Adipocytes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="Y">Inflammation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="Y">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000273" MajorTopicYN="Y">Adipose Tissue</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D041721" MajorTopicYN="Y">3T3-L1 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000067996" MajorTopicYN="N">RAW 264.7 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000071199" MajorTopicYN="N">NLR Family, Pyrin Domain-Containing 3 Protein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adipocyte</Keyword><Keyword MajorTopicYN="N">Exosome</Keyword><Keyword MajorTopicYN="N">Macrophage</Keyword><Keyword MajorTopicYN="N">MiR-500a-5p</Keyword><Keyword MajorTopicYN="N">NLRP3 inflammasome</Keyword><Keyword MajorTopicYN="N">Nrf2</Keyword></KeywordList><CoiStatement>Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>10</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>15</Day><Hour>0</Hour><Minute>42</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>2</Day><Hour>5</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>19</Hour><Minute>27</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39617207</ArticleId><ArticleId IdType="doi">10.1016/j.biocel.2024.106713</ArticleId><ArticleId IdType="pii">S1357-2725(24)00206-1</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39616659</PMID><DateCompleted><Year>2024</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-460X</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of diabetes and its complications</Title><ISOAbbreviation>J Diabetes Complications</ISOAbbreviation></Journal><ArticleTitle>Prognostic importance of baseline and changes in serum uric acid for macro/microvascular and mortality outcomes in individuals with type 2 diabetes: The Rio de Janeiro type 2 diabetes cohort.</ArticleTitle><Pagination><StartPage>108921</StartPage><MedlinePgn>108921</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jdiacomp.2024.108921</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1056-8727(24)00247-2</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">To investigate the associations between baseline/changes in serum uric acid (sUA) and the risks for cardiovascular/microvascular outcomes and mortality in a type 2 diabetes cohort.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Baseline sUA was measured in 685 individuals, and 463 had a second sUA measurement during follow-up; sUA was analyzed as a continuous variable and categorized into sex-specific tertile subgroups and low/high levels (>4.5 mg/dl women; >5.5 mg/dl men). The risks associated with baseline sUA and its changes were examined by Cox analyses for all outcomes.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Median follow up was 10.7 years, there were 173 major cardiovascular events (MACEs), 268 all-cause deaths, 127 microalbuminuria, 104 renal failure, 160 retinopathy and 178 peripheral neuropathy outcomes. Baseline sUA was predictor of all outcomes, except all-cause mortality and retinopathy. In tertile and high/low sUA analyses, the hazard ratios (HRs) varied from 1.6 (microalbuminuria development) to 2.4 (MACEs; cardiovascular mortality). There was interaction with sex for MACEs, an increased risk was observed in women (HR: 2.6), but not in men (HR: 1.2). Changes in sUA were associated with the renal failure (HR: 2.4).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">In a prospective cohort, high baseline sUA was a predictor of cardiovascular, renal and peripheral neuropathy. However, sUA changes were only predictor of renal failure.</AbstractText><CopyrightInformation>Copyright © 2024 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cardoso</LastName><ForeName>Claudia R L</ForeName><Initials>CRL</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, University Hospital Clementino Fraga Filho, School of Medicine; Universidade Federal do Rio de Janeiro, Brazil. Electronic address: claudiacardoso@hucff.ufrj.br.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>da Silva Pereira</LastName><ForeName>Lucas</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, University Hospital Clementino Fraga Filho, School of Medicine; Universidade Federal do Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leite</LastName><ForeName>Nathalie C</ForeName><Initials>NC</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, University Hospital Clementino Fraga Filho, School of Medicine; Universidade Federal do Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Salles</LastName><ForeName>Gil F</ForeName><Initials>GF</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, University Hospital Clementino Fraga Filho, School of Medicine; Universidade Federal do Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Diabetes Complications</MedlineTA><NlmUniqueID>9204583</NlmUniqueID><ISSNLinking>1056-8727</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>268B43MJ25</RegistryNumber><NameOfSubstance UI="D014527">Uric Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014527" MajorTopicYN="Y">Uric Acid</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001938" MajorTopicYN="N" Type="Geographic">Brazil</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003925" MajorTopicYN="Y">Diabetic Angiopathies</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003928" MajorTopicYN="N">Diabetic Nephropathies</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003929" MajorTopicYN="N">Diabetic Neuropathies</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003930" MajorTopicYN="N">Diabetic Retinopathy</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000419" MajorTopicYN="N">Albuminuria</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cardiovascular events</Keyword><Keyword MajorTopicYN="N">Cohort study</Keyword><Keyword MajorTopicYN="N">Microvascular complications</Keyword><Keyword MajorTopicYN="N">Mortality</Keyword><Keyword MajorTopicYN="N">Serum uric acid</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>8</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>14</Day><Hour>0</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>18</Hour><Minute>26</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>18</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39616659</ArticleId><ArticleId IdType="doi">10.1016/j.jdiacomp.2024.108921</ArticleId><ArticleId IdType="pii">S1056-8727(24)00247-2</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39616150</PMID><DateCompleted><Year>2024</Year><Month>11</Month><Day>30</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>03</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2049-3169</ISSN><JournalIssue CitedMedium="Internet"><Volume>16</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Dec</Month><Day>01</Day></PubDate></JournalIssue><Title>International journal of oral science</Title><ISOAbbreviation>Int J Oral Sci</ISOAbbreviation></Journal><ArticleTitle>A blood glucose fluctuation-responsive delivery system promotes bone regeneration and the repair function of Smpd3-reprogrammed BMSC-derived exosomes.</ArticleTitle><Pagination><StartPage>65</StartPage><MedlinePgn>65</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">65</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41368-024-00328-6</ELocationID><Abstract><AbstractText>Blood glucose fluctuation leads to poor bone defect repair in patients with type 2 diabetes (T2DM). Strategies to safely and efficiently improve the bone regeneration disorder caused by blood glucose fluctuation are still a challenge. Neutral sphingophospholipase 2 (Smpd3) is downregulated in jawbone-derived bone marrow mesenchymal stem cells (BMSCs) from T2DM patients. Here, we investigated the effect of Smpd3 on the osteogenic differentiation of BMSCs and utilized exosomes from stem cells overexpressing Smpd3 as the main treatment based on the glucose responsiveness of phenylboronic acid-based polyvinyl alcohol crosslinkers and the protease degradability of gelatin nanoparticles. The combined loading of Smpd3-overexpressing stem cell-derived exosomes (Exos-Smpd3) and nanosilver ions (Ns) to construct a hydrogel delivery system (Exos-Smpd3@Ns) promoted osteogenesis and differentiation of BMSCs in a glucose-fluctuating environment, ectopic osteogenesis of BMSCs in a glucose-fluctuating environment and jawbone regeneration of diabetic dogs in vitro. Mechanistically, Smpd3 promoted the osteogenesis and differentiation of jawbone-derived BMSCs by activating autophagy in the jawbone and inhibiting macrophage polarization and oxidative stress caused by blood glucose fluctuations. These results reveal the role and mechanism of Smpd3 and the Smpd3 overexpression exosome delivery system in promoting BMSC function and bone regeneration under blood glucose fluctuations, providing a theoretical basis and candidate methods for the treatment of bone defects in T2DM patients.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Lingxiao</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory for Tooth Regeneration and Function Reconstruction of Oral Tissues, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Haoqing</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory for Tooth Regeneration and Function Reconstruction of Oral Tissues, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Chen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory for Tooth Regeneration and Function Reconstruction of Oral Tissues, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yue</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Periodontics, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Yilin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Dental Implant Center, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory for Tooth Regeneration and Function Reconstruction of Oral Tissues, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Pan</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Dental Implant Center, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Dental Implant Center, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Zhipeng</ForeName><Initials>Z</Initials><Identifier Source="ORCID">0000-0003-0629-3476</Identifier><AffiliationInfo><Affiliation>Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory for Tooth Regeneration and Function Reconstruction of Oral Tissues, School of Stomatology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China. zpfan@ccmu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Beijing Laboratory of Oral Health, Capital Medical University, Beijing, China. zpfan@ccmu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Research Unit of Tooth Development and Regeneration, Chinese Academy of Medical Sciences, Beijing, China. zpfan@ccmu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>12</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>India</Country><MedlineTA>Int J Oral Sci</MedlineTA><NlmUniqueID>101504351</NlmUniqueID><ISSNLinking>1674-2818</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020100">Hydrogels</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D055354" MajorTopicYN="Y">Exosomes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001861" MajorTopicYN="Y">Bone Regeneration</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059630" MajorTopicYN="Y">Mesenchymal Stem Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010012" MajorTopicYN="N">Osteogenesis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020100" MajorTopicYN="N">Hydrogels</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Competing interests: The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2023</Year><Month>12</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>10</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>15</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate 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Rep.11, 4317 (2021).</Citation><ArticleIdList><ArticleId IdType="pmc">PMC7900171</ArticleId><ArticleId IdType="pubmed">33619303</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">39616149</PMID><DateCompleted><Year>2024</Year><Month>11</Month><Day>30</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>05</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2044-4052</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Nov</Month><Day>30</Day></PubDate></JournalIssue><Title>Nutrition & diabetes</Title><ISOAbbreviation>Nutr Diabetes</ISOAbbreviation></Journal><ArticleTitle>Black Tea drinks with inulin and dextrin reduced postprandial plasma glucose fluctuations in patients with type 2 diabetes: an acute, randomized, placebo-controlled, single-blind crossover study.</ArticleTitle><Pagination><StartPage>95</StartPage><MedlinePgn>95</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">95</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41387-024-00351-w</ELocationID><Abstract><AbstractText Label="BACKGROUND">This study evaluated the effects of black tea drinks with inulin and dextrin (BTID) on postprandial plasma glucose (PG) in patients with type 2 diabetes mellitus (T2DM).</AbstractText><AbstractText Label="METHODS">An acute, randomized, double-blind, placebo-controlled, crossover clinical trial was carried out on T2DM patients. The subjects were randomly assigned to groups consuming placebo black tea powder or BTID (identically packaged) followed by a mixed meal tolerance test (MMTT). Afterwards, individuals who initially consumed BTID were given the placebo and those who initially consumed the placebo were given BTID.</AbstractText><AbstractText Label="RESULTS">A total of 35 patients were included in the study, and 32 completed the study. Compared to placebo, BTID significantly reduced the change in glycaemia at 30 min, 1, 2, and 3 h during the MMTT. In the analysis of PG fluctuations at 2 h during the MMTT, the proportion of patients with minor PG fluctuations (< 2.8 mmol/L) in the BTID group was 53.1%, significantly higher than the 28.1% in the placebo group. Binary logistic regression analysis revealed that the risk of significant PG fluctuations decreased by 65.5% after consuming BTID, with a corresponding odds ratio of 0.345 (P = 0.044, 95% CI 0.122-0.974). In addition, the areas under the curve for PG and insulin secretion after BTID administration were significantly smaller than that for placebo.</AbstractText><AbstractText Label="CONCLUSIONS">Compared to placebo, BTID significantly reduced the change in PG levels during the MMTT and decreased the risk of large PG fluctuations by 65.5%. These effects were associated to a significant reduction in postprandial insulin secretion and may help to improved insulin sensitivity and a lower β-cell burden.</AbstractText><CopyrightInformation>© 2024. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Chen</LastName><ForeName>Si</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Peng</LastName><ForeName>Danfeng</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shan</LastName><ForeName>Yingyi</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0009-0004-4165-6169</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Fengjing</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0002-8956-7489</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Haikou orthopedic and diabetes hospital, Haikou, 570300, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Du</LastName><ForeName>Ronghui</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bao</LastName><ForeName>Yuqian</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Haoyong</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0002-8621-4960</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China. yuhaoyong@shsmu.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tu</LastName><ForeName>Yinfang</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0000-0001-8280-5213</Identifier><AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai, 200233, China. yinfangtian@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Haikou orthopedic and diabetes hospital, Haikou, 570300, China. yinfangtian@hotmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nutr Diabetes</MedlineTA><NlmUniqueID>101566341</NlmUniqueID><ISSNLinking>2044-4052</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013662">Tea</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003912">Dextrins</NameOfSubstance></Chemical><Chemical><RegistryNumber>9005-80-5</RegistryNumber><NameOfSubstance UI="D007444">Inulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018592" MajorTopicYN="Y">Cross-Over Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019518" MajorTopicYN="Y">Postprandial Period</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013662" MajorTopicYN="Y">Tea</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003912" MajorTopicYN="Y">Dextrins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007444" MajorTopicYN="Y">Inulin</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004311" MajorTopicYN="N">Double-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016037" MajorTopicYN="N">Single-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>Competing interests: The authors declare no competing interests. Ethical approval: The study protocols were approved by the Ethics Review Committee of Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, in compliance with the Declaration of Helsinki. The patients/participants provided their written informed consent to participate in this study.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>7</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>11</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>15</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>15</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>11</Month><Day>30</Day><Hour>23</Hour><Minute>14</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>11</Month><Day>30</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39616149</ArticleId><ArticleId IdType="pmc">PMC11608310</ArticleId><ArticleId IdType="doi">10.1038/s41387-024-00351-w</ArticleId><ArticleId IdType="pii">10.1038/s41387-024-00351-w</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA, et al. 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Nutrients. 2015;7:7995–8009.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4586571</ArticleId><ArticleId IdType="pubmed">26393646</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39616020</PMID><DateCompleted><Year>2025</Year><Month>01</Month><Day>10</Day></DateCompleted><DateRevised><Year>2025</Year><Month>01</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-114X</ISSN><JournalIssue CitedMedium="Internet"><Volume>47</Volume><Issue>1</Issue><PubDate><Year>2025</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Clinical therapeutics</Title><ISOAbbreviation>Clin Ther</ISOAbbreviation></Journal><ArticleTitle>Real-world Evidence on Oral Semaglutide for the Management of Type 2 Diabetes. A Narrative Review for Clinical Practice.</ArticleTitle><Pagination><StartPage>102</StartPage><EndPage>110</EndPage><MedlinePgn>102-110</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.clinthera.2024.11.005</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0149-2918(24)00330-8</ELocationID><Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">Oral semaglutide is the first oral glucagon-like peptide-1 receptor agonist (GLP-1RA) available for type 2 diabetes mellitus (T2DM) management, whose effectiveness and tolerability have extensively been demonstrated in the PIONEER clinical trial program. Nevertheless, data from real-world are crucial to evaluate treatment performance under routine care. The aim of this narrative review is to summarize available evidence regarding real-world utilization patterns of oral semaglutide, and discuss efficacy, safety, and dosing regimen data in routine scenarios.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We searched PubMed for real-world studies evaluating oral semaglutide up to August 2024, and specific search terms were: "oral semaglutide," and "real-world studies" or "observational studies" or "retrospective studies".</AbstractText><AbstractText Label="FINDINGS" NlmCategory="RESULTS">19 real-world studies were included in the narrative review. In real-world settings, oral semaglutide provided significant glycemic (median HbA1c reduction at 6 months of 1%) and weight (median body weight reduction of 2 to 3 kg) benefits across the spectrum of T2DM, aligning with pre-clinical evidence from the PIONEER program. No new tolerability and safety issue has emerged from oral semaglutide administration in routine clinical practice.</AbstractText><AbstractText Label="IMPLICATIONS" NlmCategory="CONCLUSIONS">Oral semaglutide constitutes an effective and safe option for T2DM management, and its increased acceptance has the potential to favor the early introduction of GLP-1RAs along the disease course. Nevertheless, continuous evaluation of real-world data is critical to better define the optimal positioning of oral semaglutide along T2DM trajectory and fully exploit its potential in everyday clinical practice.</AbstractText><CopyrightInformation>Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Marassi</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Padova, Padua, Italy. Electronic address: mare.marassi@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fadini</LastName><ForeName>G P</ForeName><Initials>GP</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Padova, Padua, Italy; Veneto Institute of Molecular Medicine, Padua, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Ther</MedlineTA><NlmUniqueID>7706726</NlmUniqueID><ISSNLinking>0149-2918</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>53AXN4NNHX</RegistryNumber><NameOfSubstance UI="C000591245">semaglutide</NameOfSubstance></Chemical><Chemical><RegistryNumber>62340-29-8</RegistryNumber><NameOfSubstance UI="D004763">Glucagon-Like Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000067757">Glucagon-Like Peptide-1 Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006442">Glycated Hemoglobin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004763" MajorTopicYN="Y">Glucagon-Like Peptides</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000284" MajorTopicYN="N">Administration, Oral</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007004" MajorTopicYN="Y">Hypoglycemic Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000067757" MajorTopicYN="N">Glucagon-Like Peptide-1 Receptor</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006442" MajorTopicYN="N">Glycated Hemoglobin</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Effectiveness</Keyword><Keyword MajorTopicYN="N">Narrative review</Keyword><Keyword MajorTopicYN="N">Oral semaglutide</Keyword><Keyword MajorTopicYN="N">Real-world</Keyword><Keyword MajorTopicYN="N">Type 2 diabetes</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Gian Paolo Fadini reports a relationship with Abbott, AstraZeneca, Boehringer, Lilly, MSD, Novo Nordisk, Novaartis, Sanofi, Servier, Takeda that includes: funding grants and speaking and lecture fees. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>6</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2024</Year><Month>9</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>11</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2025</Year><Month>1</Month><Day>11</Day><Hour>13</Hour><Minute>59</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>15</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>11</Month><Day>30</Day><Hour>21</Hour><Minute>57</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39616020</ArticleId><ArticleId IdType="doi">10.1016/j.clinthera.2024.11.005</ArticleId><ArticleId IdType="pii">S0149-2918(24)00330-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">39615896</PMID><DateCompleted><Year>2024</Year><Month>11</Month><Day>30</Day></DateCompleted><DateRevised><Year>2024</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Print">2054-4774</ISSN><JournalIssue CitedMedium="Print"><Volume>11</Volume><Issue>1</Issue><PubDate><Year>2024</Year><Month>Nov</Month><Day>29</Day></PubDate></JournalIssue><Title>BMJ open gastroenterology</Title><ISOAbbreviation>BMJ Open Gastroenterol</ISOAbbreviation></Journal><ArticleTitle>Forns index and fatty liver index, but not FIB-4, are associated with indices of glycaemia, pre-diabetes and type 2 diabetes: analysis of The Maastricht Study.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e001466</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjgast-2024-001466</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Glucose metabolism status (GMS) is linked to non-alcoholic fatty liver disease (NAFLD). Higher levels of advanced glycation end products (AGEs) are observed in people with type 2 diabetes mellitus (T2DM) and NAFLD. We examined the association between GMS, non-invasive tests and AGEs, with liver steatosis and fibrosis.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Data from The Maastricht Study, a population-based cohort, were analysed. Participants with alcohol overconsumption or missing data were excluded. GMS was determined via an oral glucose tolerance test. AGEs, measured by skin autofluorescence (SAF), were assessed using an AGE Reader. Associations of GMS and SAF with the fibrosis-4 score (FIB-4), Forns index (FI) and fatty liver index (FLI) were investigated using multivariable linear regression, adjusted for sociodemographic, lifestyle and clinical variables.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">1955 participants (56.6%) were analysed: 598 (30.6%) had T2DM, 264 (13.5%) had pre-diabetes and 1069 (54.7%) had normal glucose metabolism. Pre-diabetes was significantly associated with FLI (standardised regression coefficient (Stβ) 0.396, 95% CI 0.323 to 0.471) and FI (Stβ 0.145, 95% CI 0.059 to 0.232) but not FIB-4. T2DM was significantly associated with FLI (Stβ 0.623, 95% CI 0.552 to 0.694) and FI (Stβ 0.307, 95% CI 0.226 to 0.388) but not FIB-4. SAF was significantly associated with FLI (Stβ 0.083, 95% CI 0.036 to 0.129), FI (Stβ 0.106, 95% CI 0.069 to 0.143) and FIB-4 (Stβ 0.087, 95% CI 0.037 to 0.137).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The study showed that adverse GMS and higher glycaemia are positively associated with steatosis. FI, but not FIB-4, was related to adverse GMS concerning fibrosis. This study is the first to demonstrate that SAF is positively associated with steatosis and fibrosis.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Heyens</LastName><ForeName>Leen</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0003-4850-6011</Identifier><AffiliationInfo><Affiliation>Hasselt University Faculty of Medicine and Life Sciences, Diepenbeek, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Maastricht University Faculty of Health Medicine and Life Sciences, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Kenjic</LastName><ForeName>Hanna</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dagnelie</LastName><ForeName>Pieter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Maastricht University Medical Centre+ Internal Medicine, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schalkwijk</LastName><ForeName>Casper</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Maastricht University Medical Centre+ Internal Medicine, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stehouwer</LastName><ForeName>Coen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meex</LastName><ForeName>Steven</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department Clinical Chemistry, Central Diagnostic Laboratory, Maastricht University Medical Centre+, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kooman</LastName><ForeName>Jeroen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Maastricht University Medical Centre+ Internal Medicine, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bekers</LastName><ForeName>Otto</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department Clinical Chemistry, Central Diagnostic Laboratory, Maastricht University Medical Centre+, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Greevenbroek</LastName><ForeName>Marleen</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Maastricht University Medical Centre+ Internal Medicine, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Savelberg</LastName><ForeName>Hans</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robaeys</LastName><ForeName>Geert</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Hasselt University Faculty of Medicine and Life Sciences, Diepenbeek, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Galan</LastName><ForeName>Bastiaan</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Social Medicine, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koster</LastName><ForeName>Annemarie</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Epidemiology, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CAPHRI Care and Public Health Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Dongen</LastName><ForeName>Martien</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>CAPHRI Care and Public Health Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eussen</LastName><ForeName>Simone</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>CARIM Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Epidemiology, Maastricht University, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Koek</LastName><ForeName>Ger</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands gh.koek@mumc.nl.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Maastricht University Medical Centre+ Internal Medicine, Maastricht, The Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2024</Year><Month>11</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open Gastroenterol</MedlineTA><NlmUniqueID>101660690</NlmUniqueID><ISSNLinking>2054-4774</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017127">Glycation End Products, Advanced</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="Y">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011236" MajorTopicYN="Y">Prediabetic State</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065626" MajorTopicYN="Y">Non-alcoholic Fatty Liver Disease</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="Y">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005951" MajorTopicYN="Y">Glucose Tolerance Test</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017127" MajorTopicYN="N">Glycation End Products, Advanced</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008103" MajorTopicYN="N">Liver Cirrhosis</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009426" MajorTopicYN="N" Type="Geographic">Netherlands</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DIABETES MELLITUS</Keyword><Keyword MajorTopicYN="N">HEPATIC FIBROSIS</Keyword><Keyword MajorTopicYN="N">Non-alcoholic Fatty Liver Disease</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2024</Year><Month>5</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2024</Year><Month>10</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>15</Hour><Minute>23</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2024</Year><Month>12</Month><Day>1</Day><Hour>15</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2024</Year><Month>11</Month><Day>30</Day><Hour>20</Hour><Minute>53</Minute></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2024</Year><Month>11</Month><Day>29</Day></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">39615896</ArticleId><ArticleId IdType="pmc">PMC11624825</ArticleId><ArticleId 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-[
-{
-"PMID": 39612437,
-"Title": "Medicine",
-"ArticleTitle": "Association between serum uric acid and prediabetes in a normal Chinese population: A cross-sectional study.",
-"Abstract": "Cardiovascular events are frequent among individuals with prediabetes. And the relationship between cardiovascular diseases and elevated serum uric acid (SUA) levels has been supported by extensive scientific evidence. However, there remains controversy regarding the correlation between elevated SUA and prediabetes. The aim of this study was to investigate the association between elevated SUA levels and the prevalence of prediabetes and gender differences in the association. A total of 190,891 individuals who participated in health checkups at the Health Promotion Center of Sir Run Run Shaw Hospital of Zhejiang University from January 2017 to December 2021 were included in this cross-sectional study. The health checkups were carried out by trained general practitioners and nurses. The diagnostic criteria for diabetes and prediabetes are defined in the Standards of Medical Care in Diabetes-2022. The association between SUA levels and diabetes and prediabetes was examined based on logistic regression analysis. The dose-response effect between SUA levels and diabetes and prediabetes in both sexes was assessed using a restricted cubic spline (RCS) regression model. Among 190,891 participants, this study included 106,482 males (55.8%) and 84,409 females (44.2%). There were 46,240 (24.2%) patients with prediabetes and 20,792 (10.9%) patients with diabetes. SUA was divided into quartiles (Q). Compared to the SUA Q1 group, the prevalence of prediabetes was elevated in the SUA Q4 group (OR = 1.378, 95% CI = 1.321-1.437), but diabetes risk was decreased in the SUA Q4 group (OR = 0.690, 95% CI = 0.651-0.730). We found that SUA levels were correlated with prediabetes more significantly in male subjects (OR = 1.328, 95% CI = 1.272-1.386) than in female subjects (OR = 1.184, 95% CI = 1.122-1.249) (P for interaction < .001). Higher SUA levels were strongly related to an elevated prevalence of prediabetes but a decreased prevalence of diabetes. The association of SUA in prediabetes was more significant in men.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Humans", "Prediabetic State", "Male", "Female", "Uric Acid", "Cross-Sectional Studies", "Middle Aged", "China", "Adult", "Prevalence", "Sex Factors", "Risk Factors", "Aged", "East Asian People"]
-},
-{
-"PMID": 39612426,
-"Title": "Medicine",
-"ArticleTitle": "Exploring the link between SIRT1 gene variants and depression comorbidity in type 2 diabetes.",
-"Abstract": "This study aims to (1) analyze the clinical characteristics and risk factors of patients with type 2 diabetes and comorbid depression and (2) explore the association between SIRT1 gene single-nucleotide polymorphism sites and this comorbidity. A total of 450 type 2 diabetes patients hospitalized in the General Medicine Department at The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology from July 2022 to September 2023, and 300 healthy individuals from the physical examination department were selected as study subjects. Both groups were assessed using general information surveys and questionnaires. Statistical analyses were performed to compare clinical indicators across 3 groups: individuals with only type 2 diabetes, those with comorbid depression, and healthy controls. The age, gender, disease duration, marital status, income and drug expenditure, employment status, fasting blood glucose level, fasting insulin level difference, insulin resistance index difference, glycated hemoglobin, high-density lipoprotein level, and HCY difference among the 3 groups of patients were risk factors for type 2 diabetes comorbid depression patients. The SIRT1 mRNA level was significantly reduced in type 2 diabetes comorbid depression patients. The SIRT1 gene had 3 sites: rs12415800, rs3758391, and rs932658, which were related to the patient's type 2 diabetes comorbid depression. They were the additive model and dominant model of rs12415800 and rs3758391, respectively. In addition, the GTGGT haplotype composed of rs12415800-rs932658-rs7895833-rs2273773-rs1467568 and the AGACT haplotype composed of rs3758391-rs932658-rs33957861-rs3818292-rs1467568 were significantly associated with type 2 diabetes comorbid depression. Numerous factors influence the presence of depression in patients with type 2 diabetes, with the SIRT1 gene playing a significant role, serving as a potential biomarker for this comorbidity.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Adult", "Aged", "Female", "Humans", "Male", "Middle Aged", "Case-Control Studies", "China", "Comorbidity", "Depression", "Diabetes Mellitus, Type 2", "Genetic Predisposition to Disease", "Polymorphism, Single Nucleotide", "Risk Factors", "Sirtuin 1"]
-},
-{
-"PMID": 39612420,
-"Title": "Medicine",
-"ArticleTitle": "Effects of genetic variants of organic cation transporters on metformin response in newly diagnosed patients with type 2 diabetes.",
-"Abstract": "Type 2 diabetes mellitus (T2DM) is a chronic disease that affects millions of people worldwide. Metformin is the optimal initial therapy for patients with T2DM. Genetic factors play a vital role in metformin response, including variations in drug efficacy and potential side effects. To determine the effects of genetic variants of multidrug and toxin extrusion protein 2 (MATE2), ataxia telangiectasia mutated (ATM), and serine/threonine kinase 11 (STK11) genes on metformin response in a cohort of Saudi patients. This prospective observational study included 76 T2DM newly diagnosed Saudi patients treated with metformin monotherapy and 80 control individuals. Demographic data, lipid profiles, creatinine levels, and hemoglobin A1c (HbA1c) levels were collected before and after treatment. All participants were genotyped for 5 single-nucleotide polymorphisms (SNPs), including rs4621031, rs34399035, rs2301759, rs1800058, and rs11212617, using TaqMan R genotyping assays. This study included 156 subjects. The subjects' mean ± SD age was 50.4 ± 10.14 years. The difference in HbA1c levels in T2DM after treatment ranged from -1.20% to 8.8%, with a mean value of 0.927 ± 1.73%. In general, 73.7% of the patients with T2DM showed an adequate response to metformin (HbA1c < 7%). STK11 (rs2301759) significantly affects the response to metformin in T2DM patients. In the rs2301759 single-nucleotide polymorphisms, the prevalence of an adequate response to metformin was significantly higher among patients with C/C and T/C genotypes than among non-responders (P = .021). However, no statistically significant associations were observed for the other tested SNPs. Our study provides evidence of an association between STK11 (rs2301759) and response to metformin in Saudi patients with T2DM. The need for targeted studies on specific gene-drug associations is emphasized, and further studies with a larger population should be conducted.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Metformin", "Diabetes Mellitus, Type 2", "Female", "Middle Aged", "Male", "Polymorphism, Single Nucleotide", "Hypoglycemic Agents", "Prospective Studies", "Protein Serine-Threonine Kinases", "Organic Cation Transport Proteins", "Glycated Hemoglobin", "Saudi Arabia", "Adult", "AMP-Activated Protein Kinase Kinases", "Ataxia Telangiectasia Mutated Proteins", "Genotype"]
-},
-{
-"PMID": 39612398,
-"Title": "Medicine",
-"ArticleTitle": "A comprehensive review of biomarker research in diabetic nephropathy from a global bibliometric and visualization perspective.",
-"Abstract": "Our study comprehensively and visually summarized the important findings of global biomarker research in DN and revealed the structure, hotspots, and evolutionary trends in this field. It would inspire subsequent studies from a macroscopic perspective and provide a basis for rational allocation of resources and identification of collaborations among researchers.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Diabetic Nephropathies", "Humans", "Bibliometrics", "Biomarkers", "Biomedical Research"]
-},
-{
-"PMID": 39612259,
-"Title": "Journal of managed care & specialty pharmacy",
-"ArticleTitle": "Area deprivation index impact on type 2 diabetes outcomes in a regional health plan.",
-"Abstract": "Significant differences were identified between ADI quintiles 1 and 5 for noninsulin diabetes medication adherence, frequency of A1c test claims, all-cause health care service utilization, and total cost of care. There were no statistically significant differences between ADI quintiles for achievement of A1c goal or receipt of comorbidity-focused therapies.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Diabetes Mellitus, Type 2", "Female", "Middle Aged", "Male", "Retrospective Studies", "Aged", "Adult", "Glycated Hemoglobin", "Medication Adherence", "Pennsylvania", "Hypoglycemic Agents", "Regional Medical Programs", "Health Care Costs"]
-},
-{
-"PMID": 39612042,
-"Title": "Sleep & breathing = Schlaf & Atmung",
-"ArticleTitle": "The association between chemosensitivity and the 10-year risk of type 2 diabetes in male patients with obstructive sleep apnea.",
-"Abstract": "Higher peripheral chemosensitivity was associated with an increased 10-year T2D risk, as calculated using a risk calculator based on clinical variables. For outcomes that reflect a moderate-to-high 10-year risk of T2D, the severity of OSA did not significantly affect the risk, irrespective of whether patients exhibited relatively low or high chemosensitivity.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Sleep Apnea, Obstructive", "Male", "Diabetes Mellitus, Type 2", "Middle Aged", "Adult", "Risk Factors", "Polysomnography"]
-},
-{
-"PMID": 39612019,
-"Title": "Sleep & breathing = Schlaf & Atmung",
-"ArticleTitle": "The effect of physical activity on sleep quality in people with diabetes: systematic review and meta-analysis.",
-"Abstract": "Preliminary evidence suggests that exercise can be prescribed to manage self-reported sleep quality in this population, although its effects may not surpass those of usual care.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Diabetes Mellitus, Type 2", "Sleep Quality", "Exercise", "Exercise Therapy"]
-},
-{
-"PMID": 39611987,
-"Title": "Histochemistry and cell biology",
-"ArticleTitle": "Cratylia mollis lectin reduces inflammatory burden induced by multidrug-resistant Staphylococcus aureus in diabetic wounds.",
-"Abstract": "In diabetes, tissue repair is impaired, increasing susceptibility to Staphylococcus aureus infections, a pathogen commonly found in wounds. The emergence of S. aureus strains that are highly resistant to antimicrobial agents highlights the urgent need for alternative therapeutic options. One promising candidate is Cramoll (Cratylia mollis seed lectin), known for its immunomodulatory, mitogenic, and healing properties. However, its efficacy in infected diabetic wounds remains unexplored. This study evaluated the effects of topical Cramoll treatment on diabetic wounds infected by S. aureus. Diabetic Swiss mice (induced by streptozotocin) were subjected to an 8-mm wound on the back and subsequently infected with a suspension of multidrug-resistant S. aureus. During the treatment period, the wounds were clinically evaluated for inflammation and the area of injury. After seven days, samples were collected from the wounds to quantify the bacterial load and histopathological and immunological analyses. Wounds infected by S. aureus exhibited more pronounced areas and severity indices, which were significantly reduced by Cramoll treatment (p < 0.05). Histopathological analysis revealed a reduction in inflammatory cells and an increase in revascularization with Cramoll treatment (p < 0.05). Cramoll also promoted greater collagen production compared to controls (p < 0.05). Furthermore, Cramoll treatment significantly reduced the S. aureus load in wounds (p < 0.0001), decreased TNF-α and IL-6 levels in infected wounds, and increased ERK pathway activation (p < 0.05). In conclusion, Cramoll lectin improves the healing of diabetic wounds, and these results contribute to the understanding of Cramoll healing mechanisms, reinforcing its potential as a healing agent in various clinical conditions.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Animals", "Mice", "Diabetes Mellitus, Experimental", "Male", "Inflammation", "Wound Healing", "Staphylococcal Infections", "Staphylococcus aureus", "Methicillin-Resistant Staphylococcus aureus", "Plant Lectins"]
-},
-{
-"PMID": 39611704,
-"Title": "Nursing open",
-"ArticleTitle": "Diabetes Education Program for Nursing Students: A Systematic Review and Meta-Analysis.",
-"Abstract": "The literature search identified 464 articles, from which 13 studies were evaluated in the systematic review. Most studies (n = 12, 92.3%) used technology-based teaching methods, such as high-fidelity simulations, mobile applications, and virtual reality simulations. Regarding the evaluation of diabetes education program effectiveness, the majority of studies showed significant improvements in knowledge (n = 8, 61.5%), followed by satisfaction with learning (n = 4, 30.8%), nursing skill performance (n = 3, 23.1%), and self-confidence (n = 3, 23.1%) in nursing students. In meta-analyses, technology-based teaching interventions, compared to traditional education, showed no statistically significant improvement in diabetes knowledge (standard mean difference 9.52, 95% CI [-0.18, 19.21], p = 0.05) and self-efficacy (standard mean difference 24.09, 95% CI [-10.75, 58.92], p = 0.18). Despite this, technology-based methods demonstrated favourable effects on knowledge and self-efficacy against traditional education. Findings highlight the importance of emerging technology-based diabetes education programs tailored for nursing students, crucial for enhancing positive educational outcomes. No Patient or Public Contribution.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Humans", "Students, Nursing", "Diabetes Mellitus", "Education, Nursing"]
-},
-{
-"PMID": 39611006,
-"Title": "International journal of nanomedicine",
-"ArticleTitle": "Combination of DMDD with Nanoparticles Effective Against Diabetic Kidney Disease in vitro.",
-"Abstract": "The optimized formulation for DMDD-NPs was CS:TPP:DMDD = 10:3:3 (w), at pH 3.5, with 1.0 mg/mL of CS and stirring at 500 rpm for 30 min. In these conditions, the nanoparticles had a particle size of 320.37 ± 2.93 nm, an EE of 85.09 ± 1.43%, and a DL of 15.88 ± 0.51%. The DMDD-NPs exhibited a spherical shape, no leakage and minimal adhesion. The optimal freeze-drying protectant was a combination of 0.025% mannitol and 0.025% lactose. The drug release followed the Higuchi model. DMDD-NPs improved HK-2 cell proliferation at lower concentrations (<24 μg/mL) and showed greater cell migration inhibition than DMDD. DMDD-NPs promoted E-cadherin expression and inhibited vimentin and TGF-β1 expression, suggesting their potential role in preventing EMT for DKD treatment.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Diabetic Nephropathies", "Humans", "Nanoparticles", "Epithelial-Mesenchymal Transition", "Particle Size", "Cell Line", "Cell Movement", "Chitosan", "Drug Liberation", "Drug Carriers", "Transforming Growth Factor beta1", "Cell Survival", "Polyphosphates"]
-},
-{
-"PMID": 39610841,
-"Title": "Frontiers in endocrinology",
-"ArticleTitle": "Predicting hypoglycemia in elderly inpatients with type 2 diabetes: the ADOCHBIU model.",
-"Abstract": "ChiCTR2200062277. Registered on 31 July 2022.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Diabetes Mellitus, Type 2", "Hypoglycemia", "Male", "Female", "Aged", "Nomograms", "China", "Inpatients", "Blood Glucose", "Risk Factors", "Aged, 80 and over", "Middle Aged", "Hypoglycemic Agents", "Incidence", "Risk Assessment", "Prognosis"]
-},
-{
-"PMID": 39610135,
-"Title": "Diabetes & metabolism journal",
-"ArticleTitle": "Cardiovascular Disease & Diabetes Statistics in Korea: Nationwide Data 2010 to 2019.",
-"Abstract": "The incidence of most CVD (IHD, ischemic stroke, and PAD) decreased between 2010 and 2019, whereas the incidence of HF increased. The overall use of high-intensity statins, SGLT2i, and GLP-1RA remained low among individuals with T2DM and CVD.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Republic of Korea", "Male", "Female", "Middle Aged", "Diabetes Mellitus, Type 2", "Aged", "Cardiovascular Diseases", "Incidence", "Adult", "Nutrition Surveys", "Risk Factors", "Young Adult", "Sodium-Glucose Transporter 2 Inhibitors", "Aged, 80 and over"]
-},
-{
-"PMID": 39610132,
-"Title": "Diabetes & metabolism journal",
-"ArticleTitle": "Rate-Dependent Depression of the Hoffmann Reflex: Practical Applications in Painful Diabetic Neuropathy.",
-"Abstract": "Measurement of the rate-dependent depression (RDD) of the Hoffmann (H) reflex, a technique developed over half a century ago, is founded on repeated stimulation of the H-reflex with tracking of sequentially evoked H-wave amplitudes in the resulting electromyogram. RDD offers insight into the integrity of spinal reflex pathways and spinal inhibitory regulation. Initially, RDD was predominantly utilized in the mechanistic exploration and evaluation of movement disorders characterized by spasticity symptoms, as may occur following spinal cord injury. However, there is increasing recognition that sensory input from the periphery is modified at the spinal level before ascending to the higher central nervous system and that some pain states can arise from, or be exaggerated by, disruption of spinal processing via a mechanism termed spinal disinhibition. This, along with the urgent clinical need to identify biological markers of pain generator and/or amplifier sites to facilitate targeted pain therapies, has prompted interest in RDD as a biomarker for the contribution of spinal disinhibition to neuropathic pain states. Current research in animals and humans with diabetes has revealed specific disorders of spinal GABAergic function associated with impaired RDD. Future investigations on RDD aim to further elucidate its underlying pathways and enhance its clinical applications.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Humans", "Diabetic Neuropathies", "H-Reflex", "Animals", "Neuralgia", "Electromyography", "Spinal Cord"]
-},
-{
-"PMID": 39610131,
-"Title": "Diabetes & metabolism journal",
-"ArticleTitle": "Metabolic Dysfunction-Associated Steatotic Liver Disease in Type 2 Diabetes Mellitus: A Review and Position Statement of the Fatty Liver Research Group of the Korean Diabetes Association.",
-"Abstract": "Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist's perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Diabetes Mellitus, Type 2", "Non-alcoholic Fatty Liver Disease", "Fatty Liver", "Republic of Korea"]
-},
-{
-"PMID": 39610015,
-"Title": "Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society",
-"ArticleTitle": "Photobiomodulation studies on diabetic wound healing: An insight into the inflammatory pathway in diabetic wound healing.",
-"Abstract": "Diabetes mellitus remains a global challenge to public health as it results in non-healing chronic ulcers of the lower limb. These wounds are challenging to heal, and despite the different treatments available to improve healing, there is still a high rate of failure and relapse, often necessitating amputation. Chronic diabetic ulcers do not follow an orderly progression through the wound healing process and are associated with a persistent inflammatory state characterised by the accumulation of pro-inflammatory macrophages, cytokines and proteases. Photobiomodulation has been successfully utilised in diabetic wound healing and involves illuminating wounds at specific wavelengths using predominantly light-emitting diodes or lasers. Photobiomodulation induces wound healing through diminishing inflammation and oxidative stress, among others. Research into the application of photobiomodulation for wound healing is current and ongoing and has drawn the attention of many researchers in the healthcare sector. This review focuses on the inflammatory pathway in diabetic wound healing and the influence photobiomodulation has on this pathway using different wavelengths.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Wound Healing", "Humans", "Low-Level Light Therapy", "Inflammation", "Diabetic Foot", "Oxidative Stress", "Cytokines"]
-},
-{
-"PMID": 39609996,
-"Title": "Journal of Ayub Medical College, Abbottabad : JAMC",
-"ArticleTitle": "A NOVEL DE NOVO LIKELY PATHOGENIC VARIANT OF WFS-1 GENE IN A PAKISTANI CHILD WITH NON-CLASSIC WFS-1 SPECTRUM DISORDER.",
-"Abstract": "Access to genetic testing is not readily available in Pakistan and our population is under studied and these complex diagnoses are often missed. In this study, we present a novel de novo likely pathogenic variant in the WFS-1 gene that causes non-classic WFS-1 spectrum disorder in a child from our population.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Membrane Proteins", "Wolfram Syndrome", "Male", "Child", "Pakistan"]
-},
-{
-"PMID": 39609972,
-"Title": "Journal of Ayub Medical College, Abbottabad : JAMC",
-"ArticleTitle": "SELF-REPORTED MULTI-MORBIDITY WITH TUBERCULOSIS: DATA FROM THE KHYBER PAKHTUNKHWA INTEGRATED POPULATION HEALTH SURVEY (KPIPHS) IN PAKISTAN.",
-"Abstract": "There is a higher burden of self-reported cardiometabolic diseases among people with TB, suggesting that this high-risk group should be screened for cardiometabolic diseases, especially Diabetes.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Humans", "Pakistan", "Male", "Female", "Adult", "Middle Aged", "Tuberculosis", "Self Report", "Health Surveys", "Prevalence", "Multimorbidity", "Diabetes Mellitus"]
-},
-{
-"PMID": 39609829,
-"Title": "BMC endocrine disorders",
-"ArticleTitle": "Cognitive changes in people with diabetes with lower extremity complications compared to people with diabetes without lower extremity complications: a systematic review and meta-analysis.",
-"Abstract": "DRLECs may be related to cognition in people with diabetes, however, existing evidence is unclear due to variability in used methodologies that may challenge concluding the findings. Future high-quality studies investigating cognition among people with and without DRLECs are needed.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Humans", "Lower Extremity", "Diabetes Complications", "Cognition", "Cognitive Dysfunction", "Diabetic Neuropathies", "Diabetes Mellitus"]
-},
-{
-"PMID": 39609030,
-"Title": "BMJ open",
-"ArticleTitle": "Incidence, prevalence and risk factors for comorbid mental illness among people with hypertension and type 2 diabetes in West Africa: protocol for a systematic review and meta-analysis.",
-"Abstract": "CRD42023450732.",
-"Predictions": ["Diabetes", "Diabetes type 2"],
-"MeshTerms": ["Humans", "Diabetes Mellitus, Type 2", "Systematic Reviews as Topic", "Hypertension", "Mental Disorders", "Prevalence", "Risk Factors", "Incidence", "Africa, Western", "Comorbidity", "Research Design", "Meta-Analysis as Topic"]
-},
-{
-"PMID": 39609024,
-"Title": "BMJ open",
-"ArticleTitle": "Association of overweight and obesity with gestational diabetes mellitus among pregnant women attending antenatal care clinics in Addis Ababa, Ethiopia: a case-control study.",
-"Abstract": "Obesity, but not overweight, was significantly associated with the development of GDM. Screening for GDM is recommended for pregnant women with obesity (MUAC≥31) for targeted intervention. Antenatal care providers should provide information for women of childbearing age on maintaining a healthy body weight before and in-between pregnancies and the need for healthy, diversified food and high-level physical activity.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Humans", "Female", "Diabetes, Gestational", "Pregnancy", "Ethiopia", "Case-Control Studies", "Adult", "Prenatal Care", "Overweight", "Young Adult", "Obesity", "Risk Factors", "Logistic Models"]
-},
-{
-"PMID": 39609009,
-"Title": "BMJ open",
-"ArticleTitle": "Implementation strategies for providing optimised tuberculosis and diabetes integrated care in LMICs (POTENTIAL): protocol for a multiphase sequential and concurrent mixed-methods study.",
-"Abstract": "Ethics approval was granted by the National Bioethics Committee of Pakistan (NBCR-1010). Findings will be shared through academic publications, conferences and public outreach.",
-"Predictions": ["Diabetes"],
-"MeshTerms": ["Humans", "Pakistan", "Diabetes Mellitus", "Tuberculosis", "Delivery of Health Care, Integrated", "Developing Countries", "Quality of Life", "Research Design"]
-},
-
-{
-"PMID": 39612534,
-"Title": "Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy",
-"ArticleTitle": "Multivariate analysis of Raman spectra for discriminating human collagens: In vitro identification of extracellular matrix collagens produced by an osteosarcoma cell line.",
-"Abstract": "This study establishes Raman spectroscopy as a tool for identifying and characterizing human collagens, aiding in the diagnosis of connective tissue disorders. The creation of a spectral reference library for pure human collagen types I - VI holds potential for medical diagnostics, analytical chemistry, and materials science applications.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Spectrum Analysis, Raman", "Osteosarcoma", "Collagen", "Cell Line, Tumor", "Extracellular Matrix", "Multivariate Analysis", "Bone Neoplasms"]
-},
-{
-"PMID": 39612521,
-"Title": "Colloids and surfaces. B, Biointerfaces",
-"ArticleTitle": "Transferrin-targeting pH-responsive and biodegradable mesoporous silica nanohybrid for nitric oxide-sensitized chemotherapy of cancer.",
-"Abstract": "Weakly acidic pH, low oxygen and high glutathione levels are the main characteristics of tumor cells. Taking advantage of the unique acidic microenvironment of tumor cells, acid-responsive mesoporous organosilica nanoparticles (AMON) were designed for nitric oxide (NO)-sensitized chemotherapy of tumors. AMON served as a nanocarrier co-loaded with a nitric oxide donor (NOD) and chemotherapeutic drug doxorubicin (DOX). Transferrin (Tf) was modified on the surface as a targeting ligand to form NOD&DOX@AMON. In vitro experiments showed that AMON could be completely degraded under acidic conditions (pH 5.0) after 48 h. NOD&DOX@AMON entered cells via transferrin receptor-mediated internalization and degraded in the acidic microenvironment to release its payloads. NOD released NO in presence of one-electron reducing substances like Glutathione (GSH) and ascorbic acid, inhibiting P-glycoprotein(P-gp) function and thereby increasing the intracellular concentration of DOX. In vivo distribution studies revealed that the nanohybrids accumulated maximally in tumor tissue 12 h after intravenous injection and exhibited significant inhibitory effects on HepG2 xenograft tumors. Western blot experiments demonstrated that NOD&DOX@AMON could inhibit the expression of drug resistance-associated proteins and was expected to be employed as a therapeutic approach for drug-resistant ttumors.",
-"Predictions": [],
-"MeshTerms": ["Doxorubicin", "Humans", "Nitric Oxide", "Transferrin", "Hydrogen-Ion Concentration", "Animals", "Silicon Dioxide", "Nanoparticles", "Porosity", "Mice", "Hep G2 Cells", "Antibiotics, Antineoplastic", "Mice, Inbred BALB C", "Particle Size", "Surface Properties", "Mice, Nude", "Antineoplastic Agents", "Drug Carriers"]
-},
-{
-"PMID": 39612480,
-"Title": "JMIR research protocols",
-"ArticleTitle": "Ultrasound-Guided High-Intensity Focused Ultrasound Combined With PD-1 Blockade in Patients With Liver Metastases From Lung Cancer: Protocol for a Single-Arm Phase 2 Trial.",
-"Abstract": "DERR1-10.2196/59152.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Liver Neoplasms", "Lung Neoplasms", "High-Intensity Focused Ultrasound Ablation", "Immune Checkpoint Inhibitors", "Male", "Female", "Programmed Cell Death 1 Receptor", "Middle Aged", "Combined Modality Therapy", "Aged", "Adult", "Clinical Trials, Phase II as Topic"]
-},
-{
-"PMID": 39612472,
-"Title": "Cancer control : journal of the Moffitt Cancer Center",
-"ArticleTitle": "Pan-Cancer Analysis of PTBP1 to Identify it as a Prognostic and Immunological Biomarker.",
-"Abstract": "Our study is the first to demonstrate the oncogenic role of PTBP1 in a pan-cancer context. PTBP1 might serve as a new biomarker for prognostic prediction and immune cell infiltration across cancers in the future.",
-"Predictions": [],
-"MeshTerms": ["Polypyrimidine Tract-Binding Protein", "Humans", "Heterogeneous-Nuclear Ribonucleoproteins", "Prognosis", "Biomarkers, Tumor", "Mice", "Animals", "Cell Line, Tumor", "Gene Expression Regulation, Neoplastic", "Neoplasms", "Computational Biology", "Melanoma", "Colonic Neoplasms", "Adenocarcinoma of Lung", "RNA, Messenger"]
-},
-{
-"PMID": 39612465,
-"Title": "Medicine",
-"ArticleTitle": "Association between immune cell attributes, serum metabolites, inflammatory protein factors, and colorectal cancer: A Mendelian randomization study.",
-"Abstract": "Understanding the role of the tumor microenvironment in colorectal cancer (CRC) progression remains a challenge due to its complexity. Investigating the interplay between immune cell characteristics, serum metabolites, inflammatory protein factors, and CRC could unveil novel therapeutic avenues. We used 2-sample Mendelian randomization (MR) on Genome-Wide Association Studies (GWAS) data to explore causal links between 731 immune cell characteristics, 1400 serum metabolites, 91 inflammatory proteins, and CRC. Various MR methods, including inverse variance weighted (IVW) and MR-Egger, were applied to ensure robust analysis. Sensitivity analyses, such as the MR-Egger intercept test, Cochran's Q test, and leave-one-out analysis, were performed to check for pleiotropy, heterogeneity, and influential outliers. Following rigorous genetic variation screening, we identified 43 immune cell characteristics associated with CRC. Notably, 7 immunophenotypes, including CD39+ CD4+ T cell Absolute Count, exhibited significant associations as protective factors. Additionally, 36 other immunophenotypes showed significant causal relationships with CRC. Among serum metabolites, 37 were correlated with CRC, with 1-arachidonoyl-gpc (20: 4n6) being the most closely linked as a risk factor. Similarly, 36 serum metabolites displayed significant causal relationships with CRC. Seven inflammatory protein factors exhibited causal relationships with CRC, with 4 posing as risk factors and 3 as protective factors. Our study scrutinized 731 immune cell characteristics, 1400 serum metabolites, and 91 inflammatory protein factors within the tumor microenvironment. We confirmed causal relationships between 43 immune cell characteristics, 37 serum metabolites, and 7 inflammatory protein factors with CRC. These findings offer novel insights into the potential etiology, prevention, and treatment strategies for CRC.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Colorectal Neoplasms", "Mendelian Randomization Analysis", "Genome-Wide Association Study", "Risk Factors", "Tumor Microenvironment", "Polymorphism, Single Nucleotide"]
-},
-{
-"PMID": 39612459,
-"Title": "Medicine",
-"ArticleTitle": "Cost-effectiveness analysis of immune checkpoint inhibitors combined with targeted therapy and chemotherapy for HPV/HIV-related cervical cancer.",
-"Abstract": "Immune checkpoint inhibitors significantly improve survival benefits for patients. However, their addition is costly and unlikely to be cost-effective for HPV/HIV-related metastatic cervical cancer.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Uterine Cervical Neoplasms", "Cost-Benefit Analysis", "Female", "Immune Checkpoint Inhibitors", "Papillomavirus Infections", "Quality-Adjusted Life Years", "HIV Infections", "Antineoplastic Combined Chemotherapy Protocols", "Antibodies, Monoclonal, Humanized", "Bevacizumab", "Adult", "Middle Aged", "Cost-Effectiveness Analysis"]
-},
-{
-"PMID": 39612458,
-"Title": "Medicine",
-"ArticleTitle": "Network pharmacology and molecular docking analysis on the mechanism of Wensan tincture in the treatment of pulmonary nodules: A review.",
-"Abstract": "Network pharmacology and molecular docking methods were applied to elucidate the molecular mechanism of action of Wensan tincture (WST) in the treatment of pulmonary nodules. The Traditional Chinese Medicine Systems Pharmacology and the Traditional Chinese Medicine and Chemical Composition database were used to screen the active ingredients. Potential targets of WST were retrieved using Traditional Chinese Medicine Systems Pharmacology, SwissADME, and SwissTargetPrediction, while pulmonary nodule-associated targets were obtained from GeneCards and Online Mendelian Inheritance in Man databases. An active ingredient-target network was constructed using Cytoscape 3.9.1, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were conducted via the Database for Annotation, Visualization, and Integrated Discovery platform to identify core targets and signaling pathways. Molecular docking studies were performed using AutoDockTools. The results revealed 62 active ingredients and 344 corresponding targets within the tincture, alongside 1005 targets associated with pulmonary nodules. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses indicated that the potential therapeutic targets of WST include signal transducer and activator of transcription 3, mitogen-activated protein kinase-3, mitogen-activated protein kinase-1, Jun proto-oncogene, tumor protein 53, phosphoinositide-3-kinase regulatory subunit 1, heat shock protein 90 alpha family class A member 1, and AKT serine/threonine kinase 1. The primary pathways were the cancer pathway, mitogen-activated protein kinase signaling, advanced glycation end-products and their receptor signaling, epidermal growth factor receptor signaling, hypoxia-inducible factor-1 signaling, and the programmed cell death-ligand 1/programmed cell death protein 1 checkpoint pathways. Molecular docking demonstrated that quercetin exhibited the strongest binding affinity with mitogen-activated protein kinase-3, with a binding energy of -9.1 kcal/mol. Notably, key components of WST, such as quercetin, demonstrate considerable potential as drug candidates for the treatment of pulmonary nodules.",
-"Predictions": [],
-"MeshTerms": ["Molecular Docking Simulation", "Humans", "Drugs, Chinese Herbal", "Network Pharmacology", "Medicine, Chinese Traditional", "Lung Neoplasms", "Signal Transduction"]
-},
-{
-"PMID": 39612452,
-"Title": "Medicine",
-"ArticleTitle": "Iwilfin (eflornithine) approved by the FDA as the first and only oral maintenance therapy for high-risk neuroblastoma in adult and pediatric patients: Narrative review.",
-"Abstract": "Neural crest progenitor cells give rise to neuroblasts, the growing nerve cells of the sympathetic nervous system. These cells can undergo changes leading to neuroblastoma, a malignancy responsible for 15% of all pediatric cancer-related deaths. The molecular pathogenesis of this pediatric cancer involves complex genetic alterations, such as MYCN amplification, chromosomal abnormalities, and gene expression changes. Despite aggressive therapies, survival rates for children with high-risk neuroblastoma (HRNB) have not improved significantly compared to those with less severe forms of the disease. This highlights the challenge of managing HRNB and underscores the need for new, effective treatments. A comprehensive treatment regimen, including immunotherapy, radiation therapy, myeloablative chemotherapy, and surgical removal, has been employed to achieve remission in HRNB patients. While dinutuximab beta immunotherapy is an effective and widely used treatment, it has several potential side effects that must be carefully monitored. New drugs are being developed to reduce these side effects without compromising efficacy. One such drug is DL-alpha-difluoromethylornithine (DFMO), approved by the FDA under the brand name Iwilfin. Numerous clinical trials have shown that DFMO, when used as maintenance therapy, significantly improves event-free survival and overall survival in neuroblastoma patients. However, DFMO has adverse effects that require continuous monitoring. Further research is needed to minimize these side effects and improve its efficacy, particularly in addressing resistance caused by long-term use.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Neuroblastoma", "Child", "Eflornithine", "United States", "Adult", "Drug Approval", "Antineoplastic Agents", "United States Food and Drug Administration", "Maintenance Chemotherapy", "Administration, Oral"]
-},
-{
-"PMID": 39612448,
-"Title": "Medicine",
-"ArticleTitle": "Multimodal imaging of mixed epithelial and stromal tumor of the kidney: Case series.",
-"Abstract": "MESTK is a rare, mostly benign tumor that appears as a multilocular cystic or cystic solid, with progressive marked enhancement of the septal and solid components on enhanced scans. This imaging feature is helpful for the diagnosis of MESTK.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Female", "Kidney Neoplasms", "Middle Aged", "Multimodal Imaging", "Retrospective Studies", "Adult", "Tomography, X-Ray Computed", "Neoplasms, Complex and Mixed", "Neoplasms, Glandular and Epithelial", "Magnetic Resonance Imaging", "Kidney"]
-},
-{
-"PMID": 39612446,
-"Title": "Medicine",
-"ArticleTitle": "Talus osteoid osteoma misdiagnosed as ankle synovitis: A case report in rehabilitation therapy.",
-"Abstract": "This case highlights the diagnostic complexity of ankle osteoid osteoma and underscores the importance of a multidisciplinary approach. Rehabilitation therapists play a crucial role in managing such conditions, ensuring optimal patient outcomes through functional assessment and progress monitoring. Timely and accurate diagnosis is essential for effective treatment and improved patient quality of life.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Male", "Osteoma, Osteoid", "Adult", "Diagnostic Errors", "Talus", "Bone Neoplasms", "Synovitis", "Ankle Joint", "Magnetic Resonance Imaging"]
-},
-{
-"PMID": 39612443,
-"Title": "Medicine",
-"ArticleTitle": "A new nonsense mutation of PTCH1 gene in mother and daughter with late-onset nevus basal cell carcinoma syndrome: Case report.",
-"Abstract": "We detected a new mutation in PTCH1 gene in 2 patients with NBCCS, and both of them had ovarian mature teratomas, which are related to NM000264: exon14: c.2080C>T: p.Q694X.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Patched-1 Receptor", "Female", "Basal Cell Nevus Syndrome", "Codon, Nonsense", "Ovarian Neoplasms", "Adult", "Teratoma", "Middle Aged", "Skin Neoplasms", "Mothers"]
-},
-{
-"PMID": 39612442,
-"Title": "Medicine",
-"ArticleTitle": "Partial nephrectomy versus radiofrequency ablation in patients with cT1a renal cell carcinoma: A surveillance, epidemiology, end results (SEER) analysis.",
-"Abstract": "Radiofrequency ablation (RFA) has been proposed for T1a renal cell carcinoma (RCC). The present study compared partial nephrectomy (PN) with RFA for T1a RCC stratified by tumor sizes. We selected patients with RCC and underwent PN or RFA through the surveillance, epidemiology, end results (SEER) database. The Kaplan-Meier method and Cox proportional hazards regression model were conducted. Inverse probability of treatment weights was conducted for sensitivity analysis. We enrolled 15,692 patients in the unmatched cohort, 15,392 (98.1%) underwent PN, and 300 (1.9%) underwent RFA. For tumor ≦ 2 cm, PN was equal to RFA in terms of overall survival (OS) (P > .05) and cancer-specific survival (CSS) (P > .05). For tumor size 2 to 3 cm, PN is likely to have a better OS (P < .05)and comparable CSS (P > .05). For > 3 cm tumor, PN might be associated with higher OS (P < .05) and CSS (P < .05) compared with RFA. In conclusion, PN had a similar OS and CSS compared with RFA in tumor size ≦ 2 cm, RFA could be offered for elderly or patients with comorbidity. For > 2 cm tumors, RFA is not recommended. However, further randomized controlled trials are further required to validate our results.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Carcinoma, Renal Cell", "Kidney Neoplasms", "Nephrectomy", "Female", "Male", "SEER Program", "Middle Aged", "Radiofrequency Ablation", "Aged", "Neoplasm Staging", "Kaplan-Meier Estimate", "Proportional Hazards Models"]
-},
-{
-"PMID": 39612440,
-"Title": "Medicine",
-"ArticleTitle": "Sensitivity of major chronic diseases and patients of different ages to the collapse of the healthcare system during the COVID-19 pandemic in China.",
-"Abstract": "This study evaluates the sensitivity of major chronic diseases to the collapse of the healthcare system for developing prevention and control strategies under normal and emergency conditions. Data for the years 2018, 2019, and 2020 (coronavirus disease 2019 [COVID-19] pandemic) were curated from the National Disease Mortality Surveillance System, Chinese Center for Disease Control and Prevention for diseases such as cancer, heart disease (HD), cerebrovascular disease (CVD), and chronic obstructive pulmonary disease (COPD). The yearly death rate change for 2018, 2019, and 2020 were calculated. Similarly, expected and observed death cases, 95% confidence intervals, and Z-score were calculated for the year 2020 (COVID-19 pandemic). Furthermore, linear regression analysis was performed to analyze a correlation between the median age of various groups and the mortality rate. The observed death cases for cerebrovascular, heart, and other chronic diseases, were more than the expected death cases (430,007 vs 421,317, 369,684 vs 368,957, and 302,974 vs 300,366) as well as an upper limit of 95% confidence interval. The observed death cases for COPD and cancer are less than the expected death cases (127,786 vs 140,524, 450,346 vs 463,961) and lower limit of the 95% confidence interval. The highest Z-score was noted for cerebrovascular disease (105.14). The disease impact of severity was CVD, other chronic diseases, and HD in descending order. The unexpected decline in deaths was found for COPD and cancers with Z-scores (-166.45 and -116.32). The severity of impact was CVD, other chronic diseases, HD, cancer, and COPD in descending order. The COVID-19 pandemic has also resulted in an increase in deaths of the relatively young population as shown by the difference in rate of slop. The healthcare system collapsed due to prevention, control measures and increased burden of COVID-19 patients, affected chronic disease treatment/management and as a consequence variation in death rates occurs in different chronic diseases. A marked increase in mortality was observed in cerebrovascular disease. The unexpected decline in deaths from COPD and cancers, and increase in deaths of the relatively young population suggests that there may be opportunities for improvement in chronic disease management.",
-"Predictions": [],
-"MeshTerms": ["Humans", "COVID-19", "China", "Chronic Disease", "Aged", "Middle Aged", "Male", "Adult", "Female", "Delivery of Health Care", "SARS-CoV-2", "Neoplasms", "Pulmonary Disease, Chronic Obstructive", "Cerebrovascular Disorders", "Age Factors", "Pandemics", "Aged, 80 and over"]
-},
-{
-"PMID": 39612436,
-"Title": "Medicine",
-"ArticleTitle": "Comprehensive analysis of rheumatic diseases, comorbidities, and mortality in geriatric population: Real-world data of 515 patients in a single rheumatology clinic.",
-"Abstract": "Rheumatic diseases present unique challenges in the elderly, with changes in the immune system contributing to varied clinical presentations. More individuals are now living with chronic diseases due to greater life expectancy, but there is a lack of real-world data about rheumatic diseases and comorbidities in older people. This study aimed to investigate disease types, comorbidities, treatments, and mortality in geriatric patients in comparison to non-geriatric patients at a rheumatology clinic. This retrospective observational cohort study reviewed the medical records of 2610 patients from January 2021 to January 2024 at 2 branches of a private hospital's rheumatology clinics. Demographic information and data on rheumatic diseases, noninflammatory conditions, treatments, comorbidities, and mortality were collected, and geriatric patients were compared to non-geriatric patients. Geriatric patients (n = 515) had a significantly higher prevalence of rheumatoid arthritis (50.6% vs 28.8%, P < .001), polymyalgia rheumatica (11.1% vs 0.2%, P < .001), and crystal arthritis (19.6% vs 8.8%, P < .001), with more frequent geriatric-onset cases. Osteoarthritis was also more prevalent in geriatric patients (51.2% vs 11.3%, P < .001), while fibromyalgia was more common in the non-geriatric group (15.9% vs 4.1%, P < .001). Geriatric patients experienced higher rates of comorbidities, including hypertension (72.4% vs 17.8%, P < .001), diabetes (33.6% vs 12.1%, P < .001), and osteoporosis (64.9% vs 35.4%, P < .001). These patients used more corticosteroids (74.5% vs 44%, P < .001), and conventional synthetic disease-modifying antirheumatic drugs (62.4% vs 49.4%, P < .001) but fewer biological disease-modifying antirheumatic drugs (9.2% vs 23.1%, P < .001). Mortality rates were significantly higher in geriatric patients (6% vs 0.3%), with cancer (P = .001), ischemic heart disease (P = .04), heart failure (P = .01), chronic kidney disease (P = .02), and interstitial lung disease (P = .01) being associated with increased mortality. Geriatric rheumatology should receive greater focus in future research to help address the anticipated increases in demand and to develop tailored management strategies for elderly patients with rheumatic diseases and comorbidities.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Aged", "Female", "Male", "Rheumatic Diseases", "Retrospective Studies", "Comorbidity", "Aged, 80 and over", "Middle Aged", "Prevalence"]
-},
-{
-"PMID": 39612434,
-"Title": "Medicine",
-"ArticleTitle": "Spermatic cord myxoma: A rare case report.",
-"Abstract": "Although rare, spermatic cord myxomas should be considered in the differential diagnosis of scrotal masses. Surgical excision is both diagnostic and therapeutic, providing a favorable prognosis with minimal risk of recurrence.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Male", "Myxoma", "Middle Aged", "Spermatic Cord", "Genital Neoplasms, Male", "Diagnosis, Differential"]
-},
-{
-"PMID": 39612433,
-"Title": "Medicine",
-"ArticleTitle": "Two case reports of breast cancer combined with synchronous primary intrahepatic cholangiocarcinoma/mixed liver cancer.",
-"Abstract": "The treatment approach adopted in this case report may serve as a favorable reference for the management of similar cases. However, further extensive biological studies are still needed to investigate the biological mechanisms of multiple primary malignant tumors and to discover specific therapeutic approaches to achieve more clinical benefits for patients.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Female", "Cholangiocarcinoma", "Neoplasms, Multiple Primary", "Breast Neoplasms", "Bile Duct Neoplasms", "Liver Neoplasms", "Middle Aged", "Carcinoma, Hepatocellular", "Aged", "Carcinoma, Ductal, Breast"]
-},
-{
-"PMID": 39612432,
-"Title": "Medicine",
-"ArticleTitle": "The role of 1400 plasma metabolites in gastric cancer: A bidirectional Mendelian randomization study and metabolic pathway analysis.",
-"Abstract": "While observational studies have illustrated correlations between plasma metabolites and gastric cancer (GC), the causal association between the 2 is still unclear. Our study aims to delineate the bidirectional relationship between plasma metabolites and GC and find potential metabolic pathways. We undertook a bidirectional 2-sample Mendelian randomization (MR) analysis to investigate the causal relationship, specificity, and direction of association between 1400 plasma metabolites and GC. The GWAS data for metabolites was obtained from a cohort of 8299 European individuals. And the GC's GWAS data was from FinnGen Consortium with 2384 European individuals, and the GWAS catalog with 1029 European ancestry cases for validation. Causal estimates were primarily calculated by the inverse-variance weighted (IVW) method. To ensure robustness, we performed comprehensive sensitivity analyses to assess heterogeneity and address concerns regarding horizontal pleiotropy. We validated the forward relationship between metabolites and GC from another database and implemented meta-analysis. Furthermore, we conducted metabolic enrichment and pathway analysis of these causal metabolites using MetaboAnalyst5.0/6.0 with the database of Kyoto Encyclopedia of Genes and Genomes. All statistical analysis was carried out using R software. Metabolites like 2s, 3R-dihydroxybutyrate, 4-acetamidobutanoate, ferulic acid 4-sulfate and methyl indole-3-acetate was proven positively linked with the development of GC. Asparagine, glucose to maltose ratio, glycohyocholate, Gulonate levels, linoleoyl ethanolamide and Spermidine to (N(1) + N(8))-acetylspermidine ratio was proven to be negatively associated with GC. Moreover, linoleic acid, histidine, glutamine, bilirubin, Succinate to proline ratio were found to be potentially linked to the development of GC. Furthermore, our analysis identified 18 significant metabolic pathways, including Arginine and proline metabolism (P < .009) and Valine, leucine, and isoleucine biosynthesis (P < .031). Our findings offer evidence supporting potential casual relations between multiple plasma metabolites and GC. These findings may offer great potential for future application of these biomarkers in GC screening and clinical prevention strategies.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Mendelian Randomization Analysis", "Stomach Neoplasms", "Genome-Wide Association Study", "Metabolic Networks and Pathways", "Male", "Female"]
-},
-{
-"PMID": 39612428,
-"Title": "Medicine",
-"ArticleTitle": "Correlation between CT spectral quantitative parameters and expression levels of HIF-1α and ALX1 in non-small cell lung cancer.",
-"Abstract": "To detect the expression levels of hypoxia inducible factor-1alpha (HIF-1α) and aristaless-like homeobox 1 (ALX1) in non-small cell lung cancer and analyze the relationship between CT spectral quantitative parameters and immunohistochemical markers, in order to evaluate the biological characteristics of lung cancer by spectral CT. Spectral CT data and paraffin masses of 50 adult patients with lung cancer were collected. CT quantitative parameters including the slope of spectral curve, effective atomic number and iodine concentration in enhanced phases were acquired. Expression levels of HIF-1α and ALX1 were detected by immunohistochemical tests, and compared between different pathological types and differentiation grades of tumor cells. CT quantitative parameters at different expression levels of HIF-1α and ALX1 were compared, respectively. The relationship between CT quantitative parameters and expression levels of HIF-1α and ALX1 were analyzed. There was no significant difference of expression levels of HIF-1α and ALX1 between adenocarcinoma and squamous cell carcinoma. Expression levels of HIF-1α among different differentiation grades of tumor cells had significant difference (χ2 = 27.100, P < .001), while without significant difference in ALX1 expression. CT spectral parameters had significant difference among expression levels of HIF-1α and ALX1 (P < .01). There was a positive correlation between each CT spectral parameter and the expression level of immunohistochemical markers. CT spectral quantitative parameters are significantly different among expression levels of immunohistochemical markers. The positive correlation between CT quantitative parameter and expression level of immunohistochemical markers suggests CT spectral imaging could predict biological characteristics of tumors.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Carcinoma, Non-Small-Cell Lung", "Lung Neoplasms", "Hypoxia-Inducible Factor 1, alpha Subunit", "Male", "Middle Aged", "Female", "Tomography, X-Ray Computed", "Aged", "Homeodomain Proteins", "Adult", "Biomarkers, Tumor", "Immunohistochemistry"]
-},
-{
-"PMID": 39612421,
-"Title": "Medicine",
-"ArticleTitle": "Chemotherapy combined with immunotherapy in a patient with multiple primary gastric and rectal cancers with good prognosis: A case report.",
-"Abstract": "According to the results of NGS testing, the multiple primary cancers' patient received personalized treatment and ultimately achieved clinical complete remission. This case highlights the critical role of genetic testing in accurately identifying multiple primary cancer and the value of personalized guidance for patient treatment using NGS in clinical practice.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Male", "Rectal Neoplasms", "Stomach Neoplasms", "Aged", "Neoplasms, Multiple Primary", "Adenocarcinoma", "Antineoplastic Combined Chemotherapy Protocols", "Immunotherapy", "Chemotherapy, Adjuvant", "Capecitabine", "Neoadjuvant Therapy", "Prognosis", "Oxaloacetates"]
-},
-{
-"PMID": 39612416,
-"Title": "Medicine",
-"ArticleTitle": "High C-reactive protein is associated with the efficacy of neoadjuvant chemotherapy for hormone receptor-positive breast cancer.",
-"Abstract": "C-reactive protein (CRP) is a nonspecific biomarker for systemic inflammatory response and is linked to the prognosis of breast cancer (BC); however, few studies have investigated the correlation between CRP and the effectiveness of neoadjuvant chemotherapy treatment for BC. We recruited 177 patients with BC who underwent neoadjuvant chemotherapy in our clinical trial. the median CRP level (0.24 mg/L), patients were categorized into high and low groups. We examined the relationship between CRP levels and various clinicopathological factors, including pathological complete response (pCR), using the chi-square test or Fisher exact test. Furthermore, we evaluated the predictive capacity of CRP for different molecular subtypes by constructing receiver operating characteristic curves. To identify the independent variables associated with pCR, we conducted logistic regression multivariate analysis. No association was found between C-reactive levels at baseline and pCR rates. CRP level was significantly associated with higher body mass index, and the high CRP group had more overweight patients (47.06% vs. 16.30%, P < .001). In hormone receptor-positive patients, the high CRP group demonstrated a significantly higher pCR rate (OR = 4.115, 95% CI: 1.481-11.36, P = .009). The areas under the curve was 0.670 (95% CI: 0.550-0.792, P < .001). Multivariate logistic analysis showed that the CRP level was a significant independent predictor of pCR (OR = 5.882, 95% CI: 1.470-28.57, P = .017). High CRP levels were found to be associated with a higher pCR rate, indicating their independent predictive value in determining the efficacy of neoadjuvant chemotherapy in hormone receptor-positive BC patients.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Female", "C-Reactive Protein", "Breast Neoplasms", "Neoadjuvant Therapy", "Middle Aged", "Adult", "Aged", "Biomarkers, Tumor", "Receptors, Estrogen", "ROC Curve", "Receptors, Progesterone", "Treatment Outcome", "Chemotherapy, Adjuvant", "Prognosis", "Antineoplastic Combined Chemotherapy Protocols"]
-},
-{
-"PMID": 39612415,
-"Title": "Medicine",
-"ArticleTitle": "Development of a nomogram for predicting cancer pain in lung cancer patients: An observational study.",
-"Abstract": "During the progression of lung cancer, cancer pain is a common complication. Currently, there are no accurate tools or methods to predict the occurrence of cancer pain in lung cancer. Our study aims to construct a predictive model for lung cancer pain to assist in the early diagnosis of cancer pain and improve prognosis. We retrospectively collected clinical data from 300 lung cancer patients between March 2013 and March 2023. First, we compared the clinical data of the groups with and without cancer pain. Significant factors were further screened using random forest analysis (IncMSE% > 2) to identify those with significant differences. Finally, these factors were incorporated into a multifactorial logistic regression model to develop a predictive model for lung cancer pain. The predictive accuracy and performance of the model were assessed using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA) analysis. Our study collected data from 300 lung cancer patients, including 100 in the pain-free group and 200 in the pain group. Subsequently, we conducted univariate analysis on 22 factors and selected statistically significant factors using random forest methods. Ultimately, lymphocytes(LYM) percentage, bone metastasis, tumor necrosis factor alpha (TNFα), and interleukin-6 (IL6) were identified as key factors. These 4 factors were included in a multivariate logistic regression analysis to construct a predictive model for lung cancer pain. The model demonstrated good predictive ability, with an area under the curve (AUC) of 0.852 (95% CI: 0.806-0.899). The calibration curve indicated that the model has good accuracy in predicting the risk of lung cancer pain. DCA further emphasized the model's high accuracy. The model was finally validated using 5-fold cross-validation. We developed a reliable predictive model for cancer pain in lung cancer. This can provide a theoretical basis for future large-sample, multi-center studies and may also assist in the early prevention and intervention of cancer pain in lung cancer.",
-"Predictions": [],
-"MeshTerms": ["Humans", "Lung Neoplasms", "Female", "Male", "Nomograms", "Cancer Pain", "Middle Aged", "Retrospective Studies", "Aged", "ROC Curve", "Logistic Models", "Prognosis", "Tumor Necrosis Factor-alpha"]
-}
-]
\ No newline at end of file
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diff --git a/api/data_num.py b/dataSources/PubMed/data_num.py
similarity index 100%
rename from api/data_num.py
rename to dataSources/PubMed/data_num.py
diff --git a/PubmedInfo.md b/dataSources/PubMed/doc/PubmedInfo.md
similarity index 98%
rename from PubmedInfo.md
rename to dataSources/PubMed/doc/PubmedInfo.md
index 72b192ade33d5a83fcbe11f74f314995f6567273..c57de11807fb351f3cbc8143236c01d853848e8e 100644
--- a/PubmedInfo.md
+++ b/dataSources/PubMed/doc/PubmedInfo.md
@@ -136,7 +136,7 @@ Example: human[organism] AND topoisomerase[protein name]
When searching for terms, it is important to pay attention to how the search is structured. For example, if you search for **breast cancer** without quotes, the search engine will look for any occurrence of the terms **"breast"**, **"cancer"**, or the exact phrase **"breast cancer"**. To specifically search for the phrase **breast cancer** as a whole, you need to enclose it in quotation marks (" ").
-
+
### API syntax
@@ -205,7 +205,7 @@ Each field has a field tag (enclosed in square brackets, e.g., [TI] for Title) t
When no field tags are specified, PubMed searches across all fields. However, it also applies Automatic Term Mapping (ATM) to map your terms to MeSH terms, journal names, author names, and other indexed fields, which helps broaden the search intelligently.
-
+
### ATM
diff --git a/api/doc/data_num.json b/dataSources/PubMed/doc/data_num.json
similarity index 100%
rename from api/doc/data_num.json
rename to dataSources/PubMed/doc/data_num.json
diff --git a/docImg/SearchATMExample.png b/dataSources/PubMed/doc/img/SearchATMExample.png
similarity index 100%
rename from docImg/SearchATMExample.png
rename to dataSources/PubMed/doc/img/SearchATMExample.png
diff --git a/docImg/SearchQuotationExample.png b/dataSources/PubMed/doc/img/SearchQuotationExample.png
similarity index 100%
rename from docImg/SearchQuotationExample.png
rename to dataSources/PubMed/doc/img/SearchQuotationExample.png
diff --git a/api/pubmedApi.py b/dataSources/PubMed/pubmedApi.py
similarity index 95%
rename from api/pubmedApi.py
rename to dataSources/PubMed/pubmedApi.py
index 3bc641acbbef0dbc84152dce77f34fc783f798ab..1cb76b3ab65e2335d7687ca6f46898e98fec966c 100644
--- a/api/pubmedApi.py
+++ b/dataSources/PubMed/pubmedApi.py
@@ -1,5 +1,5 @@
from requests import get
-from api.parser.xmlParser import parseXmlFile
+from parsers.xmlParser import parseXmlFile
import json
FILENAME = "pubmedData.xml"
@@ -36,10 +36,10 @@ def getPubmedData(term, date_min, date_max, nb_items = -1, debug = False, store
response = get(url)
- with open(f"data/{FILENAME}", "w", encoding="utf-8") as file:
+ with open(f"tmp/{FILENAME}", "w", encoding="utf-8") as file:
file.write(response.text)
- obj = parseXmlFile(f"data/{FILENAME}")
+ obj = parseXmlFile(f"tmp/{FILENAME}")
data_list = []
diff --git a/api/whoApi.py b/dataSources/WHO/whoApi.py
similarity index 100%
rename from api/whoApi.py
rename to dataSources/WHO/whoApi.py
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diff --git a/model/data/arthritis_infectious.json b/model/data/arthritis_infectious.json
deleted file mode 100644
index fcf85dad7aee20988e097c06945fc203090ee196..0000000000000000000000000000000000000000
--- a/model/data/arthritis_infectious.json
+++ /dev/null
@@ -1,509 +0,0 @@
-[
- {
- "PMID": "39462905",
- "Title": "Journal of paediatrics and child health",
- "ArticleTitle": "Hospitalisation cost for paediatric osteomyelitis and septic arthritis in New Zealand.",
- "Abstract": "Direct BJI hospitalisation costs in 2018-2019 were NZ$10\u2009819\u2009474 with 11% of costs due to re-admission. Direct hospitalisation costs for paediatric BJI in NZ vary by deprivation and ethnic group. Illness complexity of paediatric BJI varies by ethnic group. Interventions are needed to reduce incidence and severity of these debilitating infections.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "New Zealand",
- "Osteomyelitis",
- "Child",
- "Arthritis, Infectious",
- "Hospitalization",
- "Male",
- "Child, Preschool",
- "Female",
- "Adolescent",
- "Infant",
- "Length of Stay",
- "Patient Readmission"
- ]
- },
- {
- "PMID": "39459423",
- "Title": "Medicina (Kaunas, Lithuania)",
- "ArticleTitle": "Arthroscopic Debridement Enhanced by Intra-Articular Antibiotic-Loaded Calcium Sulphate Beads for Septic Arthritis of a Native Knee Following Iatrogenic Joint Injection: A Case Report.",
- "Abstract": "Septic arthritis (SA) represents an orthopedics urgency and mainly affects the knee joint. Due to its devastating effects on cartilage, immediate management is crucial. SA is characterized by an annual incidence of 2 to 10 cases per 100,000 individuals, with mortality rates fluctuating between 0.5% and 15%, with a substantially higher mortality rate observed in older people (15%) in contrast to younger cohorts (4%). The etiology of septic arthritis is multifactorial: a spectrum of Gram-positive and Gram-negative bacteria can contribute to the development of this condition, especially ",
- "Predictions": [
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Aged",
- "Arthritis, Infectious",
- "Debridement",
- "Anti-Bacterial Agents",
- "Knee Joint",
- "Arthroscopy",
- "Injections, Intra-Articular",
- "Calcium Sulfate",
- "Staphylococcal Infections",
- "Staphylococcus aureus",
- "Iatrogenic Disease"
- ]
- },
- {
- "PMID": "39446985",
- "Title": "JBJS reviews",
- "ArticleTitle": "The Seasonality of Childhood Bone and Joint Infection with Focus on Kingella kingae: A Systematic Review.",
- "Abstract": "Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.",
- "Predictions": [
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Kingella kingae",
- "Seasons",
- "Child",
- "Neisseriaceae Infections",
- "Arthritis, Infectious",
- "Hospitalization",
- "Bone Diseases, Infectious",
- "Infant",
- "Child, Preschool"
- ]
- },
- {
- "PMID": "39440804",
- "Title": "Foot & ankle international",
- "ArticleTitle": "One-Stage Tibiotalocalcaneal Arthrodesis for Severe Septic Destruction of the Ankle Joint Using a Retrograde Intramedullary Nail: A Retrospective Cross-sectional Study.",
- "Abstract": "One-stage TTCA with retrograde IM nail appears to be an acceptable alternative in severe septic destruction of the ankle joint, with a high eradication rate of infection and ankle fusion.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Arthrodesis",
- "Retrospective Studies",
- "Ankle Joint",
- "Bone Nails",
- "Middle Aged",
- "Male",
- "Female",
- "Cross-Sectional Studies",
- "Aged",
- "Adult",
- "Calcaneus",
- "Arthritis, Infectious",
- "Tibia"
- ]
- },
- {
- "PMID": "39428673",
- "Title": "ANZ journal of surgery",
- "ArticleTitle": "Non-tuberculous mycobacterial bone and joint infections - a case series from a tertiary referral centre in Australia.",
- "Abstract": "Antimicrobial complications were common; however, all patients were infection free at their latest follow up. Despite the inherent limitations, these results suggest that routinely ordering mycobacterial culture is of low yield. There is potential for shorter-term oral antimicrobial treatments. Prospective research is required to optimize treatment regimens and durations.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Mycobacterium Infections, Nontuberculous",
- "Tertiary Care Centers",
- "Male",
- "Female",
- "Middle Aged",
- "Aged",
- "Osteomyelitis",
- "Queensland",
- "Nontuberculous Mycobacteria",
- "Adult",
- "Prosthesis-Related Infections",
- "Anti-Bacterial Agents",
- "Arthritis, Infectious",
- "Retrospective Studies",
- "Australia"
- ]
- },
- {
- "PMID": "39424291",
- "Title": "Journal of tropical pediatrics",
- "ArticleTitle": "A systematic review of pelvic infective osteomyelitis in children: current state of evidence.",
- "Abstract": "Musculoskeletal infection of pelvis can be confused with septic arthritis of the hip, irritable hip, sacroiliitis, and spondylodiscitis in the initial period. This study aimed to present the complete clinical picture of pelvic infective osteomyelitis (PIO) in children along with its natural course. Two researchers independently used PubMed and Scopus electronic databases for the literature review. This review includes all studies reporting PIO in the pediatric age group. The final inclusion of 11 eligible studies was done. A total of 277 patients were analyzed from the included studies with the majority of males (158/242, 65.2%). Hip and groin pain (147/195, 75.3%) and limp (155/249, 62.2%) were the common presenting symptoms. Increased systemic temperature (83/103, 80.5%) and localized tenderness at the hip joint area (90/121, 74.3%) were among the commonest signs. Magnetic resonance imaging was an investigation of choice for diagnosis (89/93, 95.6%). Blood culture showed growth in 47.6% (119/250) patients with Staphylococcus aureus (83/102, 81.3%) being the most common isolated organism. Treatment with sensitive antibiotics was the mainstay of management with surgery for debridement or biopsy being required in only 16.1% (23/142) of the patients. PIO in children is a rare condition mimicking several other disease processes affecting the neighboring tissues the diagnosis of which gets limited in low-resource settings. Further prospective clinical studies are the need of the hour to validate the guideline proposed. Explorative studies to define a clinical scoring system to differentiate septic arthritis of the hip from PIO may be considered.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Osteomyelitis",
- "Child",
- "Male",
- "Female",
- "Anti-Bacterial Agents",
- "Magnetic Resonance Imaging",
- "Child, Preschool",
- "Adolescent",
- "Arthritis, Infectious",
- "Pelvis",
- "Staphylococcal Infections",
- "Staphylococcus aureus",
- "Debridement"
- ]
- },
- {
- "PMID": "39382308",
- "Title": "Journal of clinical microbiology",
- "ArticleTitle": "Clinical performance evaluation of the BioFire Joint Infection Panel.",
- "Abstract": "The BioFire Joint Infection (JI) Panel offers a significant advancement in the rapid diagnosis of joint infections by facilitating the simultaneous detection of multiple bacterial and fungal pathogens, as well as resistance markers, directly from synovial fluid samples. An article published in the ",
- "Predictions": [
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Synovial Fluid",
- "Bacteria",
- "Fungi",
- "Retrospective Studies",
- "Prospective Studies",
- "Bacterial Infections",
- "Arthritis, Infectious",
- "Mycoses",
- "Molecular Diagnostic Techniques",
- "Sensitivity and Specificity"
- ]
- },
- {
- "PMID": "39380073",
- "Title": "Journal of medical case reports",
- "ArticleTitle": "Disseminated melioidosis-challenge to routine antibiotic therapy: a case report.",
- "Abstract": "Misidentification leads to inadequate treatment, as melioidosis medication is different from other bacterial infections. Here initiation of meropenem- and cotrimoxazole-intensive therapy for 4\u00a0weeks, and 6-month eradication phase with cotrimoxazole, resulted in gradual recovery of the patient. It took around 21\u00a0days of intensive antibiotic therapy to get bacteriological clearance from blood, which signifies the tenacious nature of this infection.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Melioidosis",
- "Male",
- "Burkholderia pseudomallei",
- "Anti-Bacterial Agents",
- "Middle Aged",
- "Meropenem",
- "Arthritis, Infectious",
- "Trimethoprim, Sulfamethoxazole Drug Combination",
- "Diagnostic Errors",
- "Thienamycins",
- "Diagnosis, Differential",
- "Treatment Outcome"
- ]
- },
- {
- "PMID": "39370286",
- "Title": "Kyobu geka. The Japanese journal of thoracic surgery",
- "ArticleTitle": "[Minimally Invasive Aortic Valve Replacement for Aortic Valve Infective Endocarditis Complicated by Septic Arthritis of the Sternoclavicular Joint:Report of a Case].",
- "Abstract": "A 54-year-old man with a history of atopic dermatitis was admitted to our hospital for persistent fever and multiple arthralgias unresponsive to antibiotics. On the second day of hospitalization, Staphylococcus aureus was detected in the blood culture, and debridement for presumed pyogenic arthritis was performed on the patient's bilateral wrists and right ankle joints. Echocardiography showed evidence of infective endocarditis of the aortic valve. The patient's fever persisted after drainage of multiple joint abscesses, and blood cultures remained positive. A right sternoclavicular joint abscess that had been noted on computed tomography (CT) at the time of admission had not decreased in size on repeat CT performed 10 days post-admission. After additional drainage of the sternoclavicular joint abscess on the 15th day, the patient's fever subsided, and blood culture was negative. On the 29th day, an aortic valve replacement was performed via a right anterior thoracotomy to prevent sternal osteomyelitis. The postoperative course was uneventful, and the patient was discharged on the 35th day after valve surgery. One year after the surgery, he continues to take antibiotics, and recurrence of infection has not been observed.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Middle Aged",
- "Arthritis, Infectious",
- "Sternoclavicular Joint",
- "Aortic Valve",
- "Minimally Invasive Surgical Procedures",
- "Heart Valve Prosthesis Implantation",
- "Endocarditis",
- "Staphylococcal Infections"
- ]
- },
- {
- "PMID": "39358640",
- "Title": "European journal of orthopaedic surgery & traumatology : orthopedie traumatologie",
- "ArticleTitle": "Clinical evaluation of a multiplex PCR-based test for joint infection: a prospective diagnostic accuracy study of forty-nine patients.",
- "Abstract": "The BJI Panel has a high accuracy for detecting the pathogens in its panel, but the absence of important common pathogens from the panel reduces its sensitivity and NPV. With a short turnaround time and precise pathogen detection, the BJI Panel has the potential to add value as a complementary diagnostic method.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Prospective Studies",
- "Prosthesis-Related Infections",
- "Female",
- "Sensitivity and Specificity",
- "Synovial Fluid",
- "Male",
- "Middle Aged",
- "Aged",
- "Multiplex Polymerase Chain Reaction",
- "Predictive Value of Tests",
- "Adult",
- "Arthritis, Infectious",
- "Aged, 80 and over",
- "Biopsy"
- ]
- },
- {
- "PMID": "39340660",
- "Title": "Inflammation research : official journal of the European Histamine Research Society ... [et al.]",
- "ArticleTitle": "Trained immunity of synovial macrophages is associated with exacerbated joint inflammation and damage after Staphylococcus aureus infection.",
- "Abstract": "There is a trained immunity phenotype in CX3CR1",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Animals",
- "Male",
- "Staphylococcal Infections",
- "Mice, Inbred C57BL",
- "Lipopolysaccharides",
- "Macrophages",
- "TOR Serine-Threonine Kinases",
- "Staphylococcus aureus",
- "CX3C Chemokine Receptor 1",
- "Synovial Membrane",
- "Arthritis, Infectious",
- "Mice",
- "Cytokines",
- "Sirolimus",
- "Inflammation",
- "Synoviocytes",
- "Nociception",
- "Trained Immunity"
- ]
- },
- {
- "PMID": "39334397",
- "Title": "Italian journal of pediatrics",
- "ArticleTitle": "The feasibility and safety of ultrasound-guided puncture for treatment of septic arthritis in children.",
- "Abstract": "IRB-MTP_2021_05_202100781.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Arthritis, Infectious",
- "Male",
- "Female",
- "Child",
- "Retrospective Studies",
- "Child, Preschool",
- "Feasibility Studies",
- "Ultrasonography, Interventional",
- "Infant",
- "Arthrocentesis",
- "Punctures",
- "Treatment Outcome",
- "Fluoroscopy"
- ]
- },
- {
- "PMID": "39332086",
- "Title": "Diagnostic microbiology and infectious disease",
- "ArticleTitle": "Innovative approach of nanopore-based metagenomic sequencing for rapid identification of bacterial pathogens in joint fluid: A pilot study.",
- "Abstract": "Analysis of 11 clinical samples of joint fluid in this pilot study demonstrated proof-of-concept for nanopore-based metagenomic sequencing to serve as a complementary real-time diagnostic technique for septic arthritis, with a sensitivity of 75.0 % and specificity of 57.1 %, compared to the gold standard method of bacterial culture.",
- "Predictions": [
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Pilot Projects",
- "Humans",
- "Metagenomics",
- "Arthritis, Infectious",
- "Bacteria",
- "Nanopore Sequencing",
- "Sensitivity and Specificity",
- "Synovial Fluid",
- "Nanopores",
- "High-Throughput Nucleotide Sequencing"
- ]
- },
- {
- "PMID": "39327035",
- "Title": "BMJ case reports",
- "ArticleTitle": {
- "i": "Aspergillus niger"
- },
- "Abstract": "This case report outlines the diagnostic and therapeutic challenges encountered in a man in his 70s suffering from knee septic arthritis caused by ",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Arthritis, Infectious",
- "Male",
- "Aspergillus niger",
- "Arthroscopy",
- "Knee Joint",
- "Antifungal Agents",
- "Debridement",
- "Aged",
- "Aspergillosis",
- "Voriconazole",
- "Postoperative Complications"
- ]
- },
- {
- "PMID": "39327034",
- "Title": "BMJ case reports",
- "ArticleTitle": "Irreversible neurological manifestations in undiagnosed disseminated gonococcal infection.",
- "Abstract": "Neisseria gonorrhoeae causes a common sexually transmitted infection with manifestations ranging from asymptomatic to urethritis and pelvic inflammatory disease to disseminated infections including septic arthritis. Serious complications may arise in unrecognised or inappropriately treated infections.We report a young, healthy woman who developed fever and joint pain and was diagnosed with an inflammatory arthritis. After starting immune suppressing treatments, she experienced right wrist drop and progressive muscle atrophy, joint contractures and sensory loss. Electrodiagnostic studies showed patchy, mixed neurogenic and myopathic features. Areas of muscle oedema on extremity MRI led to a right brachioradialis biopsy, which showed only nonspecific changes. Other testing, including lumbar puncture and MRI of the brain/spine was noncontributory. Additional history revealed unprotected intercourse with a new partner prior to symptom onset. Urine gonorrhoeae PCR was positive, and right shoulder arthrocentesis confirmed septic arthritis. After intravenous antibiotic treatment with ceftriaxone, she demonstrated slow, incomplete symptomatic improvement.",
- "Predictions": [
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Gonorrhea",
- "Arthritis, Infectious",
- "Anti-Bacterial Agents",
- "Ceftriaxone",
- "Neisseria gonorrhoeae",
- "Magnetic Resonance Imaging",
- "Adult"
- ]
- },
- {
- "PMID": "39323270",
- "Title": "Revue medicale suisse",
- "ArticleTitle": "[Acute non-traumatic single-articular pain].",
- "Abstract": "The main non-traumatic causes of acute single-joint pain are microcrystalline, degenerative, reactive and septic arthritis. Septic arthritis must be excluded quickly with puncture of the joint effusion. In the absence of sepsis, surgical drainage can be performed within 24 hours after admission to the emergency unit. Concerning gout, recommendations advise the use of imaging for diagnosis in case of joint puncture not feasible and the introduction of urate-lowering treatment during the acute attack. Regarding reactive arthritis, the presence of microbial elements in the affected joints improves the understanding of its pathophysiology. Finally, osteoarthritis guidelines emphasize the importance of self-management programs for painful crises.",
- "Predictions": [
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Acute Pain",
- "Arthralgia",
- "Arthritis, Infectious",
- "Gout"
- ]
- },
- {
- "PMID": "39312873",
- "Title": "Cellular immunology",
- "ArticleTitle": "Neutralization of TLR2 in combination with either TNF-\u03b1 or IL-1\u03b2 antibody reduces the severity of septic arthritis through STAT3/mTOR signalling in lymphocytes.",
- "Abstract": "Staphylococcus aureus induced Septic arthritis is considered a medical concern. S.aureus binds TLR2 to induce an array of inflammatory responses. Generation of pro-inflammatory cytokines induces T cell responses and control Th17/Treg cell balance. Regulation of T cell-mediated immunity in response to inflammation is significantly influenced by mTOR. Presence of elevated TNF-\u03b1, IL-1\u03b2 decreases Treg cell activity through STAT3/mTOR, promoting proliferation of T cells towards Th17 cells. Therefore, we postulated, neutralizing TLR2 with either TNF-\u03b1 or IL-1\u03b2 in combination could be useful in modifying Th17/Treg cell ratio in order to treat septic arthritis by suppressing expression of mTOR/STAT3. To date, no studies have reported effects of neutralization of TLR2 along with either TNF-\u03b1 or IL-1\u03b2 on amelioration of arthritis correlating with mTOR/STAT3 expression. Contribution of T lymphocytes collected from blood, spleen, synovial tissues, their derived cytokines IFN-\u03b3, IL-6, IL-17, TGF-\u03b2, IL-10 were noted. Expression of TLR2, TNFR1, TNFR2, NF-\u03baB along with mTOR/STAT3 also recorded. Neutralization of TLR2 along with TNF-\u03b1 and IL-1\u03b2 were able to shift Th17 cells into immunosuppressive Treg cells. Furthermore,elevated expression of IL-10, TNFR2 and demoted expression of mTOR/ STAT3 along with NF-\u03baB in lymphocytes confirms its role in resolution of arthritis. It was also effective in reducing oxidative stress via increasing expression of the antioxidant enzymes. As a result, it can be inferred that Treg-derived IL-10, which may mitigate inflammatory effects of septic arthritis by influencing the mTOR/STAT3 interaction in lymphocytes, may be selected as a different therapeutic strategy for reducing the impact of septic arthritis.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "TOR Serine-Threonine Kinases",
- "STAT3 Transcription Factor",
- "Toll-Like Receptor 2",
- "Tumor Necrosis Factor-alpha",
- "Signal Transduction",
- "Animals",
- "Arthritis, Infectious",
- "Th17 Cells",
- "T-Lymphocytes, Regulatory",
- "Interleukin-1beta",
- "Mice",
- "Male",
- "Staphylococcus aureus",
- "Antibodies, Neutralizing",
- "Staphylococcal Infections",
- "Cytokines"
- ]
- },
- {
- "PMID": "39311733",
- "Title": "South Dakota medicine : the journal of the South Dakota State Medical Association",
- "ArticleTitle": "Acute Arthritis Presentations of Gonorrhea and Syphilis - A Concise Update.",
- "Abstract": "According to the 2021 CDC sexually transmitted disease surveillance report, national cases of syphilis and gonorrhea continue to rise. Currently, South Dakota ranks #1 in syphilis and #2 in gonorrhea cases per 100,000 population. The higher incidence increases the likelihood South Dakota clinicians will encounter different presentations of syphilis and gonorrhea. Recently, we have seen patients presenting with acute STI related inflammatory arthritis. This review discusses the acute arthritic presentations associated with gonorrhea and syphilis and its treatment.",
- "Predictions": [
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Gonorrhea",
- "Syphilis",
- "Acute Disease",
- "Anti-Bacterial Agents",
- "Arthritis, Infectious",
- "Arthritis",
- "South Dakota"
- ]
- },
- {
- "PMID": "39307981",
- "Title": "Journal of pediatric orthopedics",
- "ArticleTitle": "Optimal Timing for Advanced Imaging in Childhood Bone and Joint Infection.",
- "Abstract": "Overall, children with BJI who underwent MRI scans before surgery had lower reoperation rates. Children receiving MRIs within 48 hours of admission had shorter LOS.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Retrospective Studies",
- "Magnetic Resonance Imaging",
- "Child",
- "Male",
- "Female",
- "Arthritis, Infectious",
- "Length of Stay",
- "Osteomyelitis",
- "Child, Preschool",
- "Adolescent",
- "Time Factors",
- "Recurrence",
- "Infant",
- "Reoperation"
- ]
- },
- {
- "PMID": "39289033",
- "Title": "BMJ case reports",
- "ArticleTitle": "Coccidiomycosis septic arthritis presenting as ankle monoarthritis in a patient with presumed psoriatic arthritis.",
- "Abstract": "A man in his 50s with a history of psoriasis was evaluated for acute on chronic left ankle pain. His symptoms were attributed to psoriatic arthritis, and he tried several immunosuppressive regimens without improvement. Further diagnostic workup confirmed ",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Coccidioidomycosis",
- "Arthritis, Infectious",
- "Arthritis, Psoriatic",
- "Middle Aged",
- "Diagnosis, Differential",
- "Ankle Joint",
- "Antifungal Agents",
- "Debridement",
- "Coccidioides"
- ]
- },
- {
- "PMID": "39288015",
- "Title": "The Journal of antimicrobial chemotherapy",
- "ArticleTitle": "Efficacy and safety of co-trimoxazole in device-related bone and joint infections: a CRIOGO multicentre case-control study.",
- "Abstract": "Co-trimoxazole appears to be an effective alternative for the treatment of BJI, even when it occurs on a device, but the safety profile requires close monitoring of adverse effects.",
- "Predictions": [
- "Male",
- "Arthritis, Infectious"
- ],
- "MeshTerms": [
- "Humans",
- "Trimethoprim, Sulfamethoxazole Drug Combination",
- "Male",
- "Case-Control Studies",
- "Female",
- "Aged",
- "Middle Aged",
- "Anti-Bacterial Agents",
- "Treatment Outcome",
- "Adult",
- "Prosthesis-Related Infections",
- "Aged, 80 and over",
- "Arthritis, Infectious"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/blood_cells.json b/model/data/blood_cells.json
deleted file mode 100644
index 4a300e43a02985af3afd8beba5814af8c2c5edfc..0000000000000000000000000000000000000000
--- a/model/data/blood_cells.json
+++ /dev/null
@@ -1,447 +0,0 @@
-[
- {
- "PMID": "39434567",
- "Title": "Food & function",
- "ArticleTitle": "Along the gut-bone marrow signaling pathway: use of longan polysaccharides to regenerate blood cells after chemotherapy-induced myelosuppression.",
- "Abstract": "Although it has been established that polysaccharides have an effect on bone marrow haematopoiesis, it remains unclear how polysaccharides regulate bone marrow haematopoiesis during absorption and metabolism ",
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Mice",
- "Gastrointestinal Microbiome",
- "Polysaccharides",
- "Bone Marrow",
- "Hematopoiesis",
- "Male",
- "Signal Transduction",
- "Antineoplastic Agents",
- "Blood Cells",
- "Bone Marrow Cells"
- ]
- },
- {
- "PMID": "39434350",
- "Title": "JPMA. The Journal of the Pakistan Medical Association",
- "ArticleTitle": "Fabrication of a cell irradiation technique by alpha-particles using allyl diglycol carbonate (ADC) detector and micro-capillary tubes.",
- "Abstract": "Low irradiation time had significant impact of alpha particles on the average percentage of lymphocyte and neutrophil cells.",
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Rats",
- "Alpha Particles",
- "Male",
- "Blood Cells"
- ]
- },
- {
- "PMID": "39409208",
- "Title": "Sensors (Basel, Switzerland)",
- "ArticleTitle": "TW-YOLO: An Innovative Blood Cell Detection Model Based on Multi-Scale Feature Fusion.",
- "Abstract": "As deep learning technology has progressed, automated medical image analysis is becoming ever more crucial in clinical diagnosis. However, due to the diversity and complexity of blood cell images, traditional models still exhibit deficiencies in blood cell detection. To address blood cell detection, we developed the TW-YOLO approach, leveraging multi-scale feature fusion techniques. Firstly, traditional CNN (Convolutional Neural Network) convolution has poor recognition capabilities for certain blood cell features, so the RFAConv (Receptive Field Attention Convolution) module was incorporated into the backbone of the model to enhance its capacity to extract geometric characteristics from blood cells. At the same time, utilizing the feature pyramid architecture of YOLO (You Only Look Once), we enhanced the fusion of features at different scales by incorporating the CBAM (Convolutional Block Attention Module) in the detection head and the EMA (Efficient Multi-Scale Attention) module in the neck, thereby improving the recognition ability of blood cells. Additionally, to meet the specific needs of blood cell detection, we designed the PGI-Ghost (Programmable Gradient Information-Ghost) strategy to finely describe the gradient flow throughout the process of extracting features, further improving the model's effectiveness. Experiments on blood cell detection datasets such as BloodCell-Detection-Dataset (BCD) reveal that TW-YOLO outperforms other models by 2%, demonstrating excellent performance in the task of blood cell detection. In addition to advancing blood cell image analysis research, this work offers strong technical support for future automated medical diagnostics.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Blood Cells",
- "Neural Networks, Computer",
- "Deep Learning",
- "Image Processing, Computer-Assisted",
- "Algorithms"
- ]
- },
- {
- "PMID": "39363037",
- "Title": "Scientific reports",
- "ArticleTitle": "A fine-grained image classification algorithm based on self-supervised learning and multi-feature fusion of blood cells.",
- "Abstract": "Leukemia is a prevalent and widespread blood disease, and its early diagnosis is crucial for effective patient treatment. Diagnosing leukemia types heavily relies on pathologists' morphological examination of blood cell images. However, this process is tedious and time-consuming, and the diagnostic results are subjective, leading to potential misdiagnosis and underdiagnosis. This paper proposes a blood cell image classification method that combines MAE with an enhanced Vision Transformer to tackle these challenges. Initially, pre-training occurs on two datasets, TMAMD and Red4, using the MAE self-supervised learning algorithm. Subsequently, the pre-training weights are transferred to our improved model.This paper introduces feature fusion of the outputs from each layer of the Transformer encoder to maximize the utilization of features extracted from lower layers, such as color, contour, and texture of blood cells, along with deeper semantic features. Furthermore, the dynamic margins for the subcenter Arcface Loss function are employed to enhance the model's fine-grained feature representation by achieving inter-class dispersion and intra-class aggregation. Models trained using our method achieved state-of-the-art results on both the TMAMD dataset and Red4 dataset, with classification accuracies of 93.51% and 81.41%, respectively. This achievement is expected to be a valuable reference for physicians in their clinical diagnoses.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Supervised Machine Learning",
- "Algorithms",
- "Blood Cells",
- "Leukemia",
- "Image Processing, Computer-Assisted",
- "Image Interpretation, Computer-Assisted"
- ]
- },
- {
- "PMID": "39338775",
- "Title": "Sensors (Basel, Switzerland)",
- "ArticleTitle": "A Novel Size-Based Centrifugal Microfluidic Design to Enrich and Magnetically Isolate Circulating Tumor Cells from Blood Cells through Biocompatible Magnetite-Arginine Nanoparticles.",
- "Abstract": "This paper presents a novel centrifugal microfluidic approach (so-called lab-on-a-CD) for magnetic circulating tumor cell (CTC) separation from the other healthy cells according to their physical and acquired chemical properties. This study enhances the efficiency of CTC isolation, crucial for cancer diagnosis, prognosis, and therapy. CTCs are cells that break away from primary tumors and travel through the bloodstream; however, isolating CTCs from blood cells is difficult due to their low numbers and diverse characteristics. The proposed microfluidic device consists of two sections: a passive section that uses inertial force and bifurcation law to sort CTCs into different streamlines based on size and shape and an active section that uses magnetic forces along with Dean drag, inertial, and centrifugal forces to capture magnetized CTCs at the downstream of the microchannel. The authors designed, simulated, fabricated, and tested the device with cultured cancer cells and human cells. We also proposed a cost-effective method to mitigate the surface roughness and smooth surfaces created by micromachines and a unique pulsatile technique for flow control to improve separation efficiency. The possibility of a device with fewer layers to improve the leaks and alignment concerns was also demonstrated. The fabricated device could quickly handle a large volume of samples and achieve a high separation efficiency (93%) of CTCs at an optimal angular velocity. The paper shows the feasibility and potential of the proposed centrifugal microfluidic approach to satisfy the pumping, cell sorting, and separating functions for CTC separation.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Neoplastic Cells, Circulating",
- "Cell Separation",
- "Centrifugation",
- "Magnetite Nanoparticles",
- "Microfluidic Analytical Techniques",
- "Lab-On-A-Chip Devices",
- "Cell Line, Tumor",
- "Blood Cells"
- ]
- },
- {
- "PMID": "39322696",
- "Title": "Nature",
- "ArticleTitle": "Childhood leukaemia in Down's syndrome primed by blood-cell bias.",
- "Abstract": "",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Child",
- "Humans",
- "Blood Cells",
- "Down Syndrome",
- "Leukemia"
- ]
- },
- {
- "PMID": "39294566",
- "Title": "BMC genomics",
- "ArticleTitle": "Mouse blood cells types and aging prediction using penalized Latent Dirichlet Allocation.",
- "Abstract": "pLDA learns a dimension reduced representation of the expression profile. This representation allows identification of cell types and has predictability of the age of cells.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Mice",
- "Aging",
- "Single-Cell Analysis",
- "Blood Cells",
- "Transcriptome",
- "Gene Expression Profiling",
- "Computational Biology",
- "Algorithms"
- ]
- },
- {
- "PMID": "39275304",
- "Title": "Nutrients",
- "ArticleTitle": "The Evaluation of Selected Trace Elements in Blood, Serum and Blood Cells of Type 2 Diabetes Patients with and without Renal Disorder.",
- "Abstract": "In order to ensure effective care for patients with T2DM, it is necessary to improve the standard diet, including the content of micronutrients and their modification in patients with concomitant CKD.",
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Trace Elements",
- "Male",
- "Female",
- "Middle Aged",
- "Renal Insufficiency, Chronic",
- "Aged",
- "Nickel",
- "Chromium",
- "Adult",
- "Glomerular Filtration Rate",
- "Zinc",
- "Magnesium",
- "Blood Cells",
- "Case-Control Studies"
- ]
- },
- {
- "PMID": "39273028",
- "Title": "Cells",
- "ArticleTitle": "Immunophenotyping of Peripheral Blood Cells in Patients with Chronic Lymphocytic Leukemia Treated with Ibrutinib.",
- "Abstract": "Chronic lymphocytic leukemia (CLL) is a B-cell-derived hematologic malignancy whose progression depends on active B-cell receptor (BCR) signaling. Despite the spectacular efficacy of Ibrutinib, an irreversible inhibitor of Bruton tyrosine kinase (BTK), resistance can develop in CLL patients, and alternative therapeutic strategies are therefore required. Cancer immunotherapy has revolutionized cancer care and may be an attractive approach in this context. We speculated that characterizing the immune responses of CLL patients may highlight putative immunotherapeutic targets. Here, we used high-dimensional spectral flow cytometry to compare the distribution and phenotype of non-B-cell immune populations in the circulating blood of CLL patients treated with Ibrutinib displaying a complete response or secondary progression. Although no drastic changes were observed in the composition of their immune subsets, the Ibrutinib-resistant group showed increased cycling of CD8+ T cells, leading to their overabundance at the expense of dendritic cells. In addition, the expression of 11 different surface checkpoints was similar regardless of response status. Together, this suggests that CLL relapse upon Ibrutinib treatment may not lead to major alterations in the peripheral immune response.",
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Leukemia, Lymphocytic, Chronic, B-Cell",
- "Adenine",
- "Piperidines",
- "Immunophenotyping",
- "Male",
- "Female",
- "Aged",
- "Middle Aged",
- "Aged, 80 and over",
- "CD8-Positive T-Lymphocytes",
- "Blood Cells",
- "Pyrimidines",
- "Drug Resistance, Neoplasm"
- ]
- },
- {
- "PMID": "39259469",
- "Title": "Bulletin of experimental biology and medicine",
- "ArticleTitle": "Spontaneous and Stimulated Production of Cytokines by Blood Cells Ex Vivo as a Biomarker of Initially High or Low Hypoxia Resistance in Rats.",
- "Abstract": "Spontaneous and stimulated production of cytokines by peripheral blood cells obtained from the caudal vein of male Wistar rats was assessed before testing their resistance to oxygen deficiency in a decompression chamber. To study the spontaneous production of cytokines, heparinized blood cells were incubated in a culture medium (24 h, 5% CO",
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Male",
- "Rats, Wistar",
- "Rats",
- "Hypoxia",
- "Biomarkers",
- "Interleukin-10",
- "Interleukin-6",
- "Tumor Necrosis Factor-alpha",
- "Concanavalin A",
- "Cytokines",
- "Lipopolysaccharides",
- "Phytohemagglutinins",
- "Blood Cells",
- "Interleukin-1beta"
- ]
- },
- {
- "PMID": "39168838",
- "Title": "Zhonghua yi xue za zhi",
- "ArticleTitle": "[Opportunities and expectations brought by artificial intelligence assisted peripheral blood cell morphology examination].",
- "Abstract": "The morphological examination of blood cells under manual microscopes is a classic method, but the obvious shortcomings limit the extensive development of peripheral blood cell morphological examination. By using the manual microscope method, it is difficult to ensure the effective implementation of reviewing rules on blood cell analysis, fails to meet the needs of clinical diagnosis and treatment activities, and exposes the risk of missing diagnosis and early detection of some blood system diseases. Artificial Intelligence-assisted peripheral blood cell morphological examination is an important development direction in blood cell morphological examination and diagnosis. This article primarily introduces the characteristics and current application status of artificial intelligence-assisted blood cell morphological examination, as well as the functional requirements and expectations for future technological advancements. Furthermore, it provides an outlook on potential clinical and laboratory application scenarios.With the rapid development of artificial intelligence in blood cell morphology testing, the performance of automated blood cell morphology analysis systems will be greatly improved, which can fully meet the needs of clinical diagnosis, treatment, and health management.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Artificial Intelligence",
- "Humans",
- "Blood Cells",
- "Microscopy"
- ]
- },
- {
- "PMID": "39143590",
- "Title": "BMC medical genomics",
- "ArticleTitle": "Revealing differential expression patterns of piRNA in FACS blood cells of SARS-CoV-2 infected patients.",
- "Abstract": "Non-coding RNA expression has shown to have cell type-specificity. The regulatory characteristics of these molecules are impacted by changes in their expression levels. We performed next-generation sequencing and examined small RNA-seq data obtained from 6 different types of blood cells separated by fluorescence-activated cell sorting of severe COVID-19 patients and healthy control donors. In addition to examining the behavior of piRNA in the blood cells of severe SARS-CoV-2 infected patients, our aim was to present a distinct piRNA differential expression portrait for each separate cell type. We observed that depending on the type of cell, different sorted control cells (erythrocytes, monocytes, lymphocytes, eosinophils, basophils, and neutrophils) have altering piRNA expression patterns. After analyzing the expression of piRNAs in each set of sorted cells from patients with severe COVID-19, we observed 3 significantly elevated piRNAs - piR-33,123, piR-34,765, piR-43,768 and 9 downregulated piRNAs in erythrocytes. In lymphocytes, all 19 piRNAs were upregulated. Monocytes were presented with a larger amount of statistically significant piRNA, 5 upregulated (piR-49039 piR-31623, piR-37213, piR-44721, piR-44720) and 35 downregulated. It has been previously shown that piR-31,623 has been associated with respiratory syncytial virus infection, and taking in account the major role of piRNA in transposon silencing, we presume that the differential expression patterns which we observed could be a signal of indirect antiviral activity or a specific antiviral cell state. Additionally, in lymphocytes, all 19 piRNAs were upregulated.",
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "RNA, Small Interfering",
- "SARS-CoV-2",
- "Flow Cytometry",
- "Male",
- "Female",
- "Middle Aged",
- "Monocytes",
- "Adult",
- "Blood Cells",
- "Piwi-Interacting RNA"
- ]
- },
- {
- "PMID": "39113822",
- "Title": "Frontiers in cellular and infection microbiology",
- "ArticleTitle": "The predictive value of peripheral blood cell mitochondrial gene expression in identifying the prognosis in pediatric sepsis at preschool age.",
- "Abstract": "MtDNA-CN and mitochondrial gene expression are closely linked to the severity and clinical outcomes of infectious diseases. Severe infections lead to impaired mitochondrial function in peripheral blood cells. Notably, when compared to other laboratory parameters, the expression levels of mt-CO1, mt-ND1, and mt-ATP6 demonstrate promising potential for assessing the prognosis of pediatric sepsis.",
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Sepsis",
- "Child, Preschool",
- "Female",
- "Male",
- "DNA, Mitochondrial",
- "Prospective Studies",
- "Prognosis",
- "ROC Curve",
- "Child",
- "Mitochondria",
- "NADH Dehydrogenase",
- "Mitochondrial Proton-Translocating ATPases",
- "Blood Cells",
- "Genes, Mitochondrial",
- "Gene Expression",
- "Pneumonia",
- "Predictive Value of Tests"
- ]
- },
- {
- "PMID": "39105953",
- "Title": "Clinical and experimental medicine",
- "ArticleTitle": "Application of image recognition technology in pathological diagnosis of blood smears.",
- "Abstract": "Traditional manual blood smear diagnosis methods are time-consuming and prone to errors, often relying heavily on the experience of clinical laboratory analysts for accuracy. As breakthroughs in key technologies such as neural networks and deep learning continue to drive digital transformation in the medical field, image recognition technology is increasingly being leveraged to enhance existing medical processes. In recent years, advancements in computer technology have led to improved efficiency in the identification of blood cells in blood smears through the use of image recognition technology. This paper provides a comprehensive summary of the methods and steps involved in utilizing image recognition algorithms for diagnosing diseases in blood smears, with a focus on malaria and leukemia. Furthermore, it offers a forward-looking research direction for the development of a comprehensive blood cell pathological detection system.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Pathology, Clinical",
- "Image Processing, Computer-Assisted",
- "Blood Cells",
- "Malaria",
- "Leukemia",
- "Algorithms",
- "Machine Learning",
- "Blood Cell Count",
- "Humans"
- ]
- },
- {
- "PMID": "39084628",
- "Title": "Physics in medicine and biology",
- "ArticleTitle": "Inter-subject cerebrovascular variability: a source of uncertainty for dose calculation to circulating blood cells for glioblastoma patients treated with modern radiotherapy techniques.",
- "Abstract": {
- "i": "Conclusions",
- "sub": "95%"
- },
- "Predictions": [
- "Male",
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Glioblastoma",
- "Radiotherapy Dosage",
- "Uncertainty",
- "Radiotherapy, Intensity-Modulated",
- "Brain Neoplasms",
- "Radiotherapy Planning, Computer-Assisted",
- "Radiation Dosage",
- "Blood Cells",
- "Male"
- ]
- },
- {
- "PMID": "39020094",
- "Title": "Nature aging",
- "ArticleTitle": "A metabolic atlas of blood cells in young and aged mice identifies uridine as a metabolite to rejuvenate aged hematopoietic stem cells.",
- "Abstract": "Aging of hematopoietic stem cells (HSCs) is accompanied by impaired self-renewal ability, myeloid skewing, immunodeficiencies and increased susceptibility to malignancies. Although previous studies highlighted the pivotal roles of individual metabolites in hematopoiesis, comprehensive and high-resolution metabolomic profiles of different hematopoietic cells across ages are still lacking. In this study, we created a metabolome atlas of different blood cells across ages in mice. We reveal here that purine, pyrimidine and retinol metabolism are enriched in young hematopoietic stem and progenitor cells (HSPCs), whereas glutamate and sphingolipid metabolism are concentrated in aged HSPCs. Through metabolic screening, we identified uridine as a potential regulator to rejuvenate aged HSPCs. Mechanistically, uridine treatment upregulates the FoxO signaling pathway and enhances self-renewal while suppressing inflammation in aged HSCs. Finally, we constructed an open-source platform for public easy access and metabolomic analysis in blood cells. Collectively, we provide a resource for metabolic studies in hematopoiesis that can contribute to future anti-aging metabolite screening.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Hematopoietic Stem Cells",
- "Mice",
- "Uridine",
- "Aging",
- "Metabolome",
- "Hematopoiesis",
- "Metabolomics",
- "Cellular Senescence",
- "Mice, Inbred C57BL",
- "Blood Cells",
- "Rejuvenation",
- "Signal Transduction"
- ]
- },
- {
- "PMID": "38951059",
- "Title": "Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi",
- "ArticleTitle": "[Chinese expert consensus on the technical and clinical practice specifications of artificial intelligence assisted morphology examination of blood cells (2024)].",
- "Abstract": "Blood cell morphological examination is a crucial method for the diagnosis of blood diseases, but traditional manual microscopy is characterized by low efficiency and susceptibility to subjective biases. The application of artificial intelligence (AI) technology has improved the efficiency and quality of blood cell examinations and facilitated the standardization of test results. Currently, a variety of AI devices are either in clinical use or under research, with diverse technical requirements and configurations. The Experimental Diagnostic Study Group of the Hematology Branch of the Chinese Medical Association has organized a panel of experts to formulate this consensus. The consensus covers term definitions, scope of application, technical requirements, clinical application, data management, and information security. It emphasizes the importance of specimen preparation, image acquisition, image segmentation algorithms, and cell feature extraction and classification, and sets forth basic requirements for the cell recognition spectrum. Moreover, it provides detailed explanations regarding the fine classification of pathological cells, requirements for cell training and testing, quality control standards, and assistance in issuing diagnostic reports by humans. Additionally, the consensus underscores the significance of data management and information security to ensure the safety of patient information and the accuracy of data.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Artificial Intelligence",
- "Consensus",
- "Blood Cells",
- "China",
- "Algorithms"
- ]
- },
- {
- "PMID": "38951027",
- "Title": "Genome research",
- "ArticleTitle": "Interspecies regulatory landscapes and elements revealed by novel joint systematic integration of human and mouse blood cell epigenomes.",
- "Abstract": "Knowledge of locations and activities of ",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Mice",
- "Humans",
- "Epigenesis, Genetic",
- "Epigenome",
- "Species Specificity",
- "Blood Cells",
- "Regulatory Sequences, Nucleic Acid",
- "Gene Expression Regulation",
- "Epigenomics"
- ]
- },
- {
- "PMID": "38926555",
- "Title": "Nature",
- "ArticleTitle": "Flies use blood cells to take a deep breath.",
- "Abstract": "",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Blood Cells",
- "Drosophila melanogaster",
- "Humans"
- ]
- },
- {
- "PMID": "38910248",
- "Title": "Journal of nanobiotechnology",
- "ArticleTitle": "Nanoscale insights into hematology: super-resolved imaging on blood cell structure, function, and pathology.",
- "Abstract": "Fluorescence nanoscopy, also known as super-resolution microscopy, has transcended the conventional resolution barriers and enabled visualization of biological samples at nanometric resolutions. A series of super-resolution techniques have been developed and applied to investigate the molecular distribution, organization, and interactions in blood cells, as well as the underlying mechanisms of blood-cell-associated diseases. In this review, we provide an overview of various fluorescence nanoscopy technologies, outlining their current development stage and the challenges they are facing in terms of functionality and practicality. We specifically explore how these innovations have propelled forward the analysis of thrombocytes (platelets), erythrocytes (red blood cells) and leukocytes (white blood cells), shedding light on the nanoscale arrangement of subcellular components and molecular interactions. We spotlight novel biomarkers uncovered by fluorescence nanoscopy for disease diagnosis, such as thrombocytopathies, malignancies, and infectious diseases. Furthermore, we discuss the technological hurdles and chart out prospective avenues for future research directions. This review aims to underscore the significant contributions of fluorescence nanoscopy to the field of blood cell analysis and disease diagnosis, poised to revolutionize our approach to exploring, understanding, and managing disease at the molecular level.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Animals",
- "Humans",
- "Blood Cells",
- "Blood Platelets",
- "Erythrocytes",
- "Hematology",
- "Leukocytes",
- "Microscopy, Fluorescence",
- "Nanotechnology"
- ]
- },
- {
- "PMID": "38898733",
- "Title": "International journal of laboratory hematology",
- "ArticleTitle": "Hematological cytomorphology: Where we are.",
- "Abstract": "The manuscript discusses the historical evolution of observing blood cell morphology under an optical microscope, from the earliest microscopes in the 17th century to the modern digital era, highlighting key advancements and contributions in the field. Blood has historically held symbolic importance in various cultures, with early medical observations dating back to Hippocrates and Galeno. The discovery of cells and subsequent advancements in microscopy by scientists like Hooke and van Leeuwenhoek paved the way for understanding blood cell morphology. Influential figures such as Hewson, Donn\u00e9, and Ehrlich followed. Diagnostic cytology evolved from manual cell counting to the development of automated hematological systems. Automated complete blood counting came to support microscopic examination in diagnosing hematological disorders. Morphology is crucial in predicting disease outcomes and guiding treatment decisions, particularly hematological neoplasms. The introduction of flow cytometry and its integration with traditional morphological analysis and the new cytogenetic and molecular techniques revolutionized the classification and prognostication of hematologic disorders. Digital microscopy has emerged as a powerful tool in recent years, offering rapid acquisition and sharing of blood cell images. Integrating Artificial Intelligence with digital microscopy has further enhanced morphological analysis, improving diagnostic efficiency. We also discuss the prospects of AI in pre-classifying blood cells in bone marrow aspirate samples, potentially revolutionizing diagnostic pathways for hematologic diseases. Overall, the manuscript provides a comprehensive overview of the historical development, clinical significance and technological advancements in observing blood cell morphology, underscoring its continued relevance in modern hematology practice.",
- "Predictions": [
- "Blood Cells"
- ],
- "MeshTerms": [
- "Humans",
- "Microscopy",
- "Blood Cells",
- "Hematology",
- "Hematologic Diseases",
- "History, 20th Century",
- "History, 21st Century",
- "History, 17th Century",
- "History, 19th Century",
- "Flow Cytometry",
- "Artificial Intelligence"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/cancer.json b/model/data/cancer.json
deleted file mode 100644
index 922dbc7093a616569d496e6daf2ba38dbc827b9c..0000000000000000000000000000000000000000
--- a/model/data/cancer.json
+++ /dev/null
@@ -1,445 +0,0 @@
-[
- {
- "PMID": "39738287",
- "Title": "Scientific reports",
- "ArticleTitle": "DCLRE1B as a novel prognostic biomarker associated with immune infiltration: a pancancer analysis.",
- "Abstract": "The DNA cross-link repair 1B (DCLRE1B) gene is involved in repairing cross-links between DNA strands, including those associated with Hoyeraal-Hreidarsson syndrome and congenital dyskeratosis. However, its role in tumours is not well understood. DCLRE1B expression profiles were examined in tumour tissues and normal tissues using TCGA, GTEx, and TARGET datasets. Additionally, we performed experiments with clinical melanoma samples to verify DCLRE1B expression patterns. We also performed pancancer analyses to investigate the diverse roles of DCLRE1B in the biological functions of various cancers. DCLRE1B exhibited distinct expression patterns and played crucial prognostic roles in most tumours. In particular, high expression of DCLRE1B in melanoma was significantly correlated with a poor prognosis and increased malignancy. DCLRE1B was also found to be associated with the immune landscape and various immune biomarkers and regulators. Furthermore, our analysis identified potential small molecules that could target DCLRE1B in different cancer types. The DCLRE1B gene may be involved in the development and occurrence of a variety of cancers. Additionally, DCLRE1B affects various tumour types not only by mediating DNA repair but also by shaping the differential immune microenvironment. In conclusion, our research offers fresh perspectives on the diagnosis and treatment of different types of cancers.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Biomarkers, Tumor",
- "Prognosis",
- "Tumor Microenvironment",
- "Melanoma",
- "Gene Expression Regulation, Neoplastic",
- "Neoplasms"
- ]
- },
- {
- "PMID": "39738156",
- "Title": "Nature communications",
- "ArticleTitle": "The Theranostic Genome.",
- "Abstract": "Theranostic drugs represent an emerging path to deliver on the promise of precision medicine. However, bottlenecks remain in characterizing theranostic targets, identifying theranostic lead compounds, and tailoring theranostic drugs. To overcome these bottlenecks, we present the Theranostic Genome, the part of the human genome whose expression can be utilized to combine therapeutic and diagnostic applications. Using a deep learning-based hybrid human-AI pipeline that cross-references PubMed, the Gene Expression Omnibus, DisGeNET, The Cancer Genome Atlas and the NIH Molecular Imaging and Contrast Agent Database, we bridge individual genes in human cancers with respective theranostic compounds. Cross-referencing the Theranostic Genome with RNAseq data from over 17'000 human tissues identifies theranostic targets and lead compounds for various human cancers, and allows tailoring targeted theranostics to relevant cancer subpopulations. We expect the Theranostic Genome to facilitate the development of new targeted theranostics to better diagnose, understand, treat, and monitor a variety of human cancers.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Neoplasms",
- "Precision Medicine",
- "Genome, Human",
- "Theranostic Nanomedicine",
- "Deep Learning"
- ]
- },
- {
- "PMID": "39738052",
- "Title": "Nature communications",
- "ArticleTitle": "Characterizing mutation-treatment effects using clinico-genomics data of 78,287 patients with 20 types of cancers.",
- "Abstract": "Evaluating the effectiveness of cancer treatments in relation to specific tumor mutations is essential for improving patient outcomes and advancing the field of precision medicine. Here we represent a comprehensive analysis of 78,287 U.S. cancer patients with detailed somatic mutation profiling integrated with treatment and outcomes data extracted from electronic health records. We systematically identified 776 genomic alterations associated with survival outcomes across 20 distinct cancer types treated with specific immunotherapies, chemotherapies, or targeted therapies. Additionally, we demonstrate how mutations in particular pathways correlate with treatment response. Leveraging the large number of identified predictive mutations, we developed a machine learning model to generate a risk score for response to immunotherapy in patients with advanced non-small cell lung cancer (aNSCLC). Through rigorous computational analysis of large-scale\u00a0clinico-genomic real-world data, this research provides insights and lays the groundwork for further advancements in precision oncology.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Mutation",
- "Neoplasms",
- "Precision Medicine",
- "Genomics",
- "Immunotherapy",
- "Carcinoma, Non-Small-Cell Lung",
- "Machine Learning",
- "Female",
- "Male",
- "Treatment Outcome",
- "Electronic Health Records",
- "Lung Neoplasms"
- ]
- },
- {
- "PMID": "39738026",
- "Title": "Nature communications",
- "ArticleTitle": "DNA replication initiation drives focal mutagenesis and rearrangements in human cancers.",
- "Abstract": "The rate and pattern of mutagenesis in cancer genomes is significantly influenced by DNA accessibility and active biological processes. Here we show that efficient sites of replication initiation drive and modulate specific mutational processes in cancer. Sites of replication initiation impede nucleotide excision repair in melanoma and are off-targets for activation-induced deaminase (AICDA) activity in lymphomas. Using ductal pancreatic adenocarcinoma as a cancer model, we demonstrate that the initiation of DNA synthesis is error-prone at G-quadruplex-forming sequences in tumours displaying markers of replication stress, resulting in a previously recognised but uncharacterised mutational signature. Finally, we demonstrate that replication origins serve as hotspots for genomic rearrangements, including structural and copy number variations. These findings reveal replication origins as functional determinants of tumour biology and demonstrate that replication initiation both passively and actively drives focal mutagenesis in cancer genomes.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "DNA Replication",
- "Mutagenesis",
- "Pancreatic Neoplasms",
- "Neoplasms",
- "Cell Line, Tumor",
- "DNA Copy Number Variations",
- "G-Quadruplexes",
- "Gene Rearrangement",
- "Carcinoma, Pancreatic Ductal",
- "DNA Repair",
- "Mutation"
- ]
- },
- {
- "PMID": "39738003",
- "Title": "Nature communications",
- "ArticleTitle": "An antibody cocktail targeting two different CD73 epitopes enhances enzyme inhibition and tumor control.",
- "Abstract": "CD73, an ectoenzyme responsible for adenosine production, is often elevated in immuno-suppressive tumor environments. Inhibition of CD73 activity holds great promise as a therapeutic strategy for CD73-expressing cancers. In this study, we have developed a therapeutic anti-human CD73 antibody cocktail, HB0045. HB0045 is a 1:1 mixture of two humanized monoclonal IgG1 antibodies (mAbs), HB0038 and HB0039. The cocktail not only harnesses the advantages of its parental mAbs in enzyme inhibition but also shows a significantly greater capability of promoting T cell proliferation in vitro. Structural analyses show that HB0045 effectively locks the CD73 dimer in a \"partially open\" non-active conformation through a double lock mechanism. In various animal models of syngeneic and xenograft tumors, HB0045 inhibits tumor growth more potently than the single mAbs. Collectively, our findings provide functional and structural insights into the mechanism of a CD73-targeting antibody cocktail.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "5'-Nucleotidase",
- "Animals",
- "Humans",
- "Mice",
- "GPI-Linked Proteins",
- "Epitopes",
- "Cell Line, Tumor",
- "Xenograft Model Antitumor Assays",
- "Cell Proliferation",
- "Antibodies, Monoclonal, Humanized",
- "Neoplasms",
- "Female",
- "T-Lymphocytes",
- "Antibodies, Monoclonal",
- "Mice, Inbred BALB C",
- "Combined Antibody Therapeutics"
- ]
- },
- {
- "PMID": "39737979",
- "Title": "Nature communications",
- "ArticleTitle": "Cytokine-armed pyroptosis induces antitumor immunity against diverse types of tumors.",
- "Abstract": "Inflammasomes are defense complexes that utilize cytokines and immunogenic cell death (ICD) to stimulate the immune system against pathogens. Inspired by their dual action, we present cytokine-armed pyroptosis as a strategy for boosting immune response against diverse types of tumors. To induce pyroptosis, we utilize designed tightly regulated gasdermin D variants comprising different pore-forming capabilities and diverse modes of activation, representing a toolbox of ICD inducers. We demonstrate that the electrogenic transfer of ICD effector-encoding plasmids into mouse melanoma tumors when combined with intratumoral expression of cytokines IL-1\u03b2, IL-12, or IL-18, enhanced anti-tumor immune responses. Careful selection of immunostimulatory molecules is, however, imperative as a combination of IL-1\u03b2 and IL-18 antagonized the protective effect of pyroptosis by IFN\u03b3-mediated upregulation of several immunosuppressive pathways. Additionally, we show that the intratumoral introduction of armed pyroptosis provides protection against distant tumors and proves effective across various tumor types without inducing systemic inflammation. Deconstructed inflammasomes thus serve as a powerful, tunable, and tumor-agnostic strategy to enhance antitumor response, even against the most resilient types of tumors.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Pyroptosis",
- "Animals",
- "Mice",
- "Inflammasomes",
- "Mice, Inbred C57BL",
- "Humans",
- "Cell Line, Tumor",
- "Cytokines",
- "Melanoma, Experimental",
- "Interleukin-18",
- "Interleukin-1beta",
- "Phosphate-Binding Proteins",
- "Intracellular Signaling Peptides and Proteins",
- "Neoplasms",
- "Female",
- "Interferon-gamma",
- "Interleukin-12",
- "Gasdermins"
- ]
- },
- {
- "PMID": "39737928",
- "Title": "Nature communications",
- "ArticleTitle": "Towards designing improved cancer immunotherapy targets with a peptide-MHC-I presentation model, HLApollo.",
- "Abstract": "Based on the success of cancer immunotherapy, personalized cancer vaccines have emerged as a leading oncology treatment. Antigen presentation on MHC class I (MHC-I) is crucial for the adaptive immune response to cancer cells, necessitating highly predictive computational methods to model this phenomenon. Here, we introduce HLApollo, a transformer-based model for peptide-MHC-I (pMHC-I) presentation prediction, leveraging the language of peptides, MHC, and source proteins. HLApollo provides end-to-end treatment of MHC-I sequences and deconvolution of multi-allelic data, using a negative-set switching strategy to mitigate misassigned negatives in unlabelled ligandome data. HLApollo shows a 12.65% increase in average precision (AP) on ligandome data and a 4.1% AP increase on immunogenicity test data compared to next-best models. Incorporating protein features from protein language models yields further gains and reduces the need for gene expression measurements. Guided by clinical use, we demonstrate pan-allelic generalization which effectively captures rare alleles in underrepresented ancestries.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Immunotherapy",
- "Neoplasms",
- "Histocompatibility Antigens Class I",
- "Peptides",
- "Antigen Presentation",
- "Cancer Vaccines",
- "Alleles",
- "Computational Biology"
- ]
- },
- {
- "PMID": "39737671",
- "Title": "Archiv der Pharmazie",
- "ArticleTitle": "The current landscape of 1,2,3-triazole-(fused) six-membered nitrogen-containing heteroaromatic ring hybrids with anticancer therapeutic potential.",
- "Abstract": "Cancer, characterized by uncontrolled growth and spread of abnormal cells potentially influencing almost all tissues in the body, is one of the most devastating and lethal diseases throughout the world. Chemotherapy is one of the principal approaches for cancer treatment, but multidrug resistance and severe side effects represent the main barriers to the success of therapy, creating a vital need to develop novel chemotherapeutic agents. The 1,2,3-triazole moiety can be conveniently constructed by \"click chemistry\" and could exert diverse noncovalent interactions with various enzymes in cancer cells. Hence, 1,2,3-triazole is one of the most fascinating anticancer pharmacophores. Moreover, 1,2,3-triazole could also serve as a powerful ligation tool for the complex molecular architectures to increase the anticancer efficacy of lead molecules. Notably, 1,2,3-triazole-containing hybrids with intriguing structural variations could target different biological components in cancer cells simultaneously, highlighting their potential in the treatment and eradication of cancer. This review outlines the current landscape of 1,2,3-triazole-(fused) six-membered nitrogen-containing heteroaromatic ring hybrids, inclusive of 1,2,3-triazole-quinazolines, 1,2,3-triazole-quinazolinones, 1,2,3-triazole-quinolines, 1,2,3-triazole-quinolones, 1,2,3-triazole-pyridines, and 1,2,3-triazole-pyrimidines, with anticancer therapeutic potential, and explores their mechanisms of action, critical aspects of design as well as structure-activity relationships (SARs), covering articles published from 2021 to the present, to pave the way for the development of innovative and efficient therapeutic interventions for cancer therapy.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Animals",
- "Humans",
- "Antineoplastic Agents",
- "Molecular Structure",
- "Neoplasms",
- "Nitrogen",
- "Structure-Activity Relationship",
- "Triazoles"
- ]
- },
- {
- "PMID": "39737633",
- "Title": "Journal of pediatric hematology/oncology",
- "ArticleTitle": "Assessment of Antibody Levels and Vaccine-induced Serologic Responses After Completion of Cancer Treatment in Pediatric Patients: A 6-Year Experience in Turkey on HAV, HBV, VZV, and MMR Vaccinations.",
- "Abstract": "Post-treatment serological vaccine responses in children were lower than anticipated despite multiple doses. Given the potential need for periodic serological assessments and booster vaccinations, long-term follow-ups are planned.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Child",
- "Male",
- "Female",
- "Child, Preschool",
- "Retrospective Studies",
- "Turkey",
- "Adolescent",
- "Measles-Mumps-Rubella Vaccine",
- "Neoplasms",
- "Antibodies, Viral",
- "Infant",
- "Vaccination",
- "Hepatitis B Vaccines",
- "Chickenpox Vaccine",
- "Hepatitis A Vaccines",
- "Follow-Up Studies"
- ]
- },
- {
- "PMID": "39737568",
- "Title": "Briefings in bioinformatics",
- "ArticleTitle": "A comprehensive benchmark study of methods for identifying significantly perturbed subnetworks in cancer.",
- "Abstract": "Network-based methods utilize protein-protein interaction information to identify significantly perturbed subnetworks in cancer and to propose key molecular pathways. Numerous methods have been developed, but to date, a rigorous benchmark analysis to compare the performance of existing approaches is lacking. In this paper, we proposed a novel benchmarking framework using synthetic data and conducted a comprehensive analysis to investigate the ability of existing methods to detect target genes and subnetworks and to control false positives, and how they perform in the presence of topological biases at both gene and subnetwork levels. Our analysis revealed insights into algorithmic performance that were previously unattainable. Based on the results of the benchmark study, we presented a practical guide for users on how to select appropriate detection methods and protein-protein interaction networks for cancer pathway identification, and provided suggestions for future algorithm development.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Neoplasms",
- "Humans",
- "Benchmarking",
- "Algorithms",
- "Computational Biology",
- "Protein Interaction Maps",
- "Protein Interaction Mapping",
- "Gene Regulatory Networks"
- ]
- },
- {
- "PMID": "39737564",
- "Title": "Briefings in bioinformatics",
- "ArticleTitle": "Precise identification of somatic and germline variants in the absence of matched normal samples.",
- "Abstract": "Somatic variants play a crucial role in the occurrence and progression of cancer. However, in the absence of matched normal controls, distinguishing between germline and somatic variants becomes challenging in tumor samples. The existing tumor-only genomic analysis methods either suffer from limited performance or insufficient interpretability due to an excess of features. Therefore, there is an urgent need for an alternative approach that can address these issues and have practical implications. Here, we presented OncoTOP, a computational method for genomic analysis without matched normal samples, which can accurately distinguish somatic mutations from germline variants. Reference sample analysis revealed a 0% false positive rate and 99.7% reproducibility for variant calling. Assessing 2864 tumor samples across 18 cancer types yielded a 99.8% overall positive percent agreement and a 99.9% positive predictive value. OncoTOP can also accurately detect clinically actionable variants and subclonal mutations associated with drug resistance. For the prediction of mutation origins, the positive percent agreement stood at 97.4% for predicting somatic mutations and 95.7% for germline mutations. High consistency of tumor mutational burden (TMB) was observed between the results generated by OncoTOP and tumor-normal paired analysis. In a cohort of 97 lung cancer patients treated with immunotherapy, TMB-high patients had prolonged PFS (P\u2009=\u2009.02), proving the reliability of our approach in estimating TMB to predict therapy response. Furthermore, microsatellite instability status showed a strong concordance (97%) with polymerase chain reaction results, and leukocyte antigens class I subtypes and homozygosity achieved an impressive concordance rate of 99.3% and 99.9% respectively, compared to its tumor-normal paired analysis. Thus, OncoTOP exhibited high reliability in variant calling, mutation origin prediction, and biomarker estimation. Its application will promise substantial advantages for clinical genomic testing.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Germ-Line Mutation",
- "Neoplasms",
- "Reproducibility of Results",
- "Mutation",
- "Computational Biology",
- "Genomics",
- "Lung Neoplasms",
- "Biomarkers, Tumor"
- ]
- },
- {
- "PMID": "39737563",
- "Title": "Briefings in bioinformatics",
- "ArticleTitle": "Dual-stage optimizer for systematic overestimation adjustment applied to multi-objective genetic algorithms for biomarker selection.",
- "Abstract": "The selection of biomarker panels in omics data, challenged by numerous molecular features and limited samples, often requires the use of machine learning methods paired with wrapper feature selection techniques, like genetic algorithms. They test various feature sets-potential biomarker solutions-to fine-tune a machine learning model's performance for supervised tasks, such as classifying cancer subtypes. This optimization process is undertaken using validation sets to evaluate and identify the most effective feature combinations. Evaluations have performance estimation error, measurable as discrepancy between validation and test set performance, and when the selection involves many models the best ones are almost certainly overestimated. This issue is also relevant in a multi-objective feature selection process where various characteristics of the biomarker panels are optimized, such as predictive performances and feature set size. Methods have been proposed to reduce the overestimation after a model has already been selected in single-objective problems, but no algorithm existed capable of reducing the overestimation during the optimization, improving model selection, or applied in the more general multi-objective domain. We propose Dual-stage Optimizer for Systematic overestimation Adjustment in Multi-Objective problems (DOSA-MO), a novel multi-objective optimization wrapper algorithm that learns how the original estimation, its variance, and the feature set size of the solutions predict the overestimation. DOSA-MO adjusts the expectation of the performance during the optimization, improving the composition of the solution set. We verify that DOSA-MO improves the performance of a state-of-the-art genetic algorithm on left-out or external sample sets, when predicting cancer subtypes and/or patient overall survival, using three transcriptomics datasets for kidney and breast cancer.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Algorithms",
- "Biomarkers, Tumor",
- "Machine Learning",
- "Neoplasms",
- "Computational Biology"
- ]
- },
- {
- "PMID": "39737507",
- "Title": "The Indian journal of medical research",
- "ArticleTitle": "Global burden of cancer pattern in 2020 & prediction to 2040 among older adults.",
- "Abstract": "Background & objectives Cancer is one of the leading causes of death among older adults worldwide. The global burden of cancer among older individuals is increasing due to the ageing population. The increasing burden of cancer among older adults will pose significant social and economic challenges for the delivery of healthcare services. Materials Estimated cancer new cases, deaths, age-standardized truncated incidence and mortality rate per 100,000 for older adults (60 yr or above) were reported using GLOBOCAN 2020 estimates (gco.iarc.fr). Mortality to Incidence ratio (M/I ratio) expressed in percentage by gender and continent was provided. Results Globally, of all cancer cases, 11.3 million cases (representing 62.3%) and 7.5 million deaths (representing 71.2%) were seen among older adults. The top five leading sites of cancer account for 62.2 per cent of older men and 55.9 per cent of older women; however, a widespread geographical variation across world regions is observed. The number of new cancer cases among older adults is expected to rise from 11.3 to 19.8 million (a 75.2% increase) and deaths from 3.99 to 7.3 million (82.8% increase) by 2040. Interpretation & conclusions The expected rise will bring exceptional challenges to healthcare systems, especially in lower- or lower-medium-income countries where resources are limited. Data on cancer among older adults will help health planners and policymakers develop global geriatric cancer control policies.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Neoplasms",
- "Male",
- "Female",
- "Aged",
- "Global Health",
- "Middle Aged",
- "Incidence",
- "Aged, 80 and over",
- "Global Burden of Disease"
- ]
- },
- {
- "PMID": "39737190",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "Progress of cGAS-STING signaling pathway-based modulation of immune response by traditional Chinese medicine in clinical diseases.",
- "Abstract": "The cGAS-STING signaling pathway is a critical component of the innate immune response, playing a significant role in various diseases. As a central element of this pathway, STING responds to both endogenous and exogenous DNA stimuli, triggering the production of interferons and pro-inflammatory cytokines to enhance immune defenses against tumors and pathogens. However, dysregulated activation of the STING pathway is implicated in the pathogenesis of multiple diseases, including autoinflammation, viral infections, and cancer. Traditional Chinese Medicines (TCMs), which have a long history of use, have been associated with positive effects in disease prevention and treatment. TCM formulations (e.g., Lingguizhugan Decoction, Yi-Shen-Xie-Zhuo formula) and active compounds (e.g., Glabridin, Ginsenoside Rd) can modulate the cGAS-STING signaling pathway, thereby influencing the progression of inflammatory, infectious, or oncological diseases. This review explores the mechanisms by which TCMs interact with the cGAS-STING pathway to regulate immunity, focusing on their roles in infectious diseases, malignancies, and autoimmune disorders.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Nucleotidyltransferases",
- "Signal Transduction",
- "Membrane Proteins",
- "Medicine, Chinese Traditional",
- "Animals",
- "Neoplasms",
- "Drugs, Chinese Herbal",
- "Immunity, Innate",
- "Autoimmune Diseases"
- ]
- },
- {
- "PMID": "39737177",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "Pan-cancer analysis shows that BCAP31 is a potential prognostic and immunotherapeutic biomarker for multiple cancer types.",
- "Abstract": "BCAP31 has the potential to serve as a biomarker for cancer immunology, particularly in relation to immune cell infiltration, and as an indicator of poor prognosis. These findings provide a new perspective that could inform the development of more targeted cancer therapy strategies.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Neoplasms",
- "Biomarkers, Tumor",
- "Prognosis",
- "Gene Expression Regulation, Neoplastic",
- "Cell Line, Tumor",
- "Membrane Proteins",
- "Immunotherapy",
- "Female",
- "Male",
- "Tumor Microenvironment",
- "Lymphocytes, Tumor-Infiltrating",
- "DNA Copy Number Variations"
- ]
- },
- {
- "PMID": "39736787",
- "Title": "Journal of hematology & oncology",
- "ArticleTitle": "Dual inhibition of LAG-3 and PD-1 with IBI110 and sintilimab in advanced solid tumors: the first-in-human phase Ia/Ib study.",
- "Abstract": "ClinicalTrials.gov Identifier: NCT04085185.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Middle Aged",
- "Female",
- "Antibodies, Monoclonal, Humanized",
- "Aged",
- "Adult",
- "Lymphocyte Activation Gene 3 Protein",
- "Programmed Cell Death 1 Receptor",
- "Antineoplastic Combined Chemotherapy Protocols",
- "Neoplasms",
- "Immune Checkpoint Inhibitors",
- "Antigens, CD"
- ]
- },
- {
- "PMID": "39736754",
- "Title": "Health research policy and systems",
- "ArticleTitle": "A novel social-network-analysis-based approach for analyzing complex network of actors involved in accessibility of anti-cancer medications\u00a0in Iran.",
- "Abstract": "This study highlights the importance of complex relationships among various actors and proposes a novel SNA-based approach to analyse them. Regarding the main steps of the proposed approach and the findings, it is imperative for pharmaceutical policy plans to involve a diverse group of experts from the beginning, prioritizing the preferences of stakeholders, and providing a patient-centred approach to prevent the worsening of resource shortages.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Iran",
- "Health Services Accessibility",
- "Antineoplastic Agents",
- "Neoplasms",
- "Health Policy",
- "Social Network Analysis",
- "Policy Making",
- "Stakeholder Participation",
- "Surveys and Questionnaires",
- "Social Networking",
- "Drug Industry"
- ]
- },
- {
- "PMID": "39736712",
- "Title": "BMC medical education",
- "ArticleTitle": "Patient-centered interprofessional education in cancer care: a systematic scoping review.",
- "Abstract": "The findings indicate that patient-centered IPE programs effectively promote interprofessional collaboration and enhance clinical competencies in cancer care. Future research should focus on long-term evaluations, address systemic barriers, expand geographical scope, and utilize standardized evaluation frameworks to further improve the design and implementation of patient-centered IPE programs in cancer care.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Patient-Centered Care",
- "Neoplasms",
- "Interprofessional Relations",
- "Interprofessional Education",
- "Patient Care Team",
- "Health Personnel",
- "Cooperative Behavior"
- ]
- },
- {
- "PMID": "39736689",
- "Title": "Lipids in health and disease",
- "ArticleTitle": "Cardiometabolic index and mortality risks: elevated cancer and reduced cardiovascular mortality risk in a large cohort.",
- "Abstract": "This study represents the first comprehensive assessment on the contribution of CMI to mortality across an all-age adult population, providing some insights for the comprehensive assessment of health and disease states.",
- "Predictions": [
- "Diabetes",
- "Cancer",
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Neoplasms",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Longitudinal Studies",
- "Aged",
- "Proportional Hazards Models",
- "Diabetes Mellitus",
- "Risk Factors",
- "Cardiometabolic Risk Factors",
- "Cohort Studies"
- ]
- },
- {
- "PMID": "39736601",
- "Title": "BMC public health",
- "ArticleTitle": "Research on health information avoidance behavior and influencing factors of cancer patients-an empirical analysis based on structural equation modeling.",
- "Abstract": "Sociodemographic factors influencing cancer patients' health information avoidance behaviors include per capita monthly household income, occupation, treatment modality, number of years of smart device use, and number of hours per week reading health information. Self-efficacy and negative emotions mediated the analytic model of health information avoidance behavior in cancer patients, respectively.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Neoplasms",
- "Female",
- "Male",
- "Middle Aged",
- "Adult",
- "Self Efficacy",
- "Surveys and Questionnaires",
- "Latent Class Analysis",
- "Aged",
- "Socioeconomic Factors",
- "Avoidance Learning"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/cardiovascular_diseases.json b/model/data/cardiovascular_diseases.json
deleted file mode 100644
index ebda211a1a6fb4e0e6fe7b1c284c6371b9dc8051..0000000000000000000000000000000000000000
--- a/model/data/cardiovascular_diseases.json
+++ /dev/null
@@ -1,496 +0,0 @@
-[
- {
- "PMID": "39738226",
- "Title": "Scientific reports",
- "ArticleTitle": "Excessive daytime sleepiness and its predictors among type 2 diabetes mellitus patients at central ethiopia.",
- "Abstract": "Excessive daytime sleepiness is a common finding among type 2 diabetes mellitus patients. However there is scarce data that shows the magnitude of excessive daytime sleepiness, & its association with type 2 diabetes mellitus. Hence, the study aimed to assess the prevalence of excessive daytime sleepiness and its associated factors among type 2 diabetes mellitus patients at Wolkite University Specialized Hospital. A Hospital-based cross-sectional study was employed from January 15 to March 15, 2022, among 229 Type 2 diabetes mellitus patients. Data was collected by semi-structured questionnaires, then entered into the Epi data version 4.6 and exported to SPSS version 25.0 for analysis. Binary and multiple logistic regression analysis was used to assess factors associated with excessive daytime sleepiness and statistical significance was set at P-value\u2009<\u20090.05. The prevalence of Excessive daytime sleepiness among type 2 diabetes mellitus was 27.1%. Age (AOR: 1.08; 95%CI: 1.03, 1.12), frequent snoring (AOR: 2.9; 95%CI: 1.24, 6.80), comorbid hypertension (AOR: 2.64; 95%CI: 1.17, 5.96), obesity (AOR: 2.7; 95%CI: 1.03, 7.13), and poor glycemic control (AOR: 6.68; 95%CI: 1.83, 24.41) were independently associated with Excessive daytime sleepiness among type 2 diabetes mellitus patients. Excessive daytime sleepiness was reported in more than a quarter of type 2 diabetes mellitus patients. Age, frequent snoring, hypertension, obesity, and poor glycemic control were significantly associated with Excessive daytime sleepiness among type 2 diabetes mellitus patients. Therefore health care providers should assess not only for how well their patients' diabetes is controlled but also for excessive daytime sleepiness.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Ethiopia",
- "Male",
- "Female",
- "Middle Aged",
- "Disorders of Excessive Somnolence",
- "Cross-Sectional Studies",
- "Adult",
- "Prevalence",
- "Risk Factors",
- "Aged",
- "Hypertension",
- "Surveys and Questionnaires",
- "Comorbidity",
- "Obesity",
- "Snoring"
- ]
- },
- {
- "PMID": "39738181",
- "Title": "Scientific reports",
- "ArticleTitle": "Web application using machine learning to predict cardiovascular disease and hypertension in mine workers.",
- "Abstract": "This study presents a web application for predicting cardiovascular disease (CVD) and hypertension (HTN) among mine workers using machine learning (ML) techniques. The dataset, collected from 699 participants at the Gol-Gohar mine in Iran between 2016 and 2020, includes demographic, occupational, lifestyle, and medical information. After preprocessing and feature engineering, the Random Forest algorithm was identified as the best-performing model, achieving 99% accuracy for HTN prediction and 97% for CVD, outperforming other algorithms such as Logistic Regression and Support Vector Machines. These high accuracies are crucial for occupational health management, where early detection of health risks can significantly reduce morbidity and mortality among workers exposed to environmental and occupational hazards. The web application provides personalized risk assessments based on key factors, such as age, employment history, family health background, and exposure to environmental risks like dust and noise. By offering actionable insights, the model enables targeted interventions, including workplace modifications and lifestyle recommendations, to mitigate the risk of CVD and HTN. This tool demonstrates the potential of ML to enhance preventive health strategies in high-risk occupational settings.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Hypertension",
- "Machine Learning",
- "Male",
- "Adult",
- "Middle Aged",
- "Female",
- "Iran",
- "Risk Assessment",
- "Internet",
- "Occupational Health",
- "Miners",
- "Mining",
- "Risk Factors",
- "Occupational Diseases"
- ]
- },
- {
- "PMID": "39738021",
- "Title": "Nature communications",
- "ArticleTitle": "Oxidative potential and persistent free radicals in dust storm particles and their associations with hospitalization.",
- "Abstract": "Sand and dust storms (SDS) can cause adverse health effects, with the oxidative potential (OP) and environmentally persistent free radicals (EPFRs) inducing oxidative stress. We mapped the OP and EPFRs concentrations at 1735 sites in China during SDS periods using experimental data for 2021-2023 and a random forest model. We examined 855,869 hospitalizations during SDS events for 2015-2022 in Beijing, China. An integrated exposure-response model was used to estimate the association between OP and EPFRs and hospitalization during SDS. EPFRs were strongly associated with circulatory (3.05%; 95% confidence interval [CI]: 1.01%, 4.08%) and respiratory (2.02%; 95% CI: 1.01%, 4.08%) diseases with each increase of 10",
- "Predictions": [
- "Chronic respiratory disease",
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Dust",
- "Humans",
- "Hospitalization",
- "Free Radicals",
- "Air Pollutants",
- "Oxidative Stress",
- "Particulate Matter",
- "China",
- "Environmental Exposure",
- "Beijing",
- "Sand",
- "Respiratory Tract Diseases",
- "Oxidation-Reduction",
- "Cardiovascular Diseases"
- ]
- },
- {
- "PMID": "39738016",
- "Title": "Nature communications",
- "ArticleTitle": "Alcohol-induced gut microbial reorganization and associated overproduction of phenylacetylglutamine promotes cardiovascular disease.",
- "Abstract": "The mechanism(s) underlying gut microbial metabolite (GMM) contribution towards alcohol-mediated cardiovascular disease (CVD) is unknown. Herein we observe elevation in circulating phenylacetylglutamine (PAGln), a known CVD-associated GMM, in individuals living with alcohol use disorder. In a male murine binge-on-chronic alcohol model, we confirm gut microbial reorganization, elevation in PAGln levels, and the presence of cardiovascular pathophysiology. Fecal microbiota transplantation from pair-/alcohol-fed mice into na\u00efve male mice demonstrates the transmissibility of PAGln production and the CVD phenotype. Independent of alcohol exposure, pharmacological-mediated increases in PAGln elicits direct cardiac and vascular dysfunction. PAGln induced hypercontractility and altered calcium cycling in isolated cardiomyocytes providing evidence of improper relaxation which corresponds to elevated filling pressures observed in vivo. Furthermore, PAGln directly induces vascular endothelial cell activation through induction of oxidative stress leading to endothelial cell dysfunction. We thus reveal that the alcohol-induced microbial reorganization and resultant GMM elevation, specifically PAGln, directly contributes to CVD.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Animals",
- "Gastrointestinal Microbiome",
- "Male",
- "Glutamine",
- "Cardiovascular Diseases",
- "Mice",
- "Humans",
- "Mice, Inbred C57BL",
- "Myocytes, Cardiac",
- "Ethanol",
- "Oxidative Stress",
- "Fecal Microbiota Transplantation",
- "Alcoholism",
- "Disease Models, Animal",
- "Female",
- "Glutamates",
- "Endothelial Cells",
- "Middle Aged"
- ]
- },
- {
- "PMID": "39736942",
- "Title": "Archives of Razi Institute",
- "ArticleTitle": "Morbidity profile of the patients attending Mobile Medical Unit camps in Telangana: A record-based study.",
- "Abstract": "Mobile Medical Units (MMUs) are one of the major initiatives under the National Rural Health Mission. These MMUs help people in remote, underserved areas access healthcare at affordable prices on their doorstep. The present record-based study aimed to assess the morbidity profile of the patients attending Mobile Medical Unit camps in the Yadadri-Bhuvanagiri district between April 2022 and December 2022. The MMU is run by the Department of Community and Family Medicine, AIIMS, Bibinagar, in six selected villages of the Yadadri-Bhuvanagiri district. A register is maintained to record the details of patients visiting the MMU camp. Patient's name, age, gender, place, mobile number, height, weight, blood pressure (BP), glucometer Random Blood Sugar, diagnosis, and details of medication dispensed were entered in the register. Diabetes, hypertension, and obesity were diagnosed using the World Health Organization\u00a0(WHO) criteria, the Eighth Joint National Committee guidelines, and WHO Asia Pacific guidelines, respectively. Mobile Medical Unit Camp data are entered into the Excel database at the end of every month. Since it is a record-based analysis, we used data for analysis between April 7, 2022, and December 31, 2022. A total of 1494 patients were treated in the MMU camps during this period. Among them, 89.4% were adults, and 10.6% were children (less than 18 years). Among 1,336 adult patients, the majority of participants suffered from osteoarthritis, followed by non-communicable diseases (NCDs). The mean scores of systolic and diastolic BP of the adult population were obtained at 131\u00b121 and 77\u00b113 mm Hg, respectively. The mean random blood glucose level of the adult population was 150\u00b174 mg/dl. A total of 158 children were younger than 18 years old, out of whom 78 and 80 participants were males and females, respectively. Moreover, 23.1% and 25% of males and females suffered from upper respiratory tract infections, respectively. The study further suggests that the NCD epidemic is spreading to rural areas where necessary health infrastructure is insufficient. MMUs can bring a significant change to the public health system, which needs to re-orient its priorities.",
- "Predictions": [
- "Diabetes"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Adult",
- "Mobile Health Units",
- "Middle Aged",
- "Adolescent",
- "Aged",
- "Child",
- "Young Adult",
- "India",
- "Morbidity",
- "Hypertension",
- "Child, Preschool",
- "Obesity",
- "Infant",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39736858",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Association of oxidative balance score with cardiovascular disease and all-cause and cardiovascular mortality in American adults with type 2 diabetes: data from the National Health and Nutrition examination survey 1999-2018.",
- "Abstract": "Adherence to higher OBS was associated with reduced CVD prevalence and mortality risk in T2D. Antioxidant diet and lifestyle had more significant associations with mortality and CVD prevalence, respectively. However, as these findings are merely associations and do not allow causal inferences to be drawn, future validation in high-quality randomized controlled trials is needed.",
- "Predictions": [
- "Cardiovascular diseases",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Cardiovascular Diseases",
- "Male",
- "Female",
- "Middle Aged",
- "Nutrition Surveys",
- "Adult",
- "Oxidative Stress",
- "United States",
- "Aged",
- "Life Style",
- "Diet",
- "Risk Factors",
- "Follow-Up Studies",
- "Prevalence"
- ]
- },
- {
- "PMID": "39736721",
- "Title": "BMC medicine",
- "ArticleTitle": "Changes in sarcopenia and incident cardiovascular disease in prospective cohorts.",
- "Abstract": "Changes in sarcopenia status are associated with varying risks of new-onset CVD. Progression in sarcopenia status increases the risk, while recovery from sarcopenia reduces the risk of developing cardiovascular disease.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Sarcopenia",
- "Female",
- "Male",
- "Middle Aged",
- "Prospective Studies",
- "Cardiovascular Diseases",
- "Incidence",
- "Aged",
- "China",
- "Longitudinal Studies",
- "Risk Factors",
- "Proportional Hazards Models"
- ]
- },
- {
- "PMID": "39736689",
- "Title": "Lipids in health and disease",
- "ArticleTitle": "Cardiometabolic index and mortality risks: elevated cancer and reduced cardiovascular mortality risk in a large cohort.",
- "Abstract": "This study represents the first comprehensive assessment on the contribution of CMI to mortality across an all-age adult population, providing some insights for the comprehensive assessment of health and disease states.",
- "Predictions": [
- "Diabetes",
- "Cancer",
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Neoplasms",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Longitudinal Studies",
- "Aged",
- "Proportional Hazards Models",
- "Diabetes Mellitus",
- "Risk Factors",
- "Cardiometabolic Risk Factors",
- "Cohort Studies"
- ]
- },
- {
- "PMID": "39736563",
- "Title": "BMC cardiovascular disorders",
- "ArticleTitle": "The predictive role of the hs-CRP/HDL-C ratio for long-term mortality in the general population: evidence from a cohort study.",
- "Abstract": "The hs-CRP/HDL-C ratio is a crucial predictor of long-term mortality in the general population, independent of potential confounding factors.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Cholesterol, HDL",
- "Retrospective Studies",
- "C-Reactive Protein",
- "Biomarkers",
- "Cardiovascular Diseases",
- "Risk Assessment",
- "Adult",
- "Predictive Value of Tests",
- "Time Factors",
- "Nutrition Surveys",
- "Cause of Death",
- "Prognosis",
- "United States",
- "Risk Factors",
- "Aged"
- ]
- },
- {
- "PMID": "39736518",
- "Title": "BMC cardiovascular disorders",
- "ArticleTitle": "Effect of sodium glucose cotransporter-2 inhibitors (SGLT-2is) on the clinical outcomes of patients with diabetic atrial fibrillation.",
- "Abstract": "In our study, SGLT-2i treatment was associated with a significant reduction in all-cause mortality and major bleeding in diabetic AF patients. Our study provides evidence of the clinical benefit of SGLT-2i in AF patients.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Male",
- "Atrial Fibrillation",
- "Retrospective Studies",
- "Female",
- "Aged",
- "Treatment Outcome",
- "Middle Aged",
- "Diabetes Mellitus, Type 2",
- "Time Factors",
- "Risk Factors",
- "Risk Assessment",
- "Hemorrhage",
- "Aged, 80 and over",
- "Cause of Death",
- "Myocardial Infarction"
- ]
- },
- {
- "PMID": "39736180",
- "Title": "Food chemistry",
- "ArticleTitle": "Recent developments, challenges, and prospects of dietary omega-3 PUFA-fortified foods: Focusing on their effects on cardiovascular diseases.",
- "Abstract": "Dietary omega-3 polyunsaturated fatty acids (D\u03c9-3 PUFAs) have been extensively studied and have been proven to offer notable benefits for heart health. Scientific meta-analysis strongly endorses them as potent bioactive agents capable of preventing and managing cardiovascular diseases (CVDs). Fortification of foods with D\u03c9-3 PUFAs is a potential strategy for enhancing D\u03c9-3 PUFA intake in an effort to continue strengthening public health outcomes. This review analyzed recent trends in the fortification of foods with D\u03c9-3 PUFAs in relation to technological developments, challenges linked to the method, and future scope. Additionally, recent clinical trials and research on the effect of D\u03c9-3 PUFA-fortified food consumption on cardiovascular health are reviewed. Technological trends in fortification methods, namely microencapsulation- and nanoencapsulation, have made considerable progress to date, along with excellent stability in both processing and storage conditions and favorable bioaccessibility and sensory attributes of fortified foods. There is a tremendous deal of promise for cardiovascular health based on recent clinical trial findings that fortifying food with D\u03c9-3 PUFAs decreased the incidence of heart disease, blood pressure, and lipid profiles. In summary, substantial progress has been made in addressing the challenges of D\u03c9-3 PUFA fortification. However, further multidisciplinary research is needed to inculcate effectiveness toward achieving the maximum possible D\u03c9-3 PUFAs to protect against the harmful effects of CVDs and continue global health progress.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Food, Fortified",
- "Fatty Acids, Omega-3",
- "Animals"
- ]
- },
- {
- "PMID": "39736025",
- "Title": "Polish journal of veterinary sciences",
- "ArticleTitle": "Cardiovascular problems in rabbits in reference to hypothyroidism - a four-year retrospective study.",
- "Abstract": "The effects of T4 are mainly manifested by positive ino- and chronotropism. The syndrome accompanying hypothyroidism in rabbits (impaired myocardial contractility and reduced ejection capacity) is caused by a deficiency of thyroid hormones - especially T4. The study group consisted of a total of 41 animals: 15 males and 26 females, ranging in age from 2 months to 8 years, with echocardiogram showing reduced fractional shortening (<30%), with normal results of heamatological and biochemical tests. Blood was collected in order to measure T4 level. Echocardiographic examinations were performed with two-dimensional (2D) imaging, M-mode measurements and the pulsed/colour-labelled Doppler technique. Statistical analysis was performed using Statistica 13.0. Correlations were determined: between serum thyroxine concentration and the value of the fraction of shortening in the groups: young animals (up to 5 years of age) and older animals, females and males, and sterilised and non-sterilised animals. Statistical analysis showed a positive correlation between T4 levels in the blood of the test animals and myocardial fractional shortening and heart rate and left-atrial to aortic ratio (LA/Ao) in the pre-treatment period. A positive correlation was also shown after dividing the patients into 2 groups based on their age (below 5 years vs. 5 years and over), sex (male and female rabbits) and fact of sterilization (yes/no). Our study unequivocally confirmed a positive correlation between the decreased serum T4 concentration and reduced fractional shortening, indicating decreased cardiac systolic function in hypothyroid rabbits.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Animals",
- "Rabbits",
- "Male",
- "Hypothyroidism",
- "Female",
- "Retrospective Studies",
- "Thyroxine",
- "Cardiovascular Diseases",
- "Echocardiography"
- ]
- },
- {
- "PMID": "39735642",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Leukocyte telomere length decreased the risk of mortality in patients with alcohol-associated liver disease.",
- "Abstract": "Our research found that longer LTL improved survival in patients with ALD and decreased CVD and cancer-related mortality. LTL decreased all-cause mortality especially for patients older than 65 years or men. LTL might be a useful biomarker for prognosis among patients with ALD. More prospective studies are needed to assess the relevance between LTL and mortality and explore the underlying mechanisms between them.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Leukocytes",
- "Liver Diseases, Alcoholic",
- "Telomere",
- "Adult",
- "Nutrition Surveys",
- "Prognosis",
- "Telomere Homeostasis",
- "Aged",
- "Risk Factors",
- "Cardiovascular Diseases"
- ]
- },
- {
- "PMID": "39735551",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "CD73: agent development potential and its application in diabetes and atherosclerosis.",
- "Abstract": "CD73, an important metabolic and immune escape-promoting gene, catalyzes the hydrolysis of adenosine monophosphate (AMP) to adenosine (ADO). AMP has anti-inflammatory and vascular relaxant properties, while ADO has a strong immunosuppressive effect, suggesting that CD73 has pro-inflammatory and immune escape effects. However, CD73 also decreased proinflammatory reaction, suggesting that CD73 has a positive side to the body. Indeed, CD73 plays a protective role in diabetes, while with age, CD73 changes from anti-atherosclerosis to pro-atherosclerosis. The upregulation of CD73 with agents, including AGT-5, Aire-overexpressing DCs, Aspirin, BAFFR-Fc, CD4+ peptide, ICAs, IL-2 therapies, SAgAs, sCD73, stem cells, RAD51 inhibitor, TLR9 inhibitor, and VD, decreased diabetes and atherosclerosis development. However, the downregulation of CD73 with agents, including benzothiadiazine derivatives and CD73 siRNA, reduced atherosclerosis. Notably, many CD73 agents were investigated in clinical trials. However, no agents were used to treat diabetes and atherosclerosis. Most agents were CD73 inhibitors. Only FP-1201, a CD73 agonist, was investigated in clinical trials but its further development was discontinued. In addition, many lncRNAs, circRNAs, and genes are located at the same chromosomal location as CD73. In particular, circNT5E promoted CD73 expression. circNT5E may be a promising target for agent development. This mini-review focuses on the current state of knowledge of CD73 in diabetes, atherosclerosis, and its potential role in agent development.",
- "Predictions": [
- "Diabetes"
- ],
- "MeshTerms": [
- "Humans",
- "Atherosclerosis",
- "5'-Nucleotidase",
- "Animals",
- "Diabetes Mellitus",
- "GPI-Linked Proteins",
- "Drug Development"
- ]
- },
- {
- "PMID": "39735545",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "Single chain fragment variable, a new theranostic approach for cardiovascular diseases.",
- "Abstract": "Cardiovascular diseases (CVDs) remain a significant global health challenge, leading to substantial morbidity and mortality. Despite recent advancements in CVD management, pharmaceutical treatments often suffer from poor pharmacokinetics and high toxicity. With the rapid progress of modern molecular biology and immunology, however, single-chain fragment variable (scFv) molecule engineering has emerged as a promising theranostic tool to offer specificity and versatility in targeting CVD-related antigens. To represent the latest development on the potential of scFv in the context of CVDs, this review summarized the new mechanism of action and applications as therapeutic, as well as diagnostic agents. Furthermore, the advantages of scFv, including its small size, ease of modification, and ability to be engineered for enhanced affinity and specificity, are also described. Finally, such challenges as immunogenicity, stability, and scalability, alongside strategies to overcome these hurdles, are deeply scrutinized to provide safer and more effective strategies for the diagnosis and treatment of the incurable CVDs.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Single-Chain Antibodies",
- "Animals",
- "Theranostic Nanomedicine",
- "Precision Medicine"
- ]
- },
- {
- "PMID": "39735488",
- "Title": "Turkish journal of medical sciences",
- "ArticleTitle": "Thyroid and cardiovascular diseases.",
- "Abstract": "The thyroid gland is one of the major regulator organs of hemostasis in the human body, controlling the functioning of numerous systems. Thyroid hormones exert a modulating effect on the cardiovascular system in particular, ensuring optimal functioning within the normal range. Triiodothyronine (T3), as an active form of thyroid hormone, is mainly responsible for this effect via both genomic and nongenomic mechanisms. It has been reported that overt thyroid disorders are associated with a number of cardiovascular diseases and cardiac mortality. While hyperthyroidism appears to be related to atrial fibrillation and heart failure, the most pronounced cardiovascular complication of hypothyroidism seems to be atherosclerosis. Achieving euthyroidism is of great importance for restoring cardiovascular function. However, depending on the underlying health conditions, this may not be possible for all patients. Furthermore, there has been a growing focus on the role of subclinical thyroid dysfunctions and their impacts on the cardiovascular system in recent years. The pattern of cardiovascular abnormalities in subclinical thyroid disorders appears to parallel that of overt hypothyroidism, suggesting that even mild alterations in thyroid hormone levels may also have effects on the cardiovascular system. The management of subclinical thyroid disease remains controversial. Current evidence suggests that patient age and underlying cardiovascular diseases are major factors in clinical decision-making.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Hypothyroidism",
- "Hyperthyroidism",
- "Thyroid Diseases",
- "Thyroid Gland",
- "Thyroid Hormones"
- ]
- },
- {
- "PMID": "39735485",
- "Title": "Turkish journal of medical sciences",
- "ArticleTitle": "Cardiac effects and comorbidities of neurological diseases.",
- "Abstract": "Neurological disorders encompass a complex and heterogeneous spectrum of diseases affecting the brain, spinal cord, and peripheral nervous system, each presenting unique challenges that extend well beyond primary neurological symptoms. These disorders profoundly impact cardiovascular health, prompting an intensified exploration into the intricate interconnections between the neurological and cardiovascular systems. This review synthesizes current insights and research on cardiovascular comorbidities associated with major neurological conditions, including stroke, epilepsy, Parkinson's disease, multiple sclerosis, and Alzheimer's disease. The cardiovascular sequelae of these neurological disorders are multifactorial. For instance, strokes not only predispose individuals to arrhythmia and heart failure but also exacerbate preexisting cardiovascular risk factors. Similarly, epilepsy is associated with autonomic dysregulation and an elevated risk of sudden cardiac death, underscoring the necessity for vigilant cardiac monitoring in affected individuals. Parkinson's disease manifests with orthostatic hypotension and cardiac sympathetic denervation, significantly contributing to morbidity. Additionally, multiple sclerosis and Alzheimer's disease exhibit cardiovascular autonomic dysfunction and heightened cardiovascular risk, underscoring the need for proactive management strategies. Mechanistically, these conditions disrupt autonomic nervous system regulation, induce chronic inflammation, and may share genetic susceptibilities, each contributing to cardiovascular pathology. Effective management of these complexities requires an integrative approach that includes risk factor modification, pharmacotherapy, lifestyle interventions, and comprehensive patient education. Future research directions include identifying novel therapeutic targets, conducting large-scale clinical trials, and investigating genetic biomarkers to individualize treatment strategies. By addressing the multifaceted interactions between neurological disorders and cardiovascular health, healthcare providers can optimize patient care, reducing cardiovascular morbidity and mortality in this vulnerable population.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Comorbidity",
- "Nervous System Diseases",
- "Cardiovascular Diseases",
- "Parkinson Disease",
- "Risk Factors",
- "Multiple Sclerosis"
- ]
- },
- {
- "PMID": "39735480",
- "Title": "Turkish journal of medical sciences",
- "ArticleTitle": "Burden of comorbidities in heart failure patients in T\u00fcrkiye.",
- "Abstract": "The most common comorbidities in cases of HF in T\u00fcrkiye are HT, ASCVD, dyslipidemia, DM, COPD, anemia, and AF, respectively, and more than 90% of patients have \u22652 comorbidities. While ASCVD and dyslipidemia were more common in male patients, anemia, DM, and anxiety disorders were more common in female patients. The number of comorbid conditions increased with advanced age.",
- "Predictions": [
- "Diabetes"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Heart Failure",
- "Comorbidity",
- "Middle Aged",
- "Aged",
- "Adult",
- "Turkey",
- "Prevalence",
- "Young Adult",
- "Adolescent",
- "Aged, 80 and over",
- "Hypertension",
- "Diabetes Mellitus",
- "Pulmonary Disease, Chronic Obstructive",
- "Anemia",
- "Dyslipidemias"
- ]
- },
- {
- "PMID": "39735416",
- "Title": "Journal of diabetes research",
- "ArticleTitle": "Age Characteristics of Patients With Type 2 Diabetic Foot Ulcers and Predictive Risk Factors for Lower Limb Amputation: A Population-Based Retrospective Study.",
- "Abstract": {
- "b": "Conclusion:"
- },
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetic Foot",
- "Amputation, Surgical",
- "Male",
- "Middle Aged",
- "Female",
- "Risk Factors",
- "Aged",
- "Diabetes Mellitus, Type 2",
- "Retrospective Studies",
- "Lower Extremity",
- "Age Factors",
- "China",
- "Adult",
- "Prevalence",
- "Aged, 80 and over"
- ]
- },
- {
- "PMID": "39735415",
- "Title": "Journal of diabetes research",
- "ArticleTitle": "Metabolomic Profiling Reveals Biomarkers in Coronary Heart Disease Comorbidity.",
- "Abstract": {
- "b": "Conclusion:"
- },
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Metabolomics",
- "Middle Aged",
- "Coronary Disease",
- "Biomarkers",
- "Diabetes Mellitus, Type 2",
- "Comorbidity",
- "Depression",
- "Hypertension",
- "Aged",
- "Gas Chromatography-Mass Spectrometry",
- "Metabolome",
- "Adult",
- "Case-Control Studies"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/chronic_respiratory_disease.json b/model/data/chronic_respiratory_disease.json
deleted file mode 100644
index e37b036ffe8de271bb6954e61c15127706d7289a..0000000000000000000000000000000000000000
--- a/model/data/chronic_respiratory_disease.json
+++ /dev/null
@@ -1,485 +0,0 @@
-[
- {
- "PMID": "39738052",
- "Title": "Nature communications",
- "ArticleTitle": "Characterizing mutation-treatment effects using clinico-genomics data of 78,287 patients with 20 types of cancers.",
- "Abstract": "Evaluating the effectiveness of cancer treatments in relation to specific tumor mutations is essential for improving patient outcomes and advancing the field of precision medicine. Here we represent a comprehensive analysis of 78,287 U.S. cancer patients with detailed somatic mutation profiling integrated with treatment and outcomes data extracted from electronic health records. We systematically identified 776 genomic alterations associated with survival outcomes across 20 distinct cancer types treated with specific immunotherapies, chemotherapies, or targeted therapies. Additionally, we demonstrate how mutations in particular pathways correlate with treatment response. Leveraging the large number of identified predictive mutations, we developed a machine learning model to generate a risk score for response to immunotherapy in patients with advanced non-small cell lung cancer (aNSCLC). Through rigorous computational analysis of large-scale\u00a0clinico-genomic real-world data, this research provides insights and lays the groundwork for further advancements in precision oncology.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Mutation",
- "Neoplasms",
- "Precision Medicine",
- "Genomics",
- "Immunotherapy",
- "Carcinoma, Non-Small-Cell Lung",
- "Machine Learning",
- "Female",
- "Male",
- "Treatment Outcome",
- "Electronic Health Records",
- "Lung Neoplasms"
- ]
- },
- {
- "PMID": "39738021",
- "Title": "Nature communications",
- "ArticleTitle": "Oxidative potential and persistent free radicals in dust storm particles and their associations with hospitalization.",
- "Abstract": "Sand and dust storms (SDS) can cause adverse health effects, with the oxidative potential (OP) and environmentally persistent free radicals (EPFRs) inducing oxidative stress. We mapped the OP and EPFRs concentrations at 1735 sites in China during SDS periods using experimental data for 2021-2023 and a random forest model. We examined 855,869 hospitalizations during SDS events for 2015-2022 in Beijing, China. An integrated exposure-response model was used to estimate the association between OP and EPFRs and hospitalization during SDS. EPFRs were strongly associated with circulatory (3.05%; 95% confidence interval [CI]: 1.01%, 4.08%) and respiratory (2.02%; 95% CI: 1.01%, 4.08%) diseases with each increase of 10",
- "Predictions": [
- "Chronic respiratory disease",
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Dust",
- "Humans",
- "Hospitalization",
- "Free Radicals",
- "Air Pollutants",
- "Oxidative Stress",
- "Particulate Matter",
- "China",
- "Environmental Exposure",
- "Beijing",
- "Sand",
- "Respiratory Tract Diseases",
- "Oxidation-Reduction",
- "Cardiovascular Diseases"
- ]
- },
- {
- "PMID": "39737564",
- "Title": "Briefings in bioinformatics",
- "ArticleTitle": "Precise identification of somatic and germline variants in the absence of matched normal samples.",
- "Abstract": "Somatic variants play a crucial role in the occurrence and progression of cancer. However, in the absence of matched normal controls, distinguishing between germline and somatic variants becomes challenging in tumor samples. The existing tumor-only genomic analysis methods either suffer from limited performance or insufficient interpretability due to an excess of features. Therefore, there is an urgent need for an alternative approach that can address these issues and have practical implications. Here, we presented OncoTOP, a computational method for genomic analysis without matched normal samples, which can accurately distinguish somatic mutations from germline variants. Reference sample analysis revealed a 0% false positive rate and 99.7% reproducibility for variant calling. Assessing 2864 tumor samples across 18 cancer types yielded a 99.8% overall positive percent agreement and a 99.9% positive predictive value. OncoTOP can also accurately detect clinically actionable variants and subclonal mutations associated with drug resistance. For the prediction of mutation origins, the positive percent agreement stood at 97.4% for predicting somatic mutations and 95.7% for germline mutations. High consistency of tumor mutational burden (TMB) was observed between the results generated by OncoTOP and tumor-normal paired analysis. In a cohort of 97 lung cancer patients treated with immunotherapy, TMB-high patients had prolonged PFS (P\u2009=\u2009.02), proving the reliability of our approach in estimating TMB to predict therapy response. Furthermore, microsatellite instability status showed a strong concordance (97%) with polymerase chain reaction results, and leukocyte antigens class I subtypes and homozygosity achieved an impressive concordance rate of 99.3% and 99.9% respectively, compared to its tumor-normal paired analysis. Thus, OncoTOP exhibited high reliability in variant calling, mutation origin prediction, and biomarker estimation. Its application will promise substantial advantages for clinical genomic testing.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Germ-Line Mutation",
- "Neoplasms",
- "Reproducibility of Results",
- "Mutation",
- "Computational Biology",
- "Genomics",
- "Lung Neoplasms",
- "Biomarkers, Tumor"
- ]
- },
- {
- "PMID": "39737457",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Impact of COVID-19 vaccination on adolescent and youth students' mental health and bullying behaviors after the lifting of COVID-19 restrictions in China.",
- "Abstract": "This study suggests that COVID-19 vaccination will not only protect students' physical health, but also improve mental health. It is crucial to explore the mechanism between vaccination and mental health problems and bullying behaviors in further studies.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Adolescent",
- "China",
- "COVID-19",
- "Male",
- "Female",
- "Students",
- "Bullying",
- "COVID-19 Vaccines",
- "Surveys and Questionnaires",
- "Mental Health",
- "Vaccination",
- "Depression",
- "Anxiety",
- "SARS-CoV-2",
- "Stress Disorders, Post-Traumatic"
- ]
- },
- {
- "PMID": "39735753",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Chronic impacts of natural infrastructure on the physical and psychological health of university students during and after COVID-19: a case study of Chengdu, China.",
- "Abstract": "The study emphasizes the importance of incorporating natural elements into urban planning to enhance outdoor activity and well-being, especially in post-pandemic settings. Recommendations are provided for future urban design to address the therapeutic needs of specific populations.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "China",
- "Students",
- "Universities",
- "Male",
- "Female",
- "Mental Health",
- "Young Adult",
- "Adult",
- "SARS-CoV-2",
- "City Planning"
- ]
- },
- {
- "PMID": "39735752",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Effects of a flexibly delivered group-based acceptance and commitment therapy on reducing stress and enhancing psychological wellbeing in parents of school-age children during the COVID-19 pandemic: a quasi-experimental study.",
- "Abstract": "The findings highlight the potential of group-based Acceptance and Commitment Therapy to alleviate stress and improve psychological well-being in parents of school-age children, regardless of the delivery method, especially during crises such as the COVID-19 pandemic. However, due to limitations in the study design, caution is warranted when interpreting the overall effects of group-based ACT on parent outcomes and the moderating role of delivery methods. Further research is needed to validate these findings and explore the nuances of delivery methods in similar real-world situations.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Acceptance and Commitment Therapy",
- "Female",
- "Male",
- "Parents",
- "Stress, Psychological",
- "Adult",
- "Child",
- "Hong Kong",
- "Middle Aged",
- "SARS-CoV-2",
- "Psychotherapy, Group",
- "Pandemics",
- "Mental Health"
- ]
- },
- {
- "PMID": "39735533",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "Development of a urine-based metabolomics approach for multi-cancer screening and tumor origin prediction.",
- "Abstract": "Our study demonstrates the potential of urine-based metabolomics for multi-cancer early detection. The approach offers non-invasive cancer screening, promising widespread implementation in population-based programs for early detection and improved outcomes. Further validation and expansion are needed for broader clinical applicability.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Early Detection of Cancer",
- "Metabolomics",
- "Male",
- "Female",
- "Biomarkers, Tumor",
- "Middle Aged",
- "Aged",
- "Stomach Neoplasms",
- "Colorectal Neoplasms",
- "Metabolome",
- "Adult",
- "Lung Neoplasms",
- "Neoplasms"
- ]
- },
- {
- "PMID": "39735480",
- "Title": "Turkish journal of medical sciences",
- "ArticleTitle": "Burden of comorbidities in heart failure patients in T\u00fcrkiye.",
- "Abstract": "The most common comorbidities in cases of HF in T\u00fcrkiye are HT, ASCVD, dyslipidemia, DM, COPD, anemia, and AF, respectively, and more than 90% of patients have \u22652 comorbidities. While ASCVD and dyslipidemia were more common in male patients, anemia, DM, and anxiety disorders were more common in female patients. The number of comorbid conditions increased with advanced age.",
- "Predictions": [
- "Diabetes"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Heart Failure",
- "Comorbidity",
- "Middle Aged",
- "Aged",
- "Adult",
- "Turkey",
- "Prevalence",
- "Young Adult",
- "Adolescent",
- "Aged, 80 and over",
- "Hypertension",
- "Diabetes Mellitus",
- "Pulmonary Disease, Chronic Obstructive",
- "Anemia",
- "Dyslipidemias"
- ]
- },
- {
- "PMID": "39734100",
- "Title": "Journal of research on adolescence : the official journal of the Society for Research on Adolescence",
- "ArticleTitle": "Adolescents in various contexts during the COVID-19 pandemic: A commentary.",
- "Abstract": "This commentary provides a reflection on the impact of the COVID-19 pandemic on adolescents in the context of family dynamics, school environments, peer relationships, and civic engagement. Drawing from four systematic literature reviews, the commentary highlights key findings, such as the long-term effects of COVID-19 on adolescent development, mental health, and academic well-being. The need for future research is emphasized to assess how these cohort effects will evolve over time. Cultural context and socioeconomic disparities emerge as crucial considerations, with the pandemic exacerbating existing inequalities, especially in access to education and digital resources. This commentary also underscores the importance of adopting a socio-ecological perspective to understand the multifaceted impact of COVID-19 on adolescents globally. In conclusion, it calls for targeted policies to support adolescents' mental health and academic recovery post-pandemic, particularly in underserved communities. Governments, educators, and civic organizations are encouraged to create inclusive policies that address these disparities while fostering resilience and well-being among young people. These reviews may also inform translational research that could aid in the development of evidence-based interventions and policies aimed at helping adolescents thrive in a post-pandemic world.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Adolescent",
- "Mental Health",
- "SARS-CoV-2",
- "Adolescent Development",
- "Pandemics",
- "Peer Group",
- "Socioeconomic Factors"
- ]
- },
- {
- "PMID": "39733164",
- "Title": "Scientific reports",
- "ArticleTitle": "New-onset cardiovascular diseases post SARS-CoV-2 infection in an urban population in the Bronx.",
- "Abstract": "This study investigated the incidence of new-onset cardiovascular disorders up to 3.5 years post SARS-CoV-2 infection for 56,400 individuals with COVID-19 and 1,093,904 contemporary controls without COVID-19 in the Montefiore Health System (03/11/2020 to 07/01/2023). Outcomes were new incidence of major adverse cardiovascular event (MACE), arrhythmias, inflammatory heart disease, thrombosis, cerebrovascular disorders, ischemic heart disease and other cardiac disorders between 30 days and (up to) 3.5 years post index date. Results were also compared with a pre-pandemic cohort over similar observation duration (N\u2009=\u200964,541). Cumulative incidence and hazard ratios adjusted for competitive risks were analyzed. Compared to contemporary controls, hospitalized COVID-19 patients had significantly higher risk of developing MACE (aHR\u2009=\u20092.29, 95% confidence interval [2.27, 2.31], p\u2009<\u20090.001), arrhythmias (aHR\u2009=\u20092.54[2.50, 2.58], p\u2009<\u20090.001), inflammatory heart disease (aHR\u2009=\u20095.34[4.79, 5.96], p\u2009<\u20090.001), cerebrovascular (aHR\u2009=\u20092.05[2.00, 2.11], p\u2009<\u20090.001), other cardiac disorders (aHR\u2009=\u20092.31[2.26, 2.35], p\u2009<\u20090.001), thrombosis (aHR\u2009=\u20094.25[4.15, 4.36], p\u2009<\u20090.001), and ischemic heart disease (aHR\u2009=\u20091.89[1.86, 1.92], p\u2009<\u20090.001). Non-hospitalized COVID-19 patients had slightly higher risk of developing MACE (aHR\u2009=\u20091.04[1.03, 1.06], p\u2009<\u20090.001), arrhythmias (aHR\u2009=\u20091.10[1.08, 1.12], p\u2009<\u20090.001), inflammatory heart disease (aHR\u2009=\u20092.29 [2.03, 2.59], p\u2009<\u20090.001), cerebrovascular (aHR\u2009=\u20091.11[1.07, 1.15], p\u2009<\u20090.001), and ischemic heart disease (aHR\u2009=\u20091.10[1.08, 1.13], p\u2009<\u20090.001). Race and ethnicity were mostly not associated with increased risks (p\u2009>\u20090.05). aHRs with contemporary controls as a reference were similar to those with pre-pandemic cohort as a reference. We concluded that new incident cardiovascular disorders in COVID-19 patients, especially those hospitalized for COVID-19, were higher than those in controls. Identifying risk factors for developing new-onset cardiovascular disorders may draw clinical attention for the need for careful follow-up in at-risk individuals.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Cardiovascular Diseases",
- "Male",
- "Female",
- "Middle Aged",
- "Aged",
- "Incidence",
- "SARS-CoV-2",
- "Urban Population",
- "Adult",
- "New York City",
- "Risk Factors",
- "Hospitalization",
- "Aged, 80 and over"
- ]
- },
- {
- "PMID": "39731316",
- "Title": "Nordic journal of psychiatry",
- "ArticleTitle": "Gender-stratified national mental health norms of BSI-53, BSI-18, SCL-10, ADHD-9, and ADHD-6 for Denmark.",
- "Abstract": "This study provides gender-stratified Danish mental health norms for multiple symptom scales. The considerable gender differences in the SCL-10 underscore the importance of gender-specific norms. The 2020 SCL-10 norms are biased by COVID-19 distress. Until new normative data is available, the gender-specific norms provided here are recommended.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Denmark",
- "Female",
- "Male",
- "Attention Deficit Disorder with Hyperactivity",
- "Adult",
- "Middle Aged",
- "Adolescent",
- "Young Adult",
- "Aged",
- "COVID-19",
- "Sex Factors",
- "Aged, 80 and over",
- "Reference Values",
- "Brief Psychiatric Rating Scale",
- "Mental Health"
- ]
- },
- {
- "PMID": "39730990",
- "Title": "BMC primary care",
- "ArticleTitle": "The impact of the covid-19 pandemic on perceived diabetes care and regulation, with a focus on ethnic minorities: a mixed-methods study.",
- "Abstract": "In the context of proactive care, remote healthcare and self-regulation have a crucial role for people with T2DM. It is important to identify barriers and facilitators for maintaining good glycaemic control among vulnerable groups, such as ethnic minority groups.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Adult",
- "Aged",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "COVID-19",
- "Diabetes Mellitus, Type 2",
- "Ethnic and Racial Minorities",
- "Primary Health Care",
- "Prospective Studies",
- "Telemedicine"
- ]
- },
- {
- "PMID": "39730493",
- "Title": "Scientific reports",
- "ArticleTitle": "Heart rate variability parameters indicate altered autonomic tone in subjects with COVID-19.",
- "Abstract": "COVID-19 is associated with long-term cardiovascular complications. Heart Rate Variability (HRV), a measure of sympathetic (SNS) and parasympathetic (PNS) control, has been shown to predict COVID-19 outcomes and correlate with disease progression but a comprehensive analysis that includes demographic influences has been lacking. The objective of this study was to determine the balance between SNS, PNS and heart rhythm regulation in hospitalized COVID-19 patients and compare it with similar measurements in healthy volunteers and individuals with cardiovascular diseases (CVD), while also investigating the effects of age, Body Mass Index (BMI), gender and race. Lead I ECG recordings were acquired from 50 COVID-19 patients, 31 healthy volunteers, and 51 individuals with cardiovascular diseases (CVD) without COVID-19. Fourteen HRV parameters were calculated, including time-domain, frequency-domain, nonlinear, and regularity metrics. The study population included a balanced demographic profile, with 55% of participants being under 65 years of age, 54% identifying as male, and 68% identifying as White. Among the COVID-19 patients, 52% had a BMI\u2009\u2265\u200930 compared to 29% of healthy volunteers and 33% of CVD patients. COVID-19 and CVD patients exhibited significantly reduced time-domain HRV parameters, including SDNN and RMSSD, compared to healthy volunteers (SDNN: 0.02\u2009\u00b1\u20090.02\u00a0s vs. 0.06\u2009\u00b1\u20090.03\u00a0s, p\u2009<\u20090.001; RMSSD: 0.02\u2009\u00b1\u20090.02\u00a0s vs. 0.05\u2009\u00b1\u20090.03\u00a0s, p\u2009=\u20090.08). In the frequency domain, both COVID-19 and CVD patients showed increased low-frequency (LF) power and lower high-frequency (HF) power compared to healthy volunteers (COVID-19 LF: 18.47\u2009\u00b1\u200918.18%, HF: 13.69\u2009\u00b1\u200925.80%; Healthy LF: 23.30\u2009\u00b1\u200911.79%, HF: 22.91\u2009\u00b1\u200921.86%, p\u2009<\u20090.01). The LF/HF ratio was similar in COVID-19 patients (1.038\u2009\u00b1\u20091.54) and healthy volunteers (1.03\u2009\u00b1\u20090.78). Nonlinear parameters such as SD1 were significantly lower in COVID-19 patients (0.04\u2009\u00b1\u20090.04\u00a0s vs. 0.08\u2009\u00b1\u20090.05\u00a0s, p\u2009<\u20090.01), indicating altered autonomic regulation. Variations in HRV were observed based on demographic factors, with younger patients, females, and non-white individuals showing more pronounced autonomic dysfunction. COVID-19 patients exhibit significant alterations in HRV, indicating autonomic dysfunction, characterized by decreased vagal tone and sympathetic dominance, similar to patients with severe cardiovascular comorbidities. Despite higher heart rates, the HRV analysis suggests COVID-19 is associated with substantial disruption in autonomic regulation, particularly in patients with specific demographic risk factors.",
- "Predictions": [
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Male",
- "Heart Rate",
- "Female",
- "Middle Aged",
- "Autonomic Nervous System",
- "Aged",
- "Adult",
- "Cardiovascular Diseases",
- "Electrocardiography",
- "SARS-CoV-2",
- "Body Mass Index"
- ]
- },
- {
- "PMID": "39730153",
- "Title": "BMJ open",
- "ArticleTitle": "Exploring the status of online social support for older adults with cancer: a scoping review protocol.",
- "Abstract": "No ethical approval is needed. The findings will be published in a peer-reviewed journal and presented at conferences.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Neoplasms",
- "Social Support",
- "Aged",
- "COVID-19",
- "SARS-CoV-2",
- "Online Social Networking",
- "Research Design",
- "Scoping Reviews As Topic"
- ]
- },
- {
- "PMID": "39729927",
- "Title": "Cancer genetics",
- "ArticleTitle": "Machine learning analysis of CD4+ T cell gene expression in diverse diseases: insights from cancer, metabolic, respiratory, and digestive disorders.",
- "Abstract": "CD4",
- "Predictions": [
- "Cancer",
- "Chronic respiratory disease"
- ],
- "MeshTerms": [
- "Humans",
- "CD4-Positive T-Lymphocytes",
- "Neoplasms",
- "Machine Learning",
- "Digestive System Diseases",
- "Metabolic Diseases",
- "Respiratory Tract Diseases",
- "Gene Expression Profiling",
- "Respiration Disorders"
- ]
- },
- {
- "PMID": "39729438",
- "Title": "PloS one",
- "ArticleTitle": "Implementing digital respiratory technologies for people with respiratory conditions: A protocol for a scoping review.",
- "Abstract": "The value of 'data-enabled', digital healthcare is evolving rapidly, as demonstrated in the COVID-19 pandemic, and its successful implementation remains complex and challenging. Harmonisation (within/between healthcare systems) of infrastructure and implementation strategies has the potential to promote safe, equitable and accessible digital healthcare, but guidance for implementation is lacking. Using respiratory technologies as an example, our scoping review process will capture and review the published research between 12th December 2013 to 12th December 2023. Following standard methodology (Arksey and O'Malley), we will search for studies published in ten databases: MEDLINE, EMBASE, CINAHL, PsycINFO, Cochrane Library, Web of Science, Scopus, IEEE Xplore, CABI Global Health, and WHO Medicus. Our search strategy will use the terms: digital health, respiratory conditions, and implementation. Using Covidence, screening of abstracts and full texts will be undertaken by two independent reviewers, with conflicts resolved by a third reviewer. Data will be extracted into a pilot-tested data extraction table for charting, summarising and reporting the results. We will conduct stakeholder meetings throughout to discuss the themes emerging from implementation studies and support interpretation of findings in the light of their experience within their own networks and organisations. The findings will inform the future work within the ERS CONNECT clinical research collaboration and contribute to policy statements to promote a harmonised framework for digital transformation of respiratory healthcare.",
- "Predictions": [
- "Chronic respiratory disease"
- ],
- "MeshTerms": [
- "Humans",
- "Digital Technology",
- "Respiratory Tract Diseases",
- "Telemedicine",
- "Scoping Reviews As Topic"
- ]
- },
- {
- "PMID": "39727705",
- "Title": "Current oncology (Toronto, Ont.)",
- "ArticleTitle": "Longitudinal Follow-Up of the Psychological Well-Being of Patients with Colorectal Cancer: Final Analysis of PICO-SM.",
- "Abstract": "PICO-SM was a prospective longitudinal study investigating the psychological impact of the COVID-19 pandemic on patients with colorectal cancer treated in a large UK tertiary cancer centre. Here, we present the impact of the third wave of the pandemic (December 2021 to February 2022), when the Omicron variant became prevalent in the UK, and the complete longitudinal comparison across the entire duration of this study. Patients were invited to complete a questionnaire, including screening psychometric tools. In total, n = 312 patients were included in the final analysis. Specifically, in this Omicron-predominant wave, n = 96 patients were studied in detail: the mean age was 64 years, 64% were male, 33% reported poor well-being, 27% anxiety, 11% depressive symptoms, and 3% trauma-related symptoms. The participants who had investigations cancelled (OR 9.22, 95% CI 1.09-77.85; ",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Colorectal Neoplasms",
- "Middle Aged",
- "COVID-19",
- "Female",
- "Longitudinal Studies",
- "Aged",
- "Anxiety",
- "Prospective Studies",
- "SARS-CoV-2",
- "Depression",
- "Follow-Up Studies",
- "Surveys and Questionnaires",
- "Mental Health",
- "United Kingdom",
- "Psychological Well-Being"
- ]
- },
- {
- "PMID": "39727168",
- "Title": "European journal of pain (London, England)",
- "ArticleTitle": "Monitoring Chronic Non-Cancer Pain in Denmark Over Two Decades: Prevalence, Mental Health and Loneliness.",
- "Abstract": "This study demonstrated alarming trend on chronic non-cancer pain prevalence over time in Denmark. The high estimates of prevalence and related issues, such as mental health and severe loneliness deserve further investigation and prioritisation in the public health agenda.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Denmark",
- "Loneliness",
- "Female",
- "Middle Aged",
- "Male",
- "Chronic Pain",
- "Prevalence",
- "Adult",
- "Aged",
- "Mental Health",
- "COVID-19",
- "Young Adult",
- "Adolescent",
- "Aged, 80 and over",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39726235",
- "Title": "Clinical and translational science",
- "ArticleTitle": "Population pharmacokinetics of iruplinalkib in healthy volunteers and patients with solid tumors.",
- "Abstract": "Iruplinalkib (WX-0593), a selective oral ALK/ROS1 tyrosine kinase inhibitor, was approved in China as first-line therapy for ALK-positive non-small-cell lung cancer (NSCLC) and for the treatment of locally advanced or metastatic ALK-positive NSCLC that has progressed following crizotinib therapy. Pharmacokinetics (PK) data of iruplinalkib have been collected in healthy subjects and patient populations in several studies. We developed a population PK (PopPK) model for describing iruplinalkib plasma concentrations and for evaluating whether dose adjustments are necessary based on demographic factors or disease characteristics. Plasma concentration-time data were collected from 392 participants (16 healthy volunteers and 372 patients with solid tumors) who received single or multiple doses of iruplinalkib in four trials. Data were analyzed using non-linear mixed-effects modeling. Iruplinalkib plasma concentrations were best described by a two-compartment model with first-order absorption and first-order elimination. Baseline body weight, time-varying albumin, time-varying creatinine clearance, and time-varying lactate dehydrogenase were significant covariates of apparent clearance from the central compartment (CL/F) while baseline body weight was a significant covariate of apparent volume of the central compartment (V1/F). Given the small or modest effect of all statistically significant covariates on iruplinalkib exposure at steady-state, no covariate was expected to have clinically meaningful effects on iruplinalkib exposure. Furthermore, iruplinalkib absorption was delayed 0.472\u2009h after meal, and K",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Neoplasms",
- "Aged",
- "Healthy Volunteers",
- "Protein Kinase Inhibitors",
- "Young Adult",
- "Models, Biological",
- "Aged, 80 and over",
- "Carcinoma, Non-Small-Cell Lung"
- ]
- },
- {
- "PMID": "39725931",
- "Title": "BMC palliative care",
- "ArticleTitle": "\"I have never felt so alone and vulnerable\" - A qualitative study of bereaved people's experiences of end-of-life cancer care during the Covid-19 pandemic.",
- "Abstract": "People bereaved by cancer were uniquely affected by pandemic-restrictions and disruptions to services. As services re-build post-pandemic, improvements in palliative care in hospitals, investment into community care, and ensuring compassionate communication with patients and families must be prioritised, alongside preparedness for future pandemics or similar events.",
- "Predictions": [
- "Cancer"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Neoplasms",
- "Qualitative Research",
- "Terminal Care",
- "Male",
- "Bereavement",
- "Female",
- "Middle Aged",
- "Aged",
- "Family",
- "Adult",
- "Pandemics",
- "United Kingdom",
- "SARS-CoV-2",
- "Aged, 80 and over"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/diabetes.json b/model/data/diabetes.json
deleted file mode 100644
index 4f38ac1f4bbbe36f9bd73f4fa18d32b2b693db85..0000000000000000000000000000000000000000
--- a/model/data/diabetes.json
+++ /dev/null
@@ -1,505 +0,0 @@
-[
- {
- "PMID": "39738300",
- "Title": "Scientific reports",
- "ArticleTitle": "Robust self management classification via sparse representation based discriminative model for mild cognitive impairment associated with diabetes mellitus.",
- "Abstract": "Diabetes Mellitus combined with Mild Cognitive Impairment (DM-MCI) is a high incidence disease among the elderly. Patients with DM-MCI have considerably higher risk of dementia, whose daily self-care and life management (i.e. self-management) have a significant impact on the development of their condition. Thus, the inclusion and discrimination of subsequent interventions according to their self-management is an urgent issue. A Sparse-representation-based Discriminative Classification model (SDC) is proposed in this paper to correctly classify MCI-DM patients based on their self-management ability. Specifically, an L",
- "Predictions": [
- "Diabetes"
- ],
- "MeshTerms": [
- "Humans",
- "Cognitive Dysfunction",
- "Self-Management",
- "Machine Learning",
- "Aged",
- "Male",
- "Female",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39738226",
- "Title": "Scientific reports",
- "ArticleTitle": "Excessive daytime sleepiness and its predictors among type 2 diabetes mellitus patients at central ethiopia.",
- "Abstract": "Excessive daytime sleepiness is a common finding among type 2 diabetes mellitus patients. However there is scarce data that shows the magnitude of excessive daytime sleepiness, & its association with type 2 diabetes mellitus. Hence, the study aimed to assess the prevalence of excessive daytime sleepiness and its associated factors among type 2 diabetes mellitus patients at Wolkite University Specialized Hospital. A Hospital-based cross-sectional study was employed from January 15 to March 15, 2022, among 229 Type 2 diabetes mellitus patients. Data was collected by semi-structured questionnaires, then entered into the Epi data version 4.6 and exported to SPSS version 25.0 for analysis. Binary and multiple logistic regression analysis was used to assess factors associated with excessive daytime sleepiness and statistical significance was set at P-value\u2009<\u20090.05. The prevalence of Excessive daytime sleepiness among type 2 diabetes mellitus was 27.1%. Age (AOR: 1.08; 95%CI: 1.03, 1.12), frequent snoring (AOR: 2.9; 95%CI: 1.24, 6.80), comorbid hypertension (AOR: 2.64; 95%CI: 1.17, 5.96), obesity (AOR: 2.7; 95%CI: 1.03, 7.13), and poor glycemic control (AOR: 6.68; 95%CI: 1.83, 24.41) were independently associated with Excessive daytime sleepiness among type 2 diabetes mellitus patients. Excessive daytime sleepiness was reported in more than a quarter of type 2 diabetes mellitus patients. Age, frequent snoring, hypertension, obesity, and poor glycemic control were significantly associated with Excessive daytime sleepiness among type 2 diabetes mellitus patients. Therefore health care providers should assess not only for how well their patients' diabetes is controlled but also for excessive daytime sleepiness.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Ethiopia",
- "Male",
- "Female",
- "Middle Aged",
- "Disorders of Excessive Somnolence",
- "Cross-Sectional Studies",
- "Adult",
- "Prevalence",
- "Risk Factors",
- "Aged",
- "Hypertension",
- "Surveys and Questionnaires",
- "Comorbidity",
- "Obesity",
- "Snoring"
- ]
- },
- {
- "PMID": "39737893",
- "Title": "Nutrition & diabetes",
- "ArticleTitle": "The genetic and observational nexus between diabetes and arthritis: a national health survey and mendelian randomization analysis.",
- "Abstract": "There is an association between diabetes and arthritis, with potential genetic links between Type 1 Diabetes and RA.",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Mendelian Randomization Analysis",
- "Male",
- "Female",
- "Nutrition Surveys",
- "Middle Aged",
- "Genome-Wide Association Study",
- "Arthritis, Rheumatoid",
- "Adult",
- "Arthritis",
- "Prevalence",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Aged",
- "Genetic Predisposition to Disease",
- "Logistic Models",
- "Polymorphism, Single Nucleotide"
- ]
- },
- {
- "PMID": "39737643",
- "Title": "Journal of biomedical materials research. Part B, Applied biomaterials",
- "ArticleTitle": "Beneficial Effects of Tilapia Fish Skin on Excisional Skin Wound Healing in a Type I Diabetic Rat Model.",
- "Abstract": "IntroductionProlonged hyperglycemia in diabetic patients often impairs wound healing, leading to chronic infections and complications. This study aimed to evaluate the potential of fresh Tilapia fish skin as a treatment to enhance wound healing in diabetic rats. MethodsThirty-nine healthy adult albino rats, weighing between 150 and 200\u2009g, were divided into three groups: non-diabetic rats with untreated wounds [C-], diabetic rats with untreated wounds [C+], and diabetic rats treated with fresh Tilapia skin [TT]. The healing process was monitored through clinical observation, gross examination, and histopathological analysis. ResultsThe results demonstrated that the Tilapia skin treatment accelerated wound healing, as evidenced by complete reepithelialization, full epidermal cell differentiation, an intact dermo-epidermal junction, and a reorganized dermis with fewer blood vessels. ConclusionFresh Tilapia skin proved to be a safe and effective dressing for promoting wound healing and managing infection in diabetic wounds.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Animals",
- "Tilapia",
- "Rats",
- "Skin",
- "Wound Healing",
- "Diabetes Mellitus, Experimental",
- "Diabetes Mellitus, Type 1",
- "Male"
- ]
- },
- {
- "PMID": "39737509",
- "Title": "The Indian journal of medical research",
- "ArticleTitle": "ICMR-MDRF Diabetes Biosamples: Cohort profile.",
- "Abstract": "Background & objectives Biobanks are crucial for biomedical research, enabling new treatments and medical advancements. The biobank at the Madras Diabetes Research Foundation (MDRF) aims to gather, process, store, and distribute biospecimens to assist scientific studies. Methods This article details the profile of two cohorts: the Indian Council of Medical Research-India Diabetes (ICMR-INDIAB) study and the Registry of people with diabetes in India with young age at onset (ICMR-YDR). The ICMR-INDIAB study is the largest epidemiological study on diabetes in India, encompassing a nationally representative sample of individuals aged 20 yr and older from urban and rural areas in every State across the country. The ICMR-YDR is the first national-level, multicentric clinic-based registry focusing on youth-onset diabetes in India, aiming to understand the disease patterns and variations in youth-onset diabetes across different country regions. Results Key operations at the MDRF biobank include collecting and processing samples, where serum and whole blood samples are aliquoted and transferred through a cold chain to the central laboratory, and then stored in Siruseri (29 km from the capital city of Chennai, Tamil Nadu). Samples are barcoded, linked to subject information, and stored in freezers or liquid nitrogen (LN2) vessels, with inventory tracked via software for easy retrieval. A register records access to the biobank, ensuring sample integrity and compliance with regulatory requirements. The biobank adheres to the ICMR's National Ethical Guidelines for Biomedical and Health Research involving human participants. Interpretation & conclusions The biobank enables the analysis of biomarkers in stored samples, aiding in scientifically sound decisions, treating patients, and potentially curing diabetes.",
- "Predictions": [
- "Diabetes",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "India",
- "Biological Specimen Banks",
- "Adult",
- "Female",
- "Male",
- "Diabetes Mellitus",
- "Registries",
- "Biomedical Research",
- "Young Adult",
- "Cohort Studies",
- "Age of Onset",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39736942",
- "Title": "Archives of Razi Institute",
- "ArticleTitle": "Morbidity profile of the patients attending Mobile Medical Unit camps in Telangana: A record-based study.",
- "Abstract": "Mobile Medical Units (MMUs) are one of the major initiatives under the National Rural Health Mission. These MMUs help people in remote, underserved areas access healthcare at affordable prices on their doorstep. The present record-based study aimed to assess the morbidity profile of the patients attending Mobile Medical Unit camps in the Yadadri-Bhuvanagiri district between April 2022 and December 2022. The MMU is run by the Department of Community and Family Medicine, AIIMS, Bibinagar, in six selected villages of the Yadadri-Bhuvanagiri district. A register is maintained to record the details of patients visiting the MMU camp. Patient's name, age, gender, place, mobile number, height, weight, blood pressure (BP), glucometer Random Blood Sugar, diagnosis, and details of medication dispensed were entered in the register. Diabetes, hypertension, and obesity were diagnosed using the World Health Organization\u00a0(WHO) criteria, the Eighth Joint National Committee guidelines, and WHO Asia Pacific guidelines, respectively. Mobile Medical Unit Camp data are entered into the Excel database at the end of every month. Since it is a record-based analysis, we used data for analysis between April 7, 2022, and December 31, 2022. A total of 1494 patients were treated in the MMU camps during this period. Among them, 89.4% were adults, and 10.6% were children (less than 18 years). Among 1,336 adult patients, the majority of participants suffered from osteoarthritis, followed by non-communicable diseases (NCDs). The mean scores of systolic and diastolic BP of the adult population were obtained at 131\u00b121 and 77\u00b113 mm Hg, respectively. The mean random blood glucose level of the adult population was 150\u00b174 mg/dl. A total of 158 children were younger than 18 years old, out of whom 78 and 80 participants were males and females, respectively. Moreover, 23.1% and 25% of males and females suffered from upper respiratory tract infections, respectively. The study further suggests that the NCD epidemic is spreading to rural areas where necessary health infrastructure is insufficient. MMUs can bring a significant change to the public health system, which needs to re-orient its priorities.",
- "Predictions": [
- "Diabetes"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Adult",
- "Mobile Health Units",
- "Middle Aged",
- "Adolescent",
- "Aged",
- "Child",
- "Young Adult",
- "India",
- "Morbidity",
- "Hypertension",
- "Child, Preschool",
- "Obesity",
- "Infant",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39736941",
- "Title": "Archives of Razi Institute",
- "ArticleTitle": "Involvement of \u03b3-Aminobutyric Acid and N-methyl-D-aspartate Receptors in Diabetic Gastropathy in Rats: Possible Beneficial Effect of Prolonged Treatment with Insulin and Magnesium Supplement.",
- "Abstract": "Gastrointestinal dysfunction is a severe and common complication in diabetic patients. Some evidence shows that gamma-aminobutyric acid (GABA) and glutamate contribute to diabetic gastrointestinal abnormalities. Therefore, we examined the impact of prolonged treatment with insulin and magnesium supplements on the expression pattern of GABA type A (GABA-A), GABA-B, and N-methyl-D-aspartate (NMDA) glutamate receptors as well as nitric oxide synthase 1 (NOS-1) in the stomach of type 2 diabetic rats. Twenty-four male Wistar rats were randomized to four groups (six rats each): 1) control, 2) type 2 diabetes: rats fed with a high-fat diet for three months + a low dose of streptozotocin (35 mg/kg), 3) type 2 diabetes + magnesium, and 4) type 2 diabetes + insulin. The expression of NOS-1, GABA-A, GABA-B, and NMDA receptors was detected using western blotting. The NOS-1 expression was substantially diminished (P<0.01), while the expression of GABA-A (P<0.001), GABA-B (P<0.001), and NMDA (P<0.001) receptors was enhanced in the stomach of diabetic rats relative to control. Treatment with magnesium and insulin improved NOS-1 expression in diabetic rats, although this effect was greater in magnesium treatment alone. Magnesium also restored the expression of GABA-A and GABA-B receptors in diabetic rats to control values. Moreover, insulin treatment improved GABA-A receptor expression in diabetic rats (P<0.05). No considerable alterations were detected in NMDA receptor levels in the treatment groups. The results suggest a significant role of magnesium and insulin in improving gastric motility and secretory disorders associated with diabetes through modifying the expression of GABAergic receptors.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Animals",
- "Male",
- "Rats, Wistar",
- "Receptors, N-Methyl-D-Aspartate",
- "Diabetes Mellitus, Experimental",
- "Insulin",
- "Rats",
- "Magnesium",
- "Diabetes Mellitus, Type 2",
- "Nitric Oxide Synthase Type I",
- "Dietary Supplements",
- "Random Allocation",
- "Streptozocin"
- ]
- },
- {
- "PMID": "39736870",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Construction and validation of a nomogram model for predicting diabetic peripheral neuropathy.",
- "Abstract": "The DPN nomogram prediction model, containing 7 significant variables, has exhibited excellent performance. Its generalization to clinical practice could potentially help in the early detection and prompt intervention for high-risk DPN patients.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Nomograms",
- "Diabetic Neuropathies",
- "Female",
- "Male",
- "Middle Aged",
- "Aged",
- "Risk Factors",
- "ROC Curve",
- "Diabetes Mellitus, Type 2",
- "Prognosis",
- "Adult"
- ]
- },
- {
- "PMID": "39736868",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Fear of hypoglycemia and sleep in children with type 1 diabetes and their parents.",
- "Abstract": "www.ClinicalTrials.gov, identifier NCT03103867.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Hypoglycemia",
- "Child",
- "Female",
- "Parents",
- "Adolescent",
- "Fear",
- "Cross-Over Studies",
- "Adult",
- "Sleep",
- "Middle Aged",
- "Insulin Infusion Systems",
- "Blood Glucose Self-Monitoring",
- "Insulin",
- "Blood Glucose",
- "Hypoglycemic Agents"
- ]
- },
- {
- "PMID": "39736865",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Quantitative ultrasound imaging reveals distinct fracture-associated differences in tibial intracortical pore morphology and viscoelastic properties in aged individuals with and without diabetes mellitus - an exploratory study.",
- "Abstract": "Both T1DM and T2DM showed altered bone metabolism, with T2DM linked to impaired tissue formation. CortBS provides insights into pathophysiological changes in diabetic bone and provided superior fracture risk assessment in DM patients compared to DXA.",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Ultrasonography",
- "Aged",
- "Middle Aged",
- "Bone Density",
- "Diabetes Mellitus, Type 2",
- "Tibia",
- "Absorptiometry, Photon",
- "Case-Control Studies",
- "Diabetes Mellitus, Type 1",
- "Cortical Bone",
- "Elasticity"
- ]
- },
- {
- "PMID": "39736861",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Case report: A 51-year-old diabetic patient with primary bilateral macronodular adrenal hyperplasia and primary hyperparathyroidism.",
- "Abstract": "A 51-year-old female patient with diabetes mellitus and hypertension, exhibiting poor control of blood sugar and blood pressure, was unexpectedly found to have multiple large adrenal nodules, excessive cortisol secretion, and adrenocorticotropic hormone inhibition. Cortisol levels remained unresponsive to both low-dose and high-dose dexamethasone tests, leading to a diagnosis of primary bilateral macronodular adrenal hyperplasia. Concurrently, elevated blood calcium and parathyroid hormone levels, along with 99mTc-methoxyisobutyl isonitrile (99mTc-MIBI) imaging revealing increased 99mTc-MIBI uptake in the right inferior parathyroid gland, suggest the consideration of primary hyperparathyroidism. This case is presented in light of the uncommon clinical coexistence of primary bilateral macronodular adrenal hyperplasia and primary hyperparathyroidism.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Middle Aged",
- "Hyperparathyroidism, Primary",
- "Adrenal Glands",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39736858",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Association of oxidative balance score with cardiovascular disease and all-cause and cardiovascular mortality in American adults with type 2 diabetes: data from the National Health and Nutrition examination survey 1999-2018.",
- "Abstract": "Adherence to higher OBS was associated with reduced CVD prevalence and mortality risk in T2D. Antioxidant diet and lifestyle had more significant associations with mortality and CVD prevalence, respectively. However, as these findings are merely associations and do not allow causal inferences to be drawn, future validation in high-quality randomized controlled trials is needed.",
- "Predictions": [
- "Cardiovascular diseases",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Cardiovascular Diseases",
- "Male",
- "Female",
- "Middle Aged",
- "Nutrition Surveys",
- "Adult",
- "Oxidative Stress",
- "United States",
- "Aged",
- "Life Style",
- "Diet",
- "Risk Factors",
- "Follow-Up Studies",
- "Prevalence"
- ]
- },
- {
- "PMID": "39736689",
- "Title": "Lipids in health and disease",
- "ArticleTitle": "Cardiometabolic index and mortality risks: elevated cancer and reduced cardiovascular mortality risk in a large cohort.",
- "Abstract": "This study represents the first comprehensive assessment on the contribution of CMI to mortality across an all-age adult population, providing some insights for the comprehensive assessment of health and disease states.",
- "Predictions": [
- "Diabetes",
- "Cancer",
- "Cardiovascular diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Neoplasms",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Longitudinal Studies",
- "Aged",
- "Proportional Hazards Models",
- "Diabetes Mellitus",
- "Risk Factors",
- "Cardiometabolic Risk Factors",
- "Cohort Studies"
- ]
- },
- {
- "PMID": "39736551",
- "Title": "BMC primary care",
- "ArticleTitle": "The moderating role of e-health literacy and patient-physician communication in the relationship between online diabetes information-seeking behavior and self-care practices among individuals with type 2 diabetes.",
- "Abstract": "Findings support the role of patient eHL and patient-physician communication in amplifying the positive impact of online DISB on patients' behavioral outcomes in diabetes.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Health Literacy",
- "Physician-Patient Relations",
- "Middle Aged",
- "Cross-Sectional Studies",
- "Self Care",
- "Information Seeking Behavior",
- "Medication Adherence",
- "Communication",
- "Aged",
- "Adult",
- "Internet",
- "Assessment of Medication Adherence"
- ]
- },
- {
- "PMID": "39736518",
- "Title": "BMC cardiovascular disorders",
- "ArticleTitle": "Effect of sodium glucose cotransporter-2 inhibitors (SGLT-2is) on the clinical outcomes of patients with diabetic atrial fibrillation.",
- "Abstract": "In our study, SGLT-2i treatment was associated with a significant reduction in all-cause mortality and major bleeding in diabetic AF patients. Our study provides evidence of the clinical benefit of SGLT-2i in AF patients.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Male",
- "Atrial Fibrillation",
- "Retrospective Studies",
- "Female",
- "Aged",
- "Treatment Outcome",
- "Middle Aged",
- "Diabetes Mellitus, Type 2",
- "Time Factors",
- "Risk Factors",
- "Risk Assessment",
- "Hemorrhage",
- "Aged, 80 and over",
- "Cause of Death",
- "Myocardial Infarction"
- ]
- },
- {
- "PMID": "39736351",
- "Title": "Life sciences",
- "ArticleTitle": "AAV2-mediated ABD-FGF21 gene delivery produces a sustained anti-hyperglycemic effect in type 2 diabetic mouse.",
- "Abstract": "In conclusion, we have developed a novel strategy for producing long-acting FGF21 using the AAV vector, and AAV2-ABD-FGF21 shows promise as a therapeutic approach for type 2 diabetes mellitus and other glycolipid metabolic disorders.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Animals",
- "Fibroblast Growth Factors",
- "Diabetes Mellitus, Type 2",
- "Mice",
- "Dependovirus",
- "Humans",
- "Gene Transfer Techniques",
- "Genetic Therapy",
- "Male",
- "Diabetes Mellitus, Experimental",
- "HEK293 Cells",
- "Mice, Inbred C57BL",
- "Blood Glucose",
- "Genetic Vectors",
- "Liver",
- "Hypoglycemic Agents"
- ]
- },
- {
- "PMID": "39736334",
- "Title": "Diabetes research and clinical practice",
- "ArticleTitle": "Balanced diets are associated with a lower risk of type 2 diabetes than plant-based diets.",
- "Abstract": "Adhered to a balanced diet is associated with a lower risk of diabetes compared to plant-based diet, which might be attributed to signature proteins such as AGR2, DBI, IL17RA and SERPINH1.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Cross-Sectional Studies",
- "Diet, Vegetarian",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Prospective Studies",
- "Aged",
- "Risk Factors",
- "United Kingdom",
- "Proteomics",
- "Diet, Healthy",
- "Diet, Plant-Based"
- ]
- },
- {
- "PMID": "39736162",
- "Title": "West African journal of medicine",
- "ArticleTitle": "The Impact of Diabetes Self-Management Education (DSME) on the Quality of Life of patients living with type-2 Diabetes Mellitus in Nigeria.",
- "Abstract": "The findings highlight that DSME significantly enhances the QoL, self-management competence, and glycemic control among T2DM patients in Nigeria. These results underscore the importance of structured educational interventions in diabetes care, particularly in resource-limited settings.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Quality of Life",
- "Nigeria",
- "Male",
- "Female",
- "Middle Aged",
- "Self-Management",
- "Patient Education as Topic",
- "Adult",
- "Surveys and Questionnaires",
- "Health Knowledge, Attitudes, Practice",
- "Aged",
- "Self Care"
- ]
- },
- {
- "PMID": "39735994",
- "Title": "Frontiers in bioscience (Landmark edition)",
- "ArticleTitle": "The Putative Antilipogenic Role of NRG4 and ERBB4: First Expression Study on Human Liver Samples.",
- "Abstract": "The study demonstrates a decrease in ",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Receptor, ErbB-4",
- "Neuregulins",
- "Liver",
- "Middle Aged",
- "Female",
- "Non-alcoholic Fatty Liver Disease",
- "Male",
- "Adult",
- "Lipogenesis",
- "Obesity",
- "Diabetes Mellitus, Type 2",
- "RNA, Messenger",
- "Aged"
- ]
- },
- {
- "PMID": "39735781",
- "Title": "Experimental biology and medicine (Maywood, N.J.)",
- "ArticleTitle": "Increased hip fracture risk in the patients with type 2 diabetes mellitus is correlated with urine albumin-to-creatinine ratio (ACR) and diabetes duration in men.",
- "Abstract": "Patients with type 2 diabetes mellitus (T2DM) have increased hip fracture risk. And the association between urine albumin to creatinine ratio (ACR) and an increased risk of hip fracture in patients with T2DM remains controversial. This study aimed to investigate the association between urinary ACR and hip fracture risk in postmenopausal women and aged men with T2DM. The study included 219 postmenopausal women and 216 older men (mean age >60\u00a0years) with T2DM. Women and men were divided into control group (ACR<30\u00a0mg/g), microalbuminuria group (30\u00a0mg/g \u2264 ACR<300\u00a0mg/g), and macroalbuminuria group (ACR\u2265300\u00a0mg/g) respectively. Demographic characteristics and clinical history were collected in patients. Biochemical indexes and bone turnover-related markers were measured in patients. In the study, we found that several factors, including age, T2DM duration, cerebral infarction history, serum corrected calcium levels and urine ACR were positively associated with hip fracture risk. However, 25-Hydroxyvitamin D and areal BMD were negatively associated with hip fracture risk. Furthermore, multiple regression analysis showed that urinary ACR level (\u03b2 = 0.003, p = 0.044) and duration of T2DM (\u03b2 = 0.015, p = 0.018) were positively and independently correlated with hip fracture risk in older men. In contrast, femoral neck BMD (\u03b2 = -6.765, p < 0.001) was independently and negatively correlated with hip fracture risk in older men. This study indicated that the elevated ACR levels and longer T2DM duration were related to higher hip fracture risk in older men with T2DM, which could be beneficial for developing a predictive model for osteoporotic fractures in patients with type 2 diabetes in the future. However, results were inconsistent in women, hip fracture risk didn't alter by changes in urinary microalbuminuria level in postmenopausal women with T2DM.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Hip Fractures",
- "Male",
- "Female",
- "Albuminuria",
- "Aged",
- "Middle Aged",
- "Creatinine",
- "Risk Factors",
- "Bone Density",
- "Postmenopause"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/diabetes_mellitus.json b/model/data/diabetes_mellitus.json
deleted file mode 100644
index 1e58967ffe1e608492fa8377b524cecc4c8c8d6f..0000000000000000000000000000000000000000
--- a/model/data/diabetes_mellitus.json
+++ /dev/null
@@ -1,516 +0,0 @@
-[
- {
- "PMID": "39476387",
- "Title": "Current opinion in anaesthesiology",
- "ArticleTitle": "Caring for patients with diabetes in the outpatient surgical setting: current recommendations and controversies.",
- "Abstract": "Future research needs to specifically examine chronic blood glucose control, day of surgery targets, effective home medication management and the risk of perioperative hyperglycemia in ambulatory surgery. Education, protocols and resources to support the care of perioperative patients in the outpatient setting will aid providers on the day of surgery and provide optimal diabetes care leading up to surgery.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Ambulatory Surgical Procedures",
- "Hypoglycemic Agents",
- "Diabetes Mellitus",
- "Perioperative Care",
- "Blood Glucose",
- "Insulin",
- "Ambulatory Care",
- "Postoperative Care",
- "Practice Guidelines as Topic",
- "Hyperglycemia",
- "Preoperative Care"
- ]
- },
- {
- "PMID": "39476122",
- "Title": "PloS one",
- "ArticleTitle": "Burden of diabetes mellitus in Weifang: Changing trends in prevalence and deaths from 2010 to 2021.",
- "Abstract": "The city is faced with a significant challenge of diabetes, which is influenced by factors such as gender, age, cultural background, and marital status. Unspecified diabetes mellitus (DM) with ketoacidosis (10.03%) and T2DM with renal complications (0.23%) are identified as the primary direct and underlying causes of death among diabetic patients, respectively. This study serves as a valuable reference for other regions in terms of diabetes prevention, control, and the management of chronic diseases.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Aged",
- "Middle Aged",
- "Prevalence",
- "Diabetes Mellitus",
- "Adult",
- "China",
- "Cost of Illness",
- "Adolescent",
- "Aged, 80 and over",
- "Young Adult",
- "Disability-Adjusted Life Years",
- "Cause of Death",
- "Child"
- ]
- },
- {
- "PMID": "39474868",
- "Title": "Open biology",
- "ArticleTitle": "The post-translational modification O-GlcNAc is a sensor and regulator of metabolism.",
- "Abstract": "Cells must rapidly adapt to changes in nutrient conditions through responsive signalling cascades to maintain homeostasis. One of these adaptive pathways results in the post-translational modification of proteins by O-GlcNAc. O-GlcNAc modifies thousands of nuclear and cytoplasmic proteins in response to nutrient availability through the hexosamine biosynthetic pathway. O-GlcNAc is highly dynamic and can be added and removed from proteins multiple times throughout their life cycle, setting it up to be an ideal regulator of cellular processes in response to metabolic changes. Here, we describe the link between cellular metabolism and O-GlcNAc, and we explore O-GlcNAc's role in regulating cellular processes in response to nutrient levels. Specifically, we discuss the mechanisms of elevated O-GlcNAc levels in contributing to diabetes and cancer, as well as the role of decreased O-GlcNAc levels in neurodegeneration. These studies form a foundational understanding of aberrant O-GlcNAc in human disease and provide an opportunity to further improve disease identification and treatment.",
- "Predictions": [
- "Neoplasms",
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Protein Processing, Post-Translational",
- "Humans",
- "Acetylglucosamine",
- "Animals",
- "Neoplasms",
- "Signal Transduction",
- "Glycosylation",
- "Diabetes Mellitus",
- "Neurodegenerative Diseases"
- ]
- },
- {
- "PMID": "39474832",
- "Title": "Medical decision making : an international journal of the Society for Medical Decision Making",
- "ArticleTitle": "Using QALYs as an Outcome for Assessing Global Prediction Accuracy in Diabetes Simulation Models.",
- "Abstract": "Diabetes simulation models are currently validated by examining their ability to predict the incidence of individual events (e.g., myocardial infarction, stroke, amputation) or composite events (e.g., first major adverse cardiovascular event).We introduce Q",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Quality-Adjusted Life Years",
- "Computer Simulation",
- "Hypoglycemic Agents",
- "Diabetes Mellitus, Type 2",
- "Cost-Benefit Analysis",
- "United Kingdom",
- "Technology Assessment, Biomedical",
- "Diabetes Mellitus",
- "Female",
- "Male"
- ]
- },
- {
- "PMID": "39472978",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Association between night blindness history and risk of diabetes in the Chinese population: a multi-center, cross sectional study.",
- "Abstract": "The results suggest that NB history might be associated with increased odds of diabetes in Chinese community-dwelling adults.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Cross-Sectional Studies",
- "Middle Aged",
- "Male",
- "Female",
- "Adult",
- "Aged",
- "China",
- "Diabetes Mellitus",
- "Adolescent",
- "Young Adult",
- "Night Blindness",
- "Risk Factors",
- "Aged, 80 and over",
- "East Asian People"
- ]
- },
- {
- "PMID": "39472915",
- "Title": "BMC health services research",
- "ArticleTitle": "Geographical Access to Point-of-care diagnostic tests for diabetes, anaemia, Hepatitis B, and human immunodeficiency virus in the Bono Region, Ghana.",
- "Abstract": "The findings revealed moderate access to all the tests in districts across the region. However, geographical access to glucose, Hb, Hep B, and HIV POC testing was poor (distance\u2009\u2265\u200910\u00a0km and travel time of \u2265\u200993\u00a0min), in the Banda district. This study showed the need to prioritise the Banda district for targeted improvement for all the tests. A further study is recommended to identify potential solutions to addressing the POC testing implementation in the BR, as demonstrated by this study.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Ghana",
- "HIV Infections",
- "Health Services Accessibility",
- "Anemia",
- "Hepatitis B",
- "Diabetes Mellitus",
- "Point-of-Care Testing",
- "Point-of-Care Systems"
- ]
- },
- {
- "PMID": "39471268",
- "Title": "Journal of managed care & specialty pharmacy",
- "ArticleTitle": "Potential benefits of incorporating social determinants of health screening on comprehensive medication management effectiveness.",
- "Abstract": "Although not statistically significant, the results of this pilot evaluation suggest the potential for meaningful clinical improvements from screening and referral of SDoH needs as a part of CMM encounters. These results should be corroborated using a larger, more robust study design.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Retrospective Studies",
- "Social Determinants of Health",
- "Female",
- "Male",
- "Middle Aged",
- "Medication Therapy Management",
- "Aged",
- "Pharmacists",
- "Referral and Consultation",
- "Mass Screening",
- "Adult",
- "Cohort Studies",
- "Hypertension",
- "Diabetes Mellitus",
- "Chronic Disease"
- ]
- },
- {
- "PMID": "39470899",
- "Title": "Current diabetes reports",
- "ArticleTitle": "Implementation Science and Pediatric Diabetes: A Scoping Review of the State of the Literature and Recommendations for Future Research.",
- "Abstract": "Of 23 papers identified, 19 were published since 2017 and 21 focused on type 1 diabetes. Most involved medical evidence-based practices (EBPs; n\u2009=\u200915), whereas fewer focused on psychosocial (n\u2009=\u20097) and diabetes education (n\u2009=\u20092). The majority either identified barriers and facilitators of implementing an EBP (n\u2009=\u200911) or were implementation trials (n\u2009=\u200911). Fewer studies documented gaps in EBP implementation in standard care (n\u2009=\u20097) or development of implementation strategies (n\u2009=\u20091). Five papers employed IS theories and two aimed to improve equity. There is a paucity of IS research in pediatric diabetes care literature. Few papers employed IS theory, used consistent IS terminology, or described IS strategies or outcomes. Guidance for future research to improve IS research in pediatric diabetes is offered.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Implementation Science",
- "Child",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus",
- "Pediatrics",
- "Evidence-Based Practice"
- ]
- },
- {
- "PMID": "39470889",
- "Title": "Biogerontology",
- "ArticleTitle": "A novel (-)-(2S)-7,4'-dihydroxyflavanone compound for treating age-related diabetes mellitus through immunoinformatics-guided activation of CISD3.",
- "Abstract": "The iron-sulfur domain (CISD) proteins of CDGSH are classified into three classes: CISD1, CISD2, and CISD3. During premature ageing, mutations that affect these proteins, namely their binding sites, could result in reduced protein production and an inability to preserve cellular integrity. Consequently, this leads to the development of conditions such as diabetes. Notably, CISD3 plays a crucial role in the management of age-related disorders such as Wolfram syndrome, which is often referred to as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness). Computational analyses have predicted that CISD3 regulates the redox state, safeguards the endoplasmic reticulum and mitochondria, and maintains intracellular calcium levels. CISD3, a member of a recently discovered gene family associated with the CDGSH iron protein apoptotic compensatory response, fulfils a crucial function in mitigating the effects of accelerated ageing. The compound \"(-)-(2S)-7,4'-Dihydroxyflavanone\" has been discovered by computational drug design as a possible activator of CISD3. It shows potential therapeutic benefits in ameliorating metabolic dysfunction and enhancing glucose regulation. The ligand binds to the binding pocket of the CISD3 protein, increasing the stability of the protein and enhancing its functionality. The current research investigates the binding processes of the molecule in various structures and its anticipated effects on these tissues, therefore providing valuable insights into the mitigation of age-related diabetes and metabolic dysfunction. The projected tripling of the worldwide population of individuals aged 50 and above by 2050 necessitates the urgent development of immunoinformatics-based approaches, including pharmaceutical therapies that target CISD3, to prevent age-related pathologies. The stimulation of CISD3, namely by compounds such as \"(-)-(2S)-7,4'-Dihydroxyflavanone\", has the potential to counteract telomere shortening and improve metabolic pathways.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus",
- "Aging",
- "Flavanones",
- "Hypoglycemic Agents",
- "Molecular Docking Simulation",
- "Computational Biology",
- "Drug Design",
- "Immunoinformatics"
- ]
- },
- {
- "PMID": "39470403",
- "Title": "The journals of gerontology. Series B, Psychological sciences and social sciences",
- "ArticleTitle": "Economic Disadvantage During Childhood, Obesity, and Diabetes Across Three Birth Cohorts of Older Mexicans.",
- "Abstract": "High body weight across Mexican birth cohorts seemed to offset the potential benefits from improvements in childhood conditions on adult diabetes risk.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Middle Aged",
- "Aged",
- "Mexico",
- "Diabetes Mellitus",
- "Prevalence",
- "Obesity",
- "Birth Cohort",
- "Body Mass Index",
- "Adverse Childhood Experiences",
- "Overweight",
- "Poverty",
- "North American People"
- ]
- },
- {
- "PMID": "39468609",
- "Title": "Stem cell research & therapy",
- "ArticleTitle": "Human mesenchymal stem/stromal cell based-therapy in diabetes mellitus: experimental and clinical perspectives.",
- "Abstract": "Diabetes mellitus (DM), a chronic metabolic disease, poses a significant global health challenge, with current treatments often fail to prevent the long-term disease complications. Mesenchymal stem/stromal cells (MSCs) are, adult progenitors, able to repair injured tissues, exhibiting regenerative effects and immunoregulatory and anti-inflammatory responses, so they have been emerged as a promising therapeutic approach in many immune-related and inflammatory diseases. This review summarizes the therapeutic mechanisms and outcomes of MSCs, derived from different human tissue sources (hMSCs), in the context of DM type 1 and type 2. Animal model studies and clinical trials indicate that hMSCs can facilitate pleiotropic actions in the diabetic milieu for improved metabolic indices. In addition to modulating abnormally active immune system, hMSCs can ameliorate peripheral insulin resistance, halt beta-cell destruction, preserve residual beta-cell mass, promote beta-cell regeneration and insulin production, support islet grafts, and correct lipid metabolism. Moreover, hMSC-free derivatives, importantly extracellular vesicles, have shown potent experimental anti-diabetic efficacy. Moreover, the review discusses the diverse priming strategies that are introduced to enhance the preclinical anti-diabetic actions of hMSCs. Such strategies are recommended to restore the characteristics and functions of MSCs isolated from patients with DM for autologous implications. Finally, limitations and merits for the wide spread clinical applications of MSCs in DM such as the challenge of autologous versus allogeneic MSCs, the optimal MSC tissue source and administration route, the necessity of larger clinical trials for longer evaluation duration to assess safety concerns, are briefly presented.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Mesenchymal Stem Cell Transplantation",
- "Mesenchymal Stem Cells",
- "Animals",
- "Insulin-Secreting Cells",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39468602",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Lipids as the link between central obesity and diabetes: perspectives from mediation analysis.",
- "Abstract": "In central obesity-related diabetes risk, most lipids, especially lipid ratio parameters, play a significant mediating role. Given these findings, we advocate for increased efforts in multifactorial risk monitoring and joint management of diabetes. The evaluation of lipids, particularly lipid ratio parameters, may be holds substantial value in the prevention and management of diabetes risk under close monitoring of central obesity.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Obesity, Abdominal",
- "Male",
- "Female",
- "Middle Aged",
- "Lipids",
- "Mediation Analysis",
- "Adult",
- "Risk Factors",
- "Waist Circumference",
- "Longitudinal Studies",
- "Diabetes Mellitus",
- "Biomarkers",
- "Diabetes Mellitus, Type 2",
- "Follow-Up Studies",
- "Aged",
- "Prognosis",
- "Triglycerides"
- ]
- },
- {
- "PMID": "39466432",
- "Title": "Applied microbiology and biotechnology",
- "ArticleTitle": "Gut microbiota predict retinopathy in patients with diabetes: A longitudinal cohort study.",
- "Abstract": "The gut microbiota has emerged as an independent risk factor for diabetes and its complications. This research aimed to delve into the intricate relationship between the gut microbiome and diabetic retinopathy (DR) through a dual approach of cross-sectional and prospective cohort studies. In our cross-sectional study cross-sectional investigation involving ninety-nine individuals with diabetes, distinct microbial signatures associated with DR were identified. Specifically, gut microbiome profiling revealed decreased levels of Butyricicoccus and Ruminococcus torques group, alongside upregulated methanogenesis pathways among DR patients. These individuals concurrently exhibited lower concentrations of short-chain fatty acids in their plasma. Leveraging machine learning models, including random forest classifiers, we constructed a panel of microbial genera and genes that robustly differentiated DR cases. Importantly, these genera also demonstrated significant correlations with dietary patterns and the molecular profiles of peripheral blood mononuclear cells. Building upon these findings, our prospective cohort study followed 62 diabetes patients over a 2-year period to assess the predictive value of these microbial markers. The results underlined the panel's efficacy in predicting DR incidence. By stratifying patients based on the predictive genera and metabolites identified in the cross-sectional phase, we established significant associations between reduced levels of Butyricicoccus, plasma acetate, and increased susceptibility to DR. This investigation not only deepens our understanding of how gut microbiota influences DR but also underscores the potential of microbial markers as early indicators of disease risk. These insights hold promise for developing targeted interventions aimed at mitigating the impact of diabetic complications. KEY POINTS: \u2022 Microbial signatures are differed in diabetic patients with and without retinopathy \u2022 DR-related taxa are linked to dietary habits and transcriptomic profiles \u2022 Lower abundances of Butyricicoccus and acetate were prospectively associated with DR.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Gastrointestinal Microbiome",
- "Cross-Sectional Studies",
- "Male",
- "Diabetic Retinopathy",
- "Middle Aged",
- "Longitudinal Studies",
- "Prospective Studies",
- "Female",
- "Fatty Acids, Volatile",
- "Aged",
- "Ruminococcus",
- "Clostridiales",
- "Acetates",
- "Adult",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39466337",
- "Title": "Current medical research and opinion",
- "ArticleTitle": "Technological advancements in glucose monitoring and artificial pancreas systems for shaping diabetes care.",
- "Abstract": "The management of diabetes mellitus has undergone remarkable progress with the introduction of cutting-edge technologies in glucose monitoring and artificial pancreas systems. These innovations have revolutionized diabetes care, offering patients more precise, convenient, and personalized management solutions that significantly improve their quality of life. This review aims to provide a comprehensive overview of recent technological advancements in glucose monitoring devices and artificial pancreas systems, focusing on their transformative impact on diabetes care. A detailed review of the literature was conducted to examine the evolution of glucose monitoring technologies, from traditional invasive methods to more advanced systems. The review explores minimally invasive techniques such as continuous glucose monitoring (CGM) systems and flash glucose monitoring (FGM) systems, which have already been proven to enhance glycemic control and reduce the risk of hypoglycemia. In addition, emerging non-invasive glucose monitoring technologies, including optical, electrochemical, and electro-mechanical methods, were evaluated. These techniques are paving the way for more patient-friendly options that eliminate the need for frequent finger-prick tests, thereby improving adherence and ease of use. Advancements in closed-loop artificial pancreas systems, which integrate CGM with automated insulin delivery, were also examined. These systems, often referred to as \"hybrid closed-loop\" or \"automated insulin delivery\" systems, represent a significant leap forward in diabetes care by automating the process of insulin dosing. Such advancements aim to mimic the natural function of the pancreas, allowing for better glucose regulation without the constant need for manual interventions by the patient. Technological breakthroughs in glucose monitoring and artificial pancreas systems have had a profound impact on diabetes management, providing patients with more accurate, reliable, and individualized treatment options. These innovations hold the potential to significantly improve glycemic control, reduce the incidence of diabetes-related complications, and ultimately enhance the quality of life for individuals living with diabetes. Researchers are continually exploring novel methods to measure glucose more effectively and with greater convenience, further refining the future of diabetes care. Researchers are also investigating the integration of artificial intelligence and machine learning algorithms to further enhance the precision and predictive capabilities of glucose monitoring and insulin delivery systems. With ongoing advancements in sensor technology, connectivity, and data analytics, the future of diabetes care promises to deliver even more seamless, real-time management, empowering patients with greater autonomy and improved health outcomes.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Pancreas, Artificial",
- "Blood Glucose Self-Monitoring",
- "Blood Glucose",
- "Diabetes Mellitus",
- "Insulin",
- "Insulin Infusion Systems",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39465859",
- "Title": "Medicine",
- "ArticleTitle": "Association of triglyceride-glucose index with diabetes or prediabetes in Chinese hypertensive patients: A retrospective cohort study.",
- "Abstract": "Insulin resistance is a key factor in diabetes development. This study aimed to investigate the association between baseline triglyceride-glucose (TyG) index, a surrogate marker of insulin resistance, and the onset of hyperglycemia in Chinese individuals with hypertension. Using the Rich Healthcare Group database, this retrospective cohort study included 28,687 hypertensive individuals without preexisting diabetes. A wide range of demographic information and baseline biochemical indicators was collected and rigorously analyzed. This study utilized the Cox proportional hazards model and smooth curve fitting to explore the link between TyG index and the risk of developing hyperglycemia. The robustness of the findings was validated by sensitivity and subgroup analyses. During longitudinal monitoring of hypertensive patients in our retrospective cohort study, we observed that 5.31% (1524/28,687) progressed to diabetes, while 21.66% (4620/21,326) developed prediabetes. After adjusting for confounding variables, a statistically significant positive association was observed between the TyG index and the risk of hyperglycemia. Subgroup and sensitivity analyses further supported these findings, demonstrating consistent outcomes and reinforcing the robustness of our conclusions. The TyG index, which is significantly linked to hyperglycemia in hypertensives, can aid early risk identification and intervention.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Retrospective Studies",
- "Male",
- "Female",
- "Prediabetic State",
- "Middle Aged",
- "Hypertension",
- "Triglycerides",
- "Blood Glucose",
- "China",
- "Aged",
- "Insulin Resistance",
- "Biomarkers",
- "Adult",
- "Diabetes Mellitus",
- "Proportional Hazards Models",
- "Hyperglycemia",
- "Risk Factors",
- "East Asian People"
- ]
- },
- {
- "PMID": "39465722",
- "Title": "Medicine",
- "ArticleTitle": "Association between serum globulins and diabetes mellitus in American latent tuberculosis infection patients: A cross-sectional study.",
- "Abstract": "Diabetes mellitus (DM) is predisposing to the development of latent tuberculosis infection (LTBI). An understanding of the underlying factors of LTBI-DM is important for tuberculosis prevention and control. This study aims to evaluate the association between LTBI and DM among the noninstitutionalized civilian population in the United States, focusing on the impact of serum globulins. We performed a cross-sectional study design using public data from 2011 to 2012 National Health and Nutrition Examination Survey, focusing on participants diagnosed with LTBI who were aged 20 and above. Weighted Wilcoxon rank-sum and weighted chi-square tests were used to compare group differences. A multivariable logistic regression model was constructed to assess the association between serum globulin and DM, with subgroup analyses and evaluations of nonlinear relationships. Receiver operating characteristic curves were used to assess the predictive power of the models. A total of 694 participants (512 DM and 182 nonDM) were included in our study and the incidence of DM was 22%. Higher serum globulin levels were significantly associated with an increased risk of DM, with a 21% increase in risk for each unit increase in serum globulin (odds ratio\u2005=\u20051.21, 95% confidence interval [1.03, 1.43], P\u2005<\u2005.001). The relationship between serum globulin and DM was linear, and higher serum globulin levels were associated with a higher risk of DM, particularly in males (P\u2005=\u2005.043) and obese individuals (P\u2005=\u2005.019). The area under the curve for serum globulin predicting DM was 0.795, with an optimal cutoff value of 2.9. Elevated serum globulin levels are significantly associated with an increased risk of DM among individuals with LTBI, highlighting the potential role of serum globulin as a predictive biomarker for DM in this population. However, the specific mechanism between globulin and LTBI-DM needs to be further investigated.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Cross-Sectional Studies",
- "Female",
- "Latent Tuberculosis",
- "Middle Aged",
- "Adult",
- "United States",
- "Diabetes Mellitus",
- "Nutrition Surveys",
- "Serum Globulins",
- "Risk Factors",
- "Aged",
- "Young Adult",
- "Incidence",
- "ROC Curve",
- "Biomarkers"
- ]
- },
- {
- "PMID": "39465638",
- "Title": "Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions",
- "ArticleTitle": "Drug-coated balloons in high-risk patients and diabetes mellitus: A meta-analysis of 10 studies.",
- "Abstract": "We confirmed a significant advantage of DCB versus DES in the treatment of de novo lesions in high-risk patients and mainly in DM, reducing overall mortality, MACE and target lesion revascularization.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Angioplasty, Balloon, Coronary",
- "Cardiac Catheters",
- "Cardiovascular Agents",
- "Coated Materials, Biocompatible",
- "Coronary Artery Disease",
- "Diabetes Mellitus",
- "Drug-Eluting Stents",
- "Equipment Design",
- "Odds Ratio",
- "Percutaneous Coronary Intervention",
- "Risk Assessment",
- "Risk Factors",
- "Time Factors",
- "Treatment Outcome"
- ]
- },
- {
- "PMID": "39465521",
- "Title": "Archives of Iranian medicine",
- "ArticleTitle": "Prevalence of Chronic Kidney Disease and Associated Factors among the Diabetic and Prediabetic Population in the Bandare-Kong Cohort Study; A Population-Based Study.",
- "Abstract": "The study emphasizes the importance of early detection and management of CKD risk factors, particularly among high-risk individuals, to mitigate CKD progression and associated complications. By addressing modifiable risk factors, proactive screening, and enhanced awareness, significant strides can be made in reducing CKD burden and improving patient outcomes.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Middle Aged",
- "Female",
- "Male",
- "Prediabetic State",
- "Renal Insufficiency, Chronic",
- "Adult",
- "Iran",
- "Aged",
- "Risk Factors",
- "Prevalence",
- "Glomerular Filtration Rate",
- "Prospective Studies",
- "Cohort Studies",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39464188",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "A mobile health application use among diabetes mellitus patients: a systematic review and meta-analysis.",
- "Abstract": "https://www.crd.york.ac.uk/prospero/, identifier 42024537917.",
- "Predictions": [
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus",
- "Mobile Applications",
- "Self Care",
- "Telemedicine"
- ]
- },
- {
- "PMID": "39463812",
- "Title": "Ethnicity & disease",
- "ArticleTitle": "Racial Disparities in Foot Examination among People with Diabetes in Brazil: A Nationwide Survey, 2019.",
- "Abstract": "Black Brazilians with diabetes had higher negligence of foot examination by health care professionals. Strengthening primary care would help mitigate systemic racism in Brazil.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Brazil",
- "Female",
- "Male",
- "Adult",
- "Middle Aged",
- "Diabetic Foot",
- "Adolescent",
- "Young Adult",
- "Healthcare Disparities",
- "Aged",
- "White People",
- "Physical Examination",
- "Surveys and Questionnaires",
- "Diabetes Mellitus",
- "Black People",
- "Prevalence"
- ]
- },
- {
- "PMID": "39463434",
- "Title": "Scientific reports",
- "ArticleTitle": "Cystic fibrosis-related diabetes is associated with reduced islet protein expression of GLP-1 receptor and perturbation of cell-specific transcriptional programs.",
- "Abstract": "Insulin secretion is impaired in individuals with cystic fibrosis (CF), contributing to high rates of CF-related diabetes (CFRD) and substantially increasing disease burden. To develop improved therapies for CFRD, better knowledge of pancreatic pathology in CF is needed. Glucagon like peptide-1 (GLP-1) from islet \u03b1 cells potentiates insulin secretion by binding GLP-1 receptors (GLP-1Rs) on \u03b2 cells. We determined whether expression of GLP-1 and/or its signaling components are reduced in CFRD, thereby contributing to impaired insulin secretion. Immunohistochemistry of pancreas from humans with CFRD versus no-CF/no-diabetes revealed no difference in GLP-1 immunoreactivity per islet area, whereas GLP-1R immunoreactivity per islet area or per insulin-positive islet area was reduced in CFRD. Using spatial transcriptomics, we observed several differentially expressed \u03b1- and/or \u03b2-cell genes between CFRD and control pancreas. In CFRD, we found upregulation of \u03b1-cell PCSK1 which encodes the enzyme (PC1/3) that generates GLP-1, and downregulation of \u03b1-cell PCSK1N which inhibits PC1/3. Gene set enrichment analysis also revealed \u03b1 and \u03b2 cell-specific pathway dysregulation in CFRD. Together, our data suggest intra-islet GLP-1 is not limiting in CFRD, but its action may be restricted due to reduced GLP-1R protein levels. Thus, restoring \u03b2-cell GLP-1R protein expression may improve \u03b2-cell function in CFRD.",
- "Predictions": [
- "Diabetes Mellitus",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Cystic Fibrosis",
- "Glucagon-Like Peptide-1 Receptor",
- "Male",
- "Female",
- "Adult",
- "Diabetes Mellitus",
- "Insulin-Secreting Cells",
- "Islets of Langerhans",
- "Glucagon-Secreting Cells",
- "Glucagon-Like Peptide 1",
- "Young Adult",
- "Gene Expression Regulation",
- "Adolescent",
- "Insulin"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/diabetes_type_1.json b/model/data/diabetes_type_1.json
deleted file mode 100644
index abc3610f9b907c803d5c9a42432f0924b9d43865..0000000000000000000000000000000000000000
--- a/model/data/diabetes_type_1.json
+++ /dev/null
@@ -1,472 +0,0 @@
-[
- {
- "PMID": "39737893",
- "Title": "Nutrition & diabetes",
- "ArticleTitle": "The genetic and observational nexus between diabetes and arthritis: a national health survey and mendelian randomization analysis.",
- "Abstract": "There is an association between diabetes and arthritis, with potential genetic links between Type 1 Diabetes and RA.",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Mendelian Randomization Analysis",
- "Male",
- "Female",
- "Nutrition Surveys",
- "Middle Aged",
- "Genome-Wide Association Study",
- "Arthritis, Rheumatoid",
- "Adult",
- "Arthritis",
- "Prevalence",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Aged",
- "Genetic Predisposition to Disease",
- "Logistic Models",
- "Polymorphism, Single Nucleotide"
- ]
- },
- {
- "PMID": "39737643",
- "Title": "Journal of biomedical materials research. Part B, Applied biomaterials",
- "ArticleTitle": "Beneficial Effects of Tilapia Fish Skin on Excisional Skin Wound Healing in a Type I Diabetic Rat Model.",
- "Abstract": "IntroductionProlonged hyperglycemia in diabetic patients often impairs wound healing, leading to chronic infections and complications. This study aimed to evaluate the potential of fresh Tilapia fish skin as a treatment to enhance wound healing in diabetic rats. MethodsThirty-nine healthy adult albino rats, weighing between 150 and 200\u2009g, were divided into three groups: non-diabetic rats with untreated wounds [C-], diabetic rats with untreated wounds [C+], and diabetic rats treated with fresh Tilapia skin [TT]. The healing process was monitored through clinical observation, gross examination, and histopathological analysis. ResultsThe results demonstrated that the Tilapia skin treatment accelerated wound healing, as evidenced by complete reepithelialization, full epidermal cell differentiation, an intact dermo-epidermal junction, and a reorganized dermis with fewer blood vessels. ConclusionFresh Tilapia skin proved to be a safe and effective dressing for promoting wound healing and managing infection in diabetic wounds.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Animals",
- "Tilapia",
- "Rats",
- "Skin",
- "Wound Healing",
- "Diabetes Mellitus, Experimental",
- "Diabetes Mellitus, Type 1",
- "Male"
- ]
- },
- {
- "PMID": "39736868",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Fear of hypoglycemia and sleep in children with type 1 diabetes and their parents.",
- "Abstract": "www.ClinicalTrials.gov, identifier NCT03103867.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Hypoglycemia",
- "Child",
- "Female",
- "Parents",
- "Adolescent",
- "Fear",
- "Cross-Over Studies",
- "Adult",
- "Sleep",
- "Middle Aged",
- "Insulin Infusion Systems",
- "Blood Glucose Self-Monitoring",
- "Insulin",
- "Blood Glucose",
- "Hypoglycemic Agents"
- ]
- },
- {
- "PMID": "39736865",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Quantitative ultrasound imaging reveals distinct fracture-associated differences in tibial intracortical pore morphology and viscoelastic properties in aged individuals with and without diabetes mellitus - an exploratory study.",
- "Abstract": "Both T1DM and T2DM showed altered bone metabolism, with T2DM linked to impaired tissue formation. CortBS provides insights into pathophysiological changes in diabetic bone and provided superior fracture risk assessment in DM patients compared to DXA.",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Ultrasonography",
- "Aged",
- "Middle Aged",
- "Bone Density",
- "Diabetes Mellitus, Type 2",
- "Tibia",
- "Absorptiometry, Photon",
- "Case-Control Studies",
- "Diabetes Mellitus, Type 1",
- "Cortical Bone",
- "Elasticity"
- ]
- },
- {
- "PMID": "39735417",
- "Title": "Journal of diabetes research",
- "ArticleTitle": "Identifying Promising Immunomodulators for Type 1 Diabetes (T1D) and Islet Transplantation.",
- "Abstract": "Type 1 diabetes (T1D) is an autoimmune chronic disorder that damages beta cells in the pancreatic islets of Langerhans and results in hyperglycemia due to the loss of insulin. Exogenous insulin therapy can save lives but does not stop disease progression. Thus, an effective therapy may require beta cell restoration and suppression of the autoimmune response. However, currently, there are no treatment options available that can reverse T1D. Within the National Clinical Trial (NCT) database, a majority of over 3000 trials to treat T1D are devoted to insulin therapy. This review focuses on noninsulin pharmacological therapies, specifically immunomodulators. Many investigational new drugs fall under this category, such as the recently FDA-approved CD3 monoclonal antibody teplizumab to delay the onset of T1D. In total, we identified 39 different immunomodulatory investigational drugs. FDA-approved teplizumab for Stage 2 T1D is discussed along with other immunomodulators that have been tested in Phase 3 clinical trials or higher, including otelixizumab (another anti-CD3 monoclonal antibody), daclizumab (an anti-CD25 monoclonal antibody), ladarixin (CXCR1/2 inhibitor), and antithymocyte globulin (ATG). Immunomodulators also play roles in islet transplantation and cellular therapies like FDA-approved Lantidra. Several immunomodulators involved in Phase 3 clinical studies of islet transplantation are also discussed, including alemtuzumab, basiliximab, etanercept, and reparixin, some already FDA-approved for other uses. These include alemtuzumab, basiliximab, etanercept, and reparixin, some of which have been FDA-approved for other uses. This review provides background, mechanism of action, results of completed trials, and adverse effects as well as details regarding ongoing clinical trials for each of these immunomodulators. ",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Islets of Langerhans Transplantation",
- "Immunomodulating Agents",
- "Immunologic Factors",
- "Animals",
- "Antibodies, Monoclonal, Humanized"
- ]
- },
- {
- "PMID": "39733115",
- "Title": "Scientific reports",
- "ArticleTitle": "Dynamic modeling of the Insulin-Glucose-Glucocorticoid impulsive control system.",
- "Abstract": "This paper introduces a class of insulin-glucose-glucocorticoid impulsive systems in the treatment of patients with diabetes to consider the effect of glucocorticoids. The existence and uniqueness of the positive periodic solution of the impulsive model at double fixed time is confirmed for type 1 diabetes mellitus (T1DM) using the [Formula: see text] function. Further, the global asymptotic stability of the positive periodic solution is achieved following Floquet multiplier theory and comparison principle. Additionally, the permanence of the system is confirmed in type 2 diabetes mellitus (T2DM) via the comparison theorem. Numerical analysis verifies the results of theoretical calculations and indicates that combining therapeutic strategies under hormonal interactions with the dose of exogenous insulin and glucocorticoid medicines within organisms provides more reasonable clinical strategies.",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Insulin",
- "Glucocorticoids",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Glucose",
- "Blood Glucose",
- "Models, Biological"
- ]
- },
- {
- "PMID": "39732907",
- "Title": "Scientific reports",
- "ArticleTitle": "A reinforcement learning approach to effective forecasting of pediatric hypoglycemia in diabetes I patients using an extended de Bruijn graph.",
- "Abstract": "Pediatric diabetes I is an endemic and an especially difficult disease; indeed, at this point, there does not exist a cure, but only careful management that relies on anticipating hypoglycemia. The changing physiology of children producing unique blood glucose signatures, coupled with inconsistent activities, e.g., playing, eating, napping, makes \"forecasting\" elusive. While work has been done for adult diabetes I, this does not successfully translate for children. In the work presented here, we adopt a reinforcement approach by leveraging the de Bruijn graph that has had success in detecting patterns in sequences of symbols-most notably, genomics and proteomics. We translate a continuous signal of blood glucose levels into an alphabet that then can be used to build a de Bruijn, with some extensions, to determine blood glucose states. The graph allows us to \"tune\" its efficacy by computationally ignoring edges that provide either no information or are not related to entering a hypoglycemic episode. We can then use paths in the graph to anticipate hypoglycemia in advance of about 30 minutes sufficient for a clinical setting and additionally find actionable rules that accurate and effective. All the code developed for this study can be found at: https://github.com/KurbanIntelligenceLab/dBG-Hypoglycemia-Forecast .",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Hypoglycemia",
- "Diabetes Mellitus, Type 1",
- "Child",
- "Blood Glucose",
- "Forecasting",
- "Algorithms",
- "Reinforcement, Psychology"
- ]
- },
- {
- "PMID": "39732545",
- "Title": "Endocrinologia, diabetes y nutricion",
- "ArticleTitle": "Nurse-led therapeutic patient education program on glycemic control and emotional wellbeing in adolescents with type 1 diabetes mellitus during hospital transition.",
- "Abstract": "The structured therapeutic education program for adolescents with T1DM transitioning from pediatric to adult care maintains glycemic control and emotional wellbeing.",
- "Predictions": [
- "Mental Health",
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Adolescent",
- "Male",
- "Female",
- "Patient Education as Topic",
- "Glycemic Control",
- "Transition to Adult Care",
- "Self Care",
- "Emotions",
- "Mental Health",
- "Feeding and Eating Disorders"
- ]
- },
- {
- "PMID": "39731141",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Prevalence and associated factors of psychiatric problems in children aged 6-18 years with type-1 diabetes mellitus in Gondar, Ethiopia: a cross-sectional study.",
- "Abstract": "The prevalence of psychiatric problems in diabetic children was significantly high and children living with single parent, paternal educational status, glycemic control, family history of diabetes, and family size were found to have significant association with the occurrence of psychiatric problems in diabetic children.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Adolescent",
- "Male",
- "Child",
- "Female",
- "Cross-Sectional Studies",
- "Ethiopia",
- "Diabetes Mellitus, Type 1",
- "Prevalence",
- "Mental Disorders",
- "Risk Factors",
- "Follow-Up Studies"
- ]
- },
- {
- "PMID": "39730838",
- "Title": "Scientific reports",
- "ArticleTitle": "Type 1 diabetes genetic risk score variation across ancestries using whole genome sequencing and array-based approaches.",
- "Abstract": "A Type 1 Diabetes Genetic Risk Score (T1DGRS) aids diagnosis and prediction of Type 1 Diabetes (T1D). While traditionally derived from imputed array genotypes, Whole Genome Sequencing (WGS) provides a more direct approach and is now increasingly used in clinical and research studies. We investigated the concordance between WGS-based and array-based T1DGRS across genetic ancestries in 149,265 UK Biobank participants using WGS, TOPMed-imputed, and 1000 Genomes-imputed array genotypes. In the overall cohort, WGS-based T1DGRS demonstrated strong correlation with TOPMed-imputed array-based score (r\u2009=\u20090.996, average WGS-based score 0.0028 standard deviations (SD) lower, p\u2009<\u200910",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Adult",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Diabetes Mellitus, Type 1",
- "Genetic Predisposition to Disease",
- "Genetic Risk Score",
- "Genome, Human",
- "Genome-Wide Association Study",
- "Genotype",
- "Polymorphism, Single Nucleotide",
- "Whole Genome Sequencing",
- "Racial Groups"
- ]
- },
- {
- "PMID": "39728423",
- "Title": "Medical sciences (Basel, Switzerland)",
- "ArticleTitle": "An Unusual Case of Nephrotic Range Proteinuria in a Short-Standing Type 1 Diabetic Patient with Newly Diagnosed Systemic Lupus Erythematosus: A Case Report and Literature Review.",
- "Abstract": "Lupus podocytopathy is an infrequent anatomopathological entity, so this case is presented as the first reported in Peru, and a literature review is made.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Adult",
- "Lupus Erythematosus, Systemic",
- "Diabetes Mellitus, Type 1",
- "Proteinuria",
- "Nephrotic Syndrome",
- "Podocytes"
- ]
- },
- {
- "PMID": "39727851",
- "Title": "Biosensors",
- "ArticleTitle": "Sensing Biomechanical Alterations in Red Blood Cells of Type 1 Diabetes Patients: Potential Markers for Microvascular Complications.",
- "Abstract": "In physiological conditions, red blood cells (RBCs) demonstrate remarkable deformability, allowing them to undergo considerable deformation when passing through the microcirculation. However, this deformability is compromised in Type 1 diabetes mellitus (T1DM) and related pathological conditions. This study aims to investigate the biomechanical properties of RBCs in T1DM patients, focusing on identifying significant mechanical alterations associated with microvascular complications (MCs). We conducted a case-control study involving 38 T1DM subjects recruited from the Diabetes Care Unit at Fondazione Policlinico Gemelli Hospital, comprising 22 without MCs (control group) and 16 with MCs (pathological group). Atomic Force Microscopy was employed to assess RBC biomechanical properties in a liquid environment. We observed significant RBC stiffening in individuals with MCs, particularly during large indentations that mimic microcirculatory deformations. Univariate analysis unveiled significant differences in RBC stiffness (median difference 0.0006 N/m, ",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Erythrocytes",
- "Male",
- "Female",
- "Adult",
- "Case-Control Studies",
- "Biomechanical Phenomena",
- "Biomarkers",
- "Middle Aged",
- "Microscopy, Atomic Force"
- ]
- },
- {
- "PMID": "39727210",
- "Title": "Journal of the American Heart Association",
- "ArticleTitle": "Inflammatory Markers and Measures of Cardiovascular Autonomic Neuropathy in Type 1 Diabetes.",
- "Abstract": "URL: https://www.clinicaltrials.gov; Unique identifiers: NCT02936843, NCT02017171.",
- "Predictions": [
- "Cardiovascular diseases",
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Adult",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Autonomic Nervous System",
- "Autonomic Nervous System Diseases",
- "Biomarkers",
- "Cardiovascular Diseases",
- "Cardiovascular System",
- "Cross-Sectional Studies",
- "Diabetes Mellitus, Type 1",
- "Diabetic Neuropathies",
- "Heart Rate",
- "Inflammation",
- "Inflammation Mediators",
- "Receptors, Urokinase Plasminogen Activator"
- ]
- },
- {
- "PMID": "39726058",
- "Title": "Journal of medical case reports",
- "ArticleTitle": "Immune checkpoint inhibitor-associated diabetic ketoacidosis and insulin-dependent diabetes: a case report.",
- "Abstract": "This case report underscores the risk of diabetic ketoacidosis linked to nivolumab, even in patients without predisposing factors, emphasizing the need for increased vigilance among both oncologists and physicians. It highlights the importance of monitoring for new-onset diabetes and diabetic ketoacidosis, whether immunotherapy is active or discontinued, and ensuring comprehensive care including hospitalization, insulin management, and diabetes education if diabetic ketoacidosis is diagnosed.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetic Ketoacidosis",
- "Male",
- "Aged",
- "Immune Checkpoint Inhibitors",
- "Nivolumab",
- "Diabetes Mellitus, Type 1",
- "Insulin",
- "Adenocarcinoma",
- "Hypoglycemic Agents",
- "Antineoplastic Agents, Immunological"
- ]
- },
- {
- "PMID": "39725378",
- "Title": "Experimental parasitology",
- "ArticleTitle": "Impact of acute schistosomiasis mansoni and concurrent type 1 diabetes on pancreatic architecture in mice.",
- "Abstract": "It is not well understood how type 1 diabetes (T1D) and concomitant acute schistosomiasis mansoni affect pancreatic architecture. Male Swiss mice were administered streptozotocin (single 100\u00a0mg/kg i.p.) and thirty days later infected with 80 Schistosoma mansoni cercariae. Mice were divided into groups (n\u00a0=\u00a05): A (healthy control), B (infected), C (uninfected diabetic), and D (diabetic\u00a0+\u00a0infected) and euthanized at week 9 post-infection. Blood glucose levels, biometry, stereology, and pancreatic histology were evaluated. Groups C and D showed hyperglycemia (>200\u00a0mg/dL). Group B had a higher (+79%) pancreatic mass than A. The endocrine pancreas showed fewer islets of Langerhans (-62%; -50%) and a smaller islet area (-36%; -30%) in C and D, respectively, compared to A. Group D had a smaller (-37%) islet area than B. The volume density of the islets was reduced (-33%) in group C compared to A. Within the exocrine pancreas, the volume density of the pancreatic parenchyma was reduced in groups B (-29%) and D (-26%), and increased in C (+15%) compared to A. Group D was reduced (-35%) compared to C. Group D showed generalized pancreatitis, including disrupted tissue with multiple nuclei of destroyed acinar cells and lost connective tissue and acinar cells with a paucity of zymogen granules. Pancreatic stellate cells were found around areas of distorted architecture. Paired adult worms were found within the pancreatic vessels. In conclusion, concomitant T1D and schistosomiasis mansoni promote extensive exocrine and endocrine changes in the pancreas, whereas pancreatic involvement begins in acute schistosomiasis.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Animals",
- "Mice",
- "Male",
- "Schistosomiasis mansoni",
- "Diabetes Mellitus, Type 1",
- "Pancreas",
- "Diabetes Mellitus, Experimental",
- "Blood Glucose",
- "Schistosoma mansoni",
- "Islets of Langerhans",
- "Acute Disease"
- ]
- },
- {
- "PMID": "39724143",
- "Title": "PLoS genetics",
- "ArticleTitle": "Inhibitory KIRs decrease HLA class II-mediated protection in Type 1 Diabetes.",
- "Abstract": "Inhibitory killer cell immunoglobulin-like receptors (iKIRs) are a family of inhibitory receptors that are expressed by natural killer (NK) cells and late-stage differentiated T cells. There is accumulating evidence that iKIRs regulate T cell-mediated immunity. Recently, we reported that T cell-mediated control was enhanced by iKIRs in chronic viral infections. We hypothesized that in the context of autoimmunity, where an enhanced T cell response might be considered detrimental, iKIRs would have an opposite effect. We studied Type 1 diabetes (T1D) as a paradigmatic example of autoimmunity. In T1D, variation in the Human Leucocyte Antigen (HLA) genes explains up to 50% of the genetic risk, indicating that T cells have a major role in T1D etiopathogenesis. To investigate if iKIRs affect this T cell response, we asked whether HLA associations were modified by iKIR genes. We conducted an immunogenetic analysis of a case-control T1D dataset (N = 11,961) and found that iKIR genes, in the presence of genes encoding their ligands, have a consistent and significant effect on protective HLA class II genetic associations. Our results were validated in an independent data set. We conclude that iKIRs significantly decrease HLA class II protective associations and suggest that iKIRs regulate CD4+ T cell responses in T1D.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Receptors, KIR",
- "Genetic Predisposition to Disease",
- "Histocompatibility Antigens Class II",
- "Killer Cells, Natural",
- "Case-Control Studies",
- "Autoimmunity",
- "T-Lymphocytes",
- "Male",
- "Female"
- ]
- },
- {
- "PMID": "39720308",
- "Title": "Journal of diabetes research",
- "ArticleTitle": "Young-Onset Diabetes in Sri Lanka: Experience From the Developing World.",
- "Abstract": {
- "b": "Conclusion:",
- "i": "p"
- },
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Sri Lanka",
- "Female",
- "Male",
- "Diabetes Mellitus, Type 1",
- "Adolescent",
- "Young Adult",
- "Diabetes Mellitus, Type 2",
- "Age of Onset",
- "Retrospective Studies",
- "Prevalence",
- "Developing Countries",
- "Child",
- "Adult",
- "Glycated Hemoglobin",
- "Diabetic Ketoacidosis"
- ]
- },
- {
- "PMID": "39720253",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Sclerostin as a new target of diabetes-induced osteoporosis.",
- "Abstract": "Sclerostin, a protein synthesized by bone cells, is a product of the ",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Osteoporosis",
- "Adaptor Proteins, Signal Transducing",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus, Type 2",
- "Animals",
- "Genetic Markers",
- "Wnt Signaling Pathway",
- "Bone Morphogenetic Proteins"
- ]
- },
- {
- "PMID": "39719890",
- "Title": "Journal of biomedical materials research. Part A",
- "ArticleTitle": "Supramolecular Peptide Depots for Glucose-Responsive Glucagon Delivery.",
- "Abstract": "Precise blood glucose control continues to be a critical challenge in the treatment and management of type 1 diabetes in order to mitigate both acute and chronic complications. This study investigates the development of a supramolecular peptide amphiphile (PA) material functionalized with phenylboronic acid (PBA) for glucose-responsive glucagon delivery. The PA-PBA system self-assembles into nanofibrillar hydrogels in the presence of physiological glucose levels, resulting in stable hydrogels capable of releasing glucagon under hypoglycemic conditions. Glucose responsiveness is driven by reversible binding between PBA and glucose, which modulates the electrostatic interactions necessary for hydrogel formation and dissolution. Through comprehensive in\u00a0vitro characterization, including circular dichroism, zeta potential measurements, and rheological assessments, the PA-PBA system is found to exhibit glucose-dependent assembly, enabling controlled glucagon release that is inversely related to glucose concentration. Glucagon release is accelerated under low glucose conditions, simulating a hypoglycemic state, with a reduced rate seen at higher glucose levels. Evaluation of the platform in\u00a0vivo using a type 1 diabetic mouse model demonstrates the efficacy in protecting against insulin-induced hypoglycemia by restoring blood glucose levels following an insulin overdose. The ability to tailor glucagon release in response to fluctuating glucose concentrations underscores the potential of this platform for improving glycemic control. These findings suggest that glucose-stabilized supramolecular peptide hydrogels hold significant promise for responsive drug delivery applications, offering an approach to manage glucose levels in diabetes and other metabolic disorders.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Glucagon",
- "Animals",
- "Glucose",
- "Peptides",
- "Hydrogels",
- "Diabetes Mellitus, Experimental",
- "Blood Glucose",
- "Mice",
- "Boronic Acids",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Drug Delivery Systems"
- ]
- },
- {
- "PMID": "39718005",
- "Title": "Endocrinology, diabetes & metabolism",
- "ArticleTitle": "Predicting Time in Range Without Hypoglycaemia Using a Risk Calculator for Intermittently Scanned CGM in Type 1 Diabetes.",
- "Abstract": "Clinical and socio-economic factors significantly influence OGC in type 1 diabetes. The application of statistical models offers a reliable means of predicting the likelihood of achieving OGC following isCGM system implementation.",
- "Predictions": [
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Female",
- "Male",
- "Retrospective Studies",
- "Hypoglycemia",
- "Adult",
- "Blood Glucose Self-Monitoring",
- "Blood Glucose",
- "Middle Aged",
- "Risk Assessment",
- "Glycemic Control",
- "Glycated Hemoglobin",
- "Adolescent",
- "Young Adult",
- "Time Factors"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/diabetes_type_2.json b/model/data/diabetes_type_2.json
deleted file mode 100644
index 458c30bae06223cee821a33588793c491f3376b2..0000000000000000000000000000000000000000
--- a/model/data/diabetes_type_2.json
+++ /dev/null
@@ -1,499 +0,0 @@
-[
- {
- "PMID": "39738226",
- "Title": "Scientific reports",
- "ArticleTitle": "Excessive daytime sleepiness and its predictors among type 2 diabetes mellitus patients at central ethiopia.",
- "Abstract": "Excessive daytime sleepiness is a common finding among type 2 diabetes mellitus patients. However there is scarce data that shows the magnitude of excessive daytime sleepiness, & its association with type 2 diabetes mellitus. Hence, the study aimed to assess the prevalence of excessive daytime sleepiness and its associated factors among type 2 diabetes mellitus patients at Wolkite University Specialized Hospital. A Hospital-based cross-sectional study was employed from January 15 to March 15, 2022, among 229 Type 2 diabetes mellitus patients. Data was collected by semi-structured questionnaires, then entered into the Epi data version 4.6 and exported to SPSS version 25.0 for analysis. Binary and multiple logistic regression analysis was used to assess factors associated with excessive daytime sleepiness and statistical significance was set at P-value\u2009<\u20090.05. The prevalence of Excessive daytime sleepiness among type 2 diabetes mellitus was 27.1%. Age (AOR: 1.08; 95%CI: 1.03, 1.12), frequent snoring (AOR: 2.9; 95%CI: 1.24, 6.80), comorbid hypertension (AOR: 2.64; 95%CI: 1.17, 5.96), obesity (AOR: 2.7; 95%CI: 1.03, 7.13), and poor glycemic control (AOR: 6.68; 95%CI: 1.83, 24.41) were independently associated with Excessive daytime sleepiness among type 2 diabetes mellitus patients. Excessive daytime sleepiness was reported in more than a quarter of type 2 diabetes mellitus patients. Age, frequent snoring, hypertension, obesity, and poor glycemic control were significantly associated with Excessive daytime sleepiness among type 2 diabetes mellitus patients. Therefore health care providers should assess not only for how well their patients' diabetes is controlled but also for excessive daytime sleepiness.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Ethiopia",
- "Male",
- "Female",
- "Middle Aged",
- "Disorders of Excessive Somnolence",
- "Cross-Sectional Studies",
- "Adult",
- "Prevalence",
- "Risk Factors",
- "Aged",
- "Hypertension",
- "Surveys and Questionnaires",
- "Comorbidity",
- "Obesity",
- "Snoring"
- ]
- },
- {
- "PMID": "39737893",
- "Title": "Nutrition & diabetes",
- "ArticleTitle": "The genetic and observational nexus between diabetes and arthritis: a national health survey and mendelian randomization analysis.",
- "Abstract": "There is an association between diabetes and arthritis, with potential genetic links between Type 1 Diabetes and RA.",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Mendelian Randomization Analysis",
- "Male",
- "Female",
- "Nutrition Surveys",
- "Middle Aged",
- "Genome-Wide Association Study",
- "Arthritis, Rheumatoid",
- "Adult",
- "Arthritis",
- "Prevalence",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Aged",
- "Genetic Predisposition to Disease",
- "Logistic Models",
- "Polymorphism, Single Nucleotide"
- ]
- },
- {
- "PMID": "39737509",
- "Title": "The Indian journal of medical research",
- "ArticleTitle": "ICMR-MDRF Diabetes Biosamples: Cohort profile.",
- "Abstract": "Background & objectives Biobanks are crucial for biomedical research, enabling new treatments and medical advancements. The biobank at the Madras Diabetes Research Foundation (MDRF) aims to gather, process, store, and distribute biospecimens to assist scientific studies. Methods This article details the profile of two cohorts: the Indian Council of Medical Research-India Diabetes (ICMR-INDIAB) study and the Registry of people with diabetes in India with young age at onset (ICMR-YDR). The ICMR-INDIAB study is the largest epidemiological study on diabetes in India, encompassing a nationally representative sample of individuals aged 20 yr and older from urban and rural areas in every State across the country. The ICMR-YDR is the first national-level, multicentric clinic-based registry focusing on youth-onset diabetes in India, aiming to understand the disease patterns and variations in youth-onset diabetes across different country regions. Results Key operations at the MDRF biobank include collecting and processing samples, where serum and whole blood samples are aliquoted and transferred through a cold chain to the central laboratory, and then stored in Siruseri (29 km from the capital city of Chennai, Tamil Nadu). Samples are barcoded, linked to subject information, and stored in freezers or liquid nitrogen (LN2) vessels, with inventory tracked via software for easy retrieval. A register records access to the biobank, ensuring sample integrity and compliance with regulatory requirements. The biobank adheres to the ICMR's National Ethical Guidelines for Biomedical and Health Research involving human participants. Interpretation & conclusions The biobank enables the analysis of biomarkers in stored samples, aiding in scientifically sound decisions, treating patients, and potentially curing diabetes.",
- "Predictions": [
- "Diabetes",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "India",
- "Biological Specimen Banks",
- "Adult",
- "Female",
- "Male",
- "Diabetes Mellitus",
- "Registries",
- "Biomedical Research",
- "Young Adult",
- "Cohort Studies",
- "Age of Onset",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39736941",
- "Title": "Archives of Razi Institute",
- "ArticleTitle": "Involvement of \u03b3-Aminobutyric Acid and N-methyl-D-aspartate Receptors in Diabetic Gastropathy in Rats: Possible Beneficial Effect of Prolonged Treatment with Insulin and Magnesium Supplement.",
- "Abstract": "Gastrointestinal dysfunction is a severe and common complication in diabetic patients. Some evidence shows that gamma-aminobutyric acid (GABA) and glutamate contribute to diabetic gastrointestinal abnormalities. Therefore, we examined the impact of prolonged treatment with insulin and magnesium supplements on the expression pattern of GABA type A (GABA-A), GABA-B, and N-methyl-D-aspartate (NMDA) glutamate receptors as well as nitric oxide synthase 1 (NOS-1) in the stomach of type 2 diabetic rats. Twenty-four male Wistar rats were randomized to four groups (six rats each): 1) control, 2) type 2 diabetes: rats fed with a high-fat diet for three months + a low dose of streptozotocin (35 mg/kg), 3) type 2 diabetes + magnesium, and 4) type 2 diabetes + insulin. The expression of NOS-1, GABA-A, GABA-B, and NMDA receptors was detected using western blotting. The NOS-1 expression was substantially diminished (P<0.01), while the expression of GABA-A (P<0.001), GABA-B (P<0.001), and NMDA (P<0.001) receptors was enhanced in the stomach of diabetic rats relative to control. Treatment with magnesium and insulin improved NOS-1 expression in diabetic rats, although this effect was greater in magnesium treatment alone. Magnesium also restored the expression of GABA-A and GABA-B receptors in diabetic rats to control values. Moreover, insulin treatment improved GABA-A receptor expression in diabetic rats (P<0.05). No considerable alterations were detected in NMDA receptor levels in the treatment groups. The results suggest a significant role of magnesium and insulin in improving gastric motility and secretory disorders associated with diabetes through modifying the expression of GABAergic receptors.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Animals",
- "Male",
- "Rats, Wistar",
- "Receptors, N-Methyl-D-Aspartate",
- "Diabetes Mellitus, Experimental",
- "Insulin",
- "Rats",
- "Magnesium",
- "Diabetes Mellitus, Type 2",
- "Nitric Oxide Synthase Type I",
- "Dietary Supplements",
- "Random Allocation",
- "Streptozocin"
- ]
- },
- {
- "PMID": "39736870",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Construction and validation of a nomogram model for predicting diabetic peripheral neuropathy.",
- "Abstract": "The DPN nomogram prediction model, containing 7 significant variables, has exhibited excellent performance. Its generalization to clinical practice could potentially help in the early detection and prompt intervention for high-risk DPN patients.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Nomograms",
- "Diabetic Neuropathies",
- "Female",
- "Male",
- "Middle Aged",
- "Aged",
- "Risk Factors",
- "ROC Curve",
- "Diabetes Mellitus, Type 2",
- "Prognosis",
- "Adult"
- ]
- },
- {
- "PMID": "39736865",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Quantitative ultrasound imaging reveals distinct fracture-associated differences in tibial intracortical pore morphology and viscoelastic properties in aged individuals with and without diabetes mellitus - an exploratory study.",
- "Abstract": "Both T1DM and T2DM showed altered bone metabolism, with T2DM linked to impaired tissue formation. CortBS provides insights into pathophysiological changes in diabetic bone and provided superior fracture risk assessment in DM patients compared to DXA.",
- "Predictions": [
- "Diabetes type 1",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Ultrasonography",
- "Aged",
- "Middle Aged",
- "Bone Density",
- "Diabetes Mellitus, Type 2",
- "Tibia",
- "Absorptiometry, Photon",
- "Case-Control Studies",
- "Diabetes Mellitus, Type 1",
- "Cortical Bone",
- "Elasticity"
- ]
- },
- {
- "PMID": "39736861",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Case report: A 51-year-old diabetic patient with primary bilateral macronodular adrenal hyperplasia and primary hyperparathyroidism.",
- "Abstract": "A 51-year-old female patient with diabetes mellitus and hypertension, exhibiting poor control of blood sugar and blood pressure, was unexpectedly found to have multiple large adrenal nodules, excessive cortisol secretion, and adrenocorticotropic hormone inhibition. Cortisol levels remained unresponsive to both low-dose and high-dose dexamethasone tests, leading to a diagnosis of primary bilateral macronodular adrenal hyperplasia. Concurrently, elevated blood calcium and parathyroid hormone levels, along with 99mTc-methoxyisobutyl isonitrile (99mTc-MIBI) imaging revealing increased 99mTc-MIBI uptake in the right inferior parathyroid gland, suggest the consideration of primary hyperparathyroidism. This case is presented in light of the uncommon clinical coexistence of primary bilateral macronodular adrenal hyperplasia and primary hyperparathyroidism.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Middle Aged",
- "Hyperparathyroidism, Primary",
- "Adrenal Glands",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39736858",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Association of oxidative balance score with cardiovascular disease and all-cause and cardiovascular mortality in American adults with type 2 diabetes: data from the National Health and Nutrition examination survey 1999-2018.",
- "Abstract": "Adherence to higher OBS was associated with reduced CVD prevalence and mortality risk in T2D. Antioxidant diet and lifestyle had more significant associations with mortality and CVD prevalence, respectively. However, as these findings are merely associations and do not allow causal inferences to be drawn, future validation in high-quality randomized controlled trials is needed.",
- "Predictions": [
- "Cardiovascular diseases",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Cardiovascular Diseases",
- "Male",
- "Female",
- "Middle Aged",
- "Nutrition Surveys",
- "Adult",
- "Oxidative Stress",
- "United States",
- "Aged",
- "Life Style",
- "Diet",
- "Risk Factors",
- "Follow-Up Studies",
- "Prevalence"
- ]
- },
- {
- "PMID": "39736551",
- "Title": "BMC primary care",
- "ArticleTitle": "The moderating role of e-health literacy and patient-physician communication in the relationship between online diabetes information-seeking behavior and self-care practices among individuals with type 2 diabetes.",
- "Abstract": "Findings support the role of patient eHL and patient-physician communication in amplifying the positive impact of online DISB on patients' behavioral outcomes in diabetes.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Health Literacy",
- "Physician-Patient Relations",
- "Middle Aged",
- "Cross-Sectional Studies",
- "Self Care",
- "Information Seeking Behavior",
- "Medication Adherence",
- "Communication",
- "Aged",
- "Adult",
- "Internet",
- "Assessment of Medication Adherence"
- ]
- },
- {
- "PMID": "39736518",
- "Title": "BMC cardiovascular disorders",
- "ArticleTitle": "Effect of sodium glucose cotransporter-2 inhibitors (SGLT-2is) on the clinical outcomes of patients with diabetic atrial fibrillation.",
- "Abstract": "In our study, SGLT-2i treatment was associated with a significant reduction in all-cause mortality and major bleeding in diabetic AF patients. Our study provides evidence of the clinical benefit of SGLT-2i in AF patients.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Male",
- "Atrial Fibrillation",
- "Retrospective Studies",
- "Female",
- "Aged",
- "Treatment Outcome",
- "Middle Aged",
- "Diabetes Mellitus, Type 2",
- "Time Factors",
- "Risk Factors",
- "Risk Assessment",
- "Hemorrhage",
- "Aged, 80 and over",
- "Cause of Death",
- "Myocardial Infarction"
- ]
- },
- {
- "PMID": "39736351",
- "Title": "Life sciences",
- "ArticleTitle": "AAV2-mediated ABD-FGF21 gene delivery produces a sustained anti-hyperglycemic effect in type 2 diabetic mouse.",
- "Abstract": "In conclusion, we have developed a novel strategy for producing long-acting FGF21 using the AAV vector, and AAV2-ABD-FGF21 shows promise as a therapeutic approach for type 2 diabetes mellitus and other glycolipid metabolic disorders.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Animals",
- "Fibroblast Growth Factors",
- "Diabetes Mellitus, Type 2",
- "Mice",
- "Dependovirus",
- "Humans",
- "Gene Transfer Techniques",
- "Genetic Therapy",
- "Male",
- "Diabetes Mellitus, Experimental",
- "HEK293 Cells",
- "Mice, Inbred C57BL",
- "Blood Glucose",
- "Genetic Vectors",
- "Liver",
- "Hypoglycemic Agents"
- ]
- },
- {
- "PMID": "39736334",
- "Title": "Diabetes research and clinical practice",
- "ArticleTitle": "Balanced diets are associated with a lower risk of type 2 diabetes than plant-based diets.",
- "Abstract": "Adhered to a balanced diet is associated with a lower risk of diabetes compared to plant-based diet, which might be attributed to signature proteins such as AGR2, DBI, IL17RA and SERPINH1.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Cross-Sectional Studies",
- "Diet, Vegetarian",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Prospective Studies",
- "Aged",
- "Risk Factors",
- "United Kingdom",
- "Proteomics",
- "Diet, Healthy",
- "Diet, Plant-Based"
- ]
- },
- {
- "PMID": "39736162",
- "Title": "West African journal of medicine",
- "ArticleTitle": "The Impact of Diabetes Self-Management Education (DSME) on the Quality of Life of patients living with type-2 Diabetes Mellitus in Nigeria.",
- "Abstract": "The findings highlight that DSME significantly enhances the QoL, self-management competence, and glycemic control among T2DM patients in Nigeria. These results underscore the importance of structured educational interventions in diabetes care, particularly in resource-limited settings.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Quality of Life",
- "Nigeria",
- "Male",
- "Female",
- "Middle Aged",
- "Self-Management",
- "Patient Education as Topic",
- "Adult",
- "Surveys and Questionnaires",
- "Health Knowledge, Attitudes, Practice",
- "Aged",
- "Self Care"
- ]
- },
- {
- "PMID": "39735994",
- "Title": "Frontiers in bioscience (Landmark edition)",
- "ArticleTitle": "The Putative Antilipogenic Role of NRG4 and ERBB4: First Expression Study on Human Liver Samples.",
- "Abstract": "The study demonstrates a decrease in ",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Receptor, ErbB-4",
- "Neuregulins",
- "Liver",
- "Middle Aged",
- "Female",
- "Non-alcoholic Fatty Liver Disease",
- "Male",
- "Adult",
- "Lipogenesis",
- "Obesity",
- "Diabetes Mellitus, Type 2",
- "RNA, Messenger",
- "Aged"
- ]
- },
- {
- "PMID": "39735781",
- "Title": "Experimental biology and medicine (Maywood, N.J.)",
- "ArticleTitle": "Increased hip fracture risk in the patients with type 2 diabetes mellitus is correlated with urine albumin-to-creatinine ratio (ACR) and diabetes duration in men.",
- "Abstract": "Patients with type 2 diabetes mellitus (T2DM) have increased hip fracture risk. And the association between urine albumin to creatinine ratio (ACR) and an increased risk of hip fracture in patients with T2DM remains controversial. This study aimed to investigate the association between urinary ACR and hip fracture risk in postmenopausal women and aged men with T2DM. The study included 219 postmenopausal women and 216 older men (mean age >60\u00a0years) with T2DM. Women and men were divided into control group (ACR<30\u00a0mg/g), microalbuminuria group (30\u00a0mg/g \u2264 ACR<300\u00a0mg/g), and macroalbuminuria group (ACR\u2265300\u00a0mg/g) respectively. Demographic characteristics and clinical history were collected in patients. Biochemical indexes and bone turnover-related markers were measured in patients. In the study, we found that several factors, including age, T2DM duration, cerebral infarction history, serum corrected calcium levels and urine ACR were positively associated with hip fracture risk. However, 25-Hydroxyvitamin D and areal BMD were negatively associated with hip fracture risk. Furthermore, multiple regression analysis showed that urinary ACR level (\u03b2 = 0.003, p = 0.044) and duration of T2DM (\u03b2 = 0.015, p = 0.018) were positively and independently correlated with hip fracture risk in older men. In contrast, femoral neck BMD (\u03b2 = -6.765, p < 0.001) was independently and negatively correlated with hip fracture risk in older men. This study indicated that the elevated ACR levels and longer T2DM duration were related to higher hip fracture risk in older men with T2DM, which could be beneficial for developing a predictive model for osteoporotic fractures in patients with type 2 diabetes in the future. However, results were inconsistent in women, hip fracture risk didn't alter by changes in urinary microalbuminuria level in postmenopausal women with T2DM.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Hip Fractures",
- "Male",
- "Female",
- "Albuminuria",
- "Aged",
- "Middle Aged",
- "Creatinine",
- "Risk Factors",
- "Bone Density",
- "Postmenopause"
- ]
- },
- {
- "PMID": "39735651",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Association between changes in thyroid hormones and incident type 2 diabetes using joint models of longitudinal and time-to-event data: more than a decade follow up in the Tehran thyroid study.",
- "Abstract": "The findings of this study suggest that dynamic changes in serum thyroid hormones are associated with the development of T2DM. Rising TSH and decreasing FT4 over time are associated with a lower risk of diabetes. These findings suggest a complex interplay between thyroid function and the risk of T2DM, emphasizing the importance of monitoring thyroid hormone levels as a part of T2DM prevention strategies.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Iran",
- "Middle Aged",
- "Follow-Up Studies",
- "Incidence",
- "Adult",
- "Thyrotropin",
- "Thyroxine",
- "Longitudinal Studies",
- "Thyroid Hormones",
- "Risk Factors",
- "Thyroid Function Tests",
- "Thyroid Gland",
- "Thyroid Diseases"
- ]
- },
- {
- "PMID": "39735647",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "The role of fecal microbiota transplantation in type 2 diabetes mellitus treatment.",
- "Abstract": "In contemporary microbial research, the exploration of interactions between microorganisms and multicellular hosts constitutes a burgeoning field. The gut microbiota is increasingly acknowledged as a pivotal contributor to various disorders within the endocrine system, encompassing conditions such as diabetes and thyroid diseases. A surge in research activities has been witnessed in recent years, elucidating the intricate interplay between the gut microbiota and disorders of the endocrine system. Simultaneously, fecal microbiota transplantation (FMT) has emerged as a focal point, garnering substantial attention in both biomedical and clinical spheres. Research endeavors have uncovered the remarkable therapeutic efficacy of FMT across diverse diseases, with particular emphasis on its application in addressing type 2 diabetes mellitus (T2DM) and associated com-plications. Consequently, this manuscript accentuates the intimate connection between the gut microbiota and disorders within the endocrine system, with a specific focus on exploring the potential of FMT as an intervention in the therapeutic landscape of T2DM and its complications. Furthermore, the article scrutinizes concerns inherent in treatment modalities centered around the gut microbiota, proposing viable solutions to address these issues.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Fecal Microbiota Transplantation",
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Gastrointestinal Microbiome",
- "Animals"
- ]
- },
- {
- "PMID": "39735646",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Pasireotide-induced hyperglycemia in Cushing's disease and Acromegaly: A clinical perspective and algorithms proposal.",
- "Abstract": "Pasireotide is an effective treatment for both Cushing's disease (CD) and acromegaly due to its ability to suppress adrenocorticotropic hormone and growth hormone, and to normalize insulin-like growth factor-1 levels, resulting in tumor shrinkage. However, it may also cause hyperglycemia as a side effect in some patients. The aim of this study was to review previous recommendations regarding the management of pasireotide-induced hyperglycemia in patients with CD and acromegaly and to propose efficient monitoring and treatment algorithms based on recent evidence and current guidelines for type 2 diabetes treatment. In about 25% of patients with CD and 50% of patients with acromegaly, pasireotide-induced hyperglycemia does not require drug therapy or can be managed with diet and oral antidiabetic agents. The risk of pasireotide-induced hyperglycemia is higher in patients with diabetes or prediabetes at baseline. Moreover, pasireotide used in the treatment of CD may lead to more frequent and difficult-to-treat glycemic disorders than those observed in acromegaly. Based on the pathomechanism of hyperglycemia, we suggest using metformin as the first-line therapy, followed by glucagon-like peptide-1 and/or sodium-glucose co-transporter-2 inhibitor, and finally insulin in patients with pasireotide-induced hyperglycemia. We propose algorithms for the management of glucose metabolic disorders caused by pasireotide treatment in patients with CD and acromegaly, including those with chronic kidney disease and at high cardiovascular risk.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Somatostatin",
- "Acromegaly",
- "Pituitary ACTH Hypersecretion",
- "Hyperglycemia",
- "Algorithms",
- "Hypoglycemic Agents",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39735639",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Association of circulating adiponectin and leptin levels with the risk of diabetic peripheral neuropathy.",
- "Abstract": "Circulating adiponectin and leptin levels correlate with DPN risk in diabetic patients, suggesting their potential as biomarkers for high-risk DPN identification and guiding targeted prevention and management.",
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Adiponectin",
- "Leptin",
- "Diabetic Neuropathies",
- "Male",
- "Female",
- "Middle Aged",
- "Case-Control Studies",
- "Diabetes Mellitus, Type 2",
- "Aged",
- "Biomarkers",
- "Risk Factors",
- "Adult"
- ]
- },
- {
- "PMID": "39735416",
- "Title": "Journal of diabetes research",
- "ArticleTitle": "Age Characteristics of Patients With Type 2 Diabetic Foot Ulcers and Predictive Risk Factors for Lower Limb Amputation: A Population-Based Retrospective Study.",
- "Abstract": {
- "b": "Conclusion:"
- },
- "Predictions": [
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetic Foot",
- "Amputation, Surgical",
- "Male",
- "Middle Aged",
- "Female",
- "Risk Factors",
- "Aged",
- "Diabetes Mellitus, Type 2",
- "Retrospective Studies",
- "Lower Extremity",
- "Age Factors",
- "China",
- "Adult",
- "Prevalence",
- "Aged, 80 and over"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/male.json b/model/data/male.json
deleted file mode 100644
index fc2b3ae5228a022f142a934fedd589af92c15213..0000000000000000000000000000000000000000
--- a/model/data/male.json
+++ /dev/null
@@ -1,494 +0,0 @@
-[
- {
- "PMID": "39476418",
- "Title": "Annual review of psychology",
- "ArticleTitle": "Gender Identity and Aggression.",
- "Abstract": "Gender identity, or people's deeply felt, internal sense of their gender, plays an important role in aggression perpetration and victimization. In this article, I review and organize the psychological research literatures on gender identity-based aggression. I first discuss the need to move beyond binary, cisgender understandings of gender by embracing expansive definitions that more fully capture people's experiences and identities. Next, I summarize relevant research indicating two paths from gender identity to aggression. In one path, individuals with a more masculine (i.e., dominant, agentic) gender identity use aggression proactively, motivated by pursuit of social dominance. In another path, individuals with a more uncertain (i.e., insecure, precarious) gender identity use aggression defensively-and often toward vulnerable, gender nonconforming targets-as a means of protecting their gender identity against threats. I end by identifying important areas for future research and considering how interventions might best mitigate gender identity-based aggression.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Aggression",
- "Gender Identity",
- "Female",
- "Male"
- ]
- },
- {
- "PMID": "39476405",
- "Title": "Scandinavian journal of work, environment & health",
- "ArticleTitle": "Multidimensional employment trajectories and dynamic links with mental health: Evidence from the UK Household Longitudinal Study.",
- "Abstract": "This paper shows the importance of high-quality employment for individuals' mental health over time. Researchers need to consider dynamic associations between employment quality and mental health across the life-course.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Longitudinal Studies",
- "Employment",
- "United Kingdom",
- "Adult",
- "Mental Health",
- "Unemployment",
- "Surveys and Questionnaires",
- "Psychological Distress"
- ]
- },
- {
- "PMID": "39476404",
- "Title": "Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme",
- "ArticleTitle": "Characterization of the cardiac cycle in Royal Canadian Mounted Police cadets.",
- "Abstract": "Royal Canadian Mounted Police (RCMP) cadets experience high volumes of potentially psychologically traumatic events, suggesting a need of normal cardiac cycle interval data on the cadets for comparison. We characterize the cardiac cycle of incoming RCMP cadets starting the 26-week training program. The cadets collected their cardiac data using the LLA Recordis\u2122 device. Male RCMP cadets had higher (",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Police",
- "Male",
- "Female",
- "Canada",
- "Young Adult",
- "Adult",
- "Heart",
- "Heart Rate",
- "Stress, Psychological",
- "Aortic Valve"
- ]
- },
- {
- "PMID": "39476402",
- "Title": "Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases",
- "ArticleTitle": "Periprosthetic Joint Infection in Patients With Inflammatory Arthritis: Optimal Tests to Differentiate From Flares.",
- "Abstract": "Although synovial %PMNs, CRP, and alpha-defensin are sensitive tests for diagnosing PJI, they are less specific and may be positive in IA flares.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Prosthesis-Related Infections",
- "Female",
- "Male",
- "Aged",
- "C-Reactive Protein",
- "Middle Aged",
- "Synovial Fluid",
- "Biomarkers",
- "alpha-Defensins",
- "Cross-Sectional Studies",
- "Osteoarthritis",
- "Arthritis, Rheumatoid",
- "Arthritis, Psoriatic",
- "Diagnosis, Differential",
- "Sensitivity and Specificity",
- "Leukocyte Count",
- "Fibrin Fibrinogen Degradation Products",
- "Blood Sedimentation",
- "Reoperation"
- ]
- },
- {
- "PMID": "39476390",
- "Title": "JMIR public health and surveillance",
- "ArticleTitle": "Determinants of Citizens' Intention to Participate in Self-Led Contact Tracing: Cross-Sectional Online Questionnaire Study.",
- "Abstract": "Overall, Dutch citizens are positive toward participating in self-led CT. Our results provide directions for the development and implementation of self-led CT, which may be particularly useful in preparing for future, large-scale outbreaks.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Cross-Sectional Studies",
- "Male",
- "Female",
- "Intention",
- "Netherlands",
- "Surveys and Questionnaires",
- "Adult",
- "Middle Aged",
- "Contact Tracing",
- "Aged",
- "Adolescent",
- "Young Adult"
- ]
- },
- {
- "PMID": "39476381",
- "Title": "Advanced science (Weinheim, Baden-Wurttemberg, Germany)",
- "ArticleTitle": "Posterior Basolateral Amygdala is a Critical Amygdaloid Area for Temporal Lobe Epilepsy.",
- "Abstract": "The amygdaloid complex consists of multiple nuclei and is a key node in controlling temporal lobe epilepsy (TLE) in both human and animal model studies. However, the specific nucleus in the amygdaloid complex and the neural circuitry governing seizures remain unknown. Here, it is discovered that activation of glutamatergic neurons in the posterior basolateral amygdala (pBLA) induces severe seizures and even mortality. The pBLA glutamatergic neurons project collateral connections to multiple brain regions, including the insular cortex (IC), bed nucleus of the stria terminalis (BNST), and central amygdala (CeA). Stimulation of pBLA-targeted IC neurons triggers seizures, whereas ablation of IC neurons suppresses seizures induced by activating pBLA glutamatergic neurons. GABAergic neurons in the BNST and CeA establish feedback inhibition on pBLA glutamatergic neurons. Deleting GABAergic neurons in the BNST or CeA leads to sporadic seizures, highlighting their role in balancing pBLA activity. Furthermore, pBLA neurons receive glutamatergic inputs from the ventral hippocampal CA1 (vCA1). Ablation of pBLA glutamatergic neurons mitigates both acute and chronic seizures in the intrahippocampal kainic acid-induced mouse model of TLE. Together, these findings identify the pBLA as a pivotal nucleus in the amygdaloid complex for regulating epileptic seizures in TLE.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Epilepsy, Temporal Lobe",
- "Animals",
- "Mice",
- "Basolateral Nuclear Complex",
- "Disease Models, Animal",
- "Male",
- "Amygdala",
- "Neurons"
- ]
- },
- {
- "PMID": "39476377",
- "Title": "JMIR aging",
- "ArticleTitle": "Decoding the Influence of eHealth on Autonomy, Competence, and Relatedness in Older Adults: Qualitative Analysis of Self-Determination Through the Motivational Technology Model.",
- "Abstract": "Participants confirmed the features that increased internal motivation, such as interactivity correlating with feelings of relatedness, but they also found other ways to support autonomous health behavior change beyond narrow views of navigability, interactivity, and customization.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Aged",
- "Personal Autonomy",
- "Female",
- "Male",
- "Motivation",
- "Telemedicine",
- "Qualitative Research",
- "Aged, 80 and over",
- "Mobile Applications",
- "Middle Aged"
- ]
- },
- {
- "PMID": "39476374",
- "Title": "Journal of medical Internet research",
- "ArticleTitle": "The Impact of Different Types of Social Media Use on the Mental Health of UK Adults: Longitudinal Observational Study.",
- "Abstract": "We found that a high frequency of posting on social media was associated with increased mental health problems a year later. However, we did not find evidence of a similar association based on the frequency of viewing social media content. This provides evidence that some types of active social media use (ie, posting) have a stronger link to mental health outcomes than some types of passive social media use (viewing). These results highlighted that the relationship between social media use and mental health is complex, and more research is needed to understand the mechanisms underlying these patterns to inform targeted interventions and policies.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Social Media",
- "Longitudinal Studies",
- "United Kingdom",
- "Adult",
- "Male",
- "Female",
- "Mental Health",
- "Middle Aged",
- "Adolescent",
- "Young Adult",
- "Aged",
- "Mental Disorders",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39476373",
- "Title": "Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine",
- "ArticleTitle": "Prevalence of Asymptomatic Changes in the Groin Region Among Adult Professional Soccer Players and Their Association With Limb Dominance.",
- "Abstract": "In adult professional soccer players with no prior groin pain complaints in recent history (12 months), asymptomatic changes are extremely common in the pubic joint and adjacent areas, including those that are very likely to be considered the main cause of pain when investigated in soccer players with groin pain. None of these changes were associated with limb dominance.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Soccer",
- "Male",
- "Adult",
- "Cross-Sectional Studies",
- "Groin",
- "Magnetic Resonance Imaging",
- "Prevalence",
- "Young Adult",
- "Pubic Symphysis",
- "Pubic Bone",
- "Functional Laterality",
- "Asymptomatic Diseases"
- ]
- },
- {
- "PMID": "39476372",
- "Title": "Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine",
- "ArticleTitle": "Prior Concussion History and Clinical Recovery Following Sport-Related Concussion in College Athletes.",
- "Abstract": "In summary, concussion history was not associated with time to return to sports following a subsequent sport-related concussion in these college athletes. On average, athletes with prior concussions did not take longer to return to school, although a slightly greater proportion of college athletes with \u22652 prior concussions had not fully returned to school, without accommodations, by 28 days following injury.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Brain Concussion",
- "Athletic Injuries",
- "Return to Sport",
- "Male",
- "Female",
- "Young Adult",
- "Universities",
- "Students",
- "Athletes",
- "Recovery of Function",
- "Adolescent",
- "Cohort Studies",
- "Time Factors"
- ]
- },
- {
- "PMID": "39476371",
- "Title": "Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine",
- "ArticleTitle": "Early Targeted Heart Rate Aerobic Exercise Reduces Proportion of Subacute Musculoskeletal Injuries After Recovery From Sport-Related Concussion.",
- "Abstract": "Adolescent male athletes prescribed aerobic exercise within 10 days of SRC had a significantly lower proportion of individuals injured in the 3 months following clinical recovery when compared with stretching. This may be due to a habituation/rehabilitation effect of aerobic activities to improve autonomic, vestibular, and/or oculomotor function after SRC.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Adolescent",
- "Brain Concussion",
- "Athletic Injuries",
- "Female",
- "Exercise",
- "Return to Sport",
- "Heart Rate",
- "Muscle Stretching Exercises",
- "Exercise Therapy"
- ]
- },
- {
- "PMID": "39476370",
- "Title": "Journal of medical Internet research",
- "ArticleTitle": "Characterization of Telecare Conversations on Lifestyle Management and Their Relation to Health Care Utilization for Patients with Heart Failure: Mixed Methods Study.",
- "Abstract": "Our approach and findings offer novel perspectives on the content, structure, and clinical associations of telehealth conversations on lifestyle management for patients with HF. Hence, our study could inform ways to enhance telehealth programs for self-care management in chronic conditions.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Heart Failure",
- "Telemedicine",
- "Female",
- "Male",
- "Life Style",
- "Aged",
- "Middle Aged",
- "Patient Acceptance of Health Care",
- "Diabetes Mellitus, Type 2",
- "Communication"
- ]
- },
- {
- "PMID": "39476368",
- "Title": "JMIR formative research",
- "ArticleTitle": "Self-Reported Patient and Provider Satisfaction With Neurology Telemedicine Visits After Rapid Telemedicine Implementation in an Urban Academic Center: Cross-Sectional Survey.",
- "Abstract": "Our study found adequate satisfaction among patients and providers regarding telemedicine implementation and its utility for patient care in a diverse urban population. Additionally, while access to technology and technology literacy are barriers to telemedical care, a substantial majority of patients who responded to the survey had access to devices (101/117, 86.3%) and were able to connect with few to no technological difficulties (84/117, 71.8%). One area identified by patients in need of improvement was comfortability in communicating via telemedicine with their providers. Furthermore, while providers agreed that telemedicine is a useful tool for patient care, it limits their ability to perform physical exams. More research and quality studies are needed to further appreciate and support the expansion of telemedical care into underserved and rural populations, especially in the area of subspecialty neurological care.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Telemedicine",
- "Patient Satisfaction",
- "Male",
- "Cross-Sectional Studies",
- "Female",
- "Neurology",
- "Academic Medical Centers",
- "Adult",
- "Middle Aged",
- "COVID-19",
- "Self Report",
- "Aged",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39476366",
- "Title": "Journal of medical Internet research",
- "ArticleTitle": "Evaluating the Implementation and Clinical Effectiveness of an Innovative Digital First Care Model for Behavioral Health Using the RE-AIM Framework: Quantitative Evaluation.",
- "Abstract": "PBH as a care model with evidence-based DMHIs, human support for patients, and integration within routine settings offers a credible service to support patients with mild to moderate mental health challenges. This type of model has the potential to address real-life access to care problems faced by health care settings.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Mental Health Services",
- "Adult",
- "Middle Aged",
- "Primary Health Care",
- "United States"
- ]
- },
- {
- "PMID": "39476363",
- "Title": "Advanced science (Weinheim, Baden-Wurttemberg, Germany)",
- "ArticleTitle": "Adipose Tissue-Resident Sphingomonas Paucimobilis Suppresses Adaptive Thermogenesis by Reducing 15-HETE Production and Inhibiting AMPK Pathway.",
- "Abstract": "Obesity represents a low-grade chronic inflammation status, which is associated with compromised adaptive thermogenesis. However, the mechanisms underlying the defective activation of thermogenesis in chronic inflammation remain unclear. Here, a chronic inflammatory model is first estabolished by injecting mice with low-dose lipopolysaccharide (LPS) before cold exposure, and then it is verified that LPS treatment can decrease the core body temperature of mice and alter the microbial distribution in epididymal white adipose tissue (eWAT). An adipose tissue-resident bacterium Sphingomonas paucimobilis is identified as a potential inhibitor on the activation of brown fat and browning of inguinal WAT, resulting in defective adaptive thermogenesis. Mechanically, LPS and S. paucimobilis inhibit the production and release of 15-HETE by suppressing its main metabolic enzyme 12 lipoxygenase (12-LOX) and 15- Hydroxyeicosatetraenoic acid (15-HETE) rescues the impaired thermogenesis. Interestingly, 15-HETE directly binds to AMP-activated protein kinase \u03b1 (AMPK\u03b1) and elevates the phosphorylation of AMPK, leading to the activation of uncoupling protein 1 (UCP1) and mitochondrial oxidative phosphorylation (OXPHOS) complexes. Further analysis with human obesity subjects reveals that individuals with high body mass index displayed lower 15-HETE levels. Taken together, this work improves the understanding of how chronic inflammation impairs adaptive thermogenesis and provides novel targets for alleviating obesity.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Animals",
- "Sphingomonas",
- "Mice",
- "Thermogenesis",
- "Male",
- "Hydroxyeicosatetraenoic Acids",
- "AMP-Activated Protein Kinases",
- "Mice, Inbred C57BL",
- "Disease Models, Animal",
- "Humans",
- "Obesity",
- "Signal Transduction",
- "Adipose Tissue"
- ]
- },
- {
- "PMID": "39476341",
- "Title": "The New England journal of medicine",
- "ArticleTitle": "Total Hip Replacement or Resistance Training for Severe Hip Osteoarthritis.",
- "Abstract": "In patients 50 years of age or older who had severe hip osteoarthritis and an indication for surgery, total hip replacement resulted in a clinically important, superior reduction in hip pain and improved hip function, as reported by patients, at 6 months as compared with resistance training. (Funded by the Danish Rheumatism Association and others; PROHIP ClinicalTrials.gov number, NCT04070027.).",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Aged",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Arthroplasty, Replacement, Hip",
- "Intention to Treat Analysis",
- "Osteoarthritis, Hip",
- "Pain Measurement",
- "Resistance Training",
- "Arthralgia"
- ]
- },
- {
- "PMID": "39476340",
- "Title": "The New England journal of medicine",
- "ArticleTitle": "Inavolisib-Based Therapy in ",
- "Abstract": "In patients with ",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Adult",
- "Aged",
- "Female",
- "Humans",
- "Middle Aged",
- "Antineoplastic Combined Chemotherapy Protocols",
- "Breast Neoplasms",
- "Class I Phosphatidylinositol 3-Kinases",
- "Double-Blind Method",
- "Kaplan-Meier Estimate",
- "Mutation",
- "Piperazines",
- "Progression-Free Survival",
- "Pyridines",
- "Male",
- "Breast Neoplasms, Male",
- "Phosphoinositide-3 Kinase Inhibitors",
- "Imidazoles",
- "Oxazoles"
- ]
- },
- {
- "PMID": "39476339",
- "Title": "The New England journal of medicine",
- "ArticleTitle": "Once-Weekly Semaglutide in Persons with Obesity and Knee Osteoarthritis.",
- "Abstract": "Among participants with obesity and knee osteoarthritis with moderate-to-severe pain, treatment with once-weekly injectable semaglutide resulted in significantly greater reductions in body weight and pain related to knee osteoarthritis than placebo. (Funded by Novo Nordisk; STEP 9 ClinicalTrials.gov number, NCT05064735.).",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Aged",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Body Mass Index",
- "Combined Modality Therapy",
- "Double-Blind Method",
- "Drug Administration Schedule",
- "Injections, Subcutaneous",
- "Obesity",
- "Osteoarthritis, Knee",
- "Weight Loss",
- "Glucagon-Like Peptide-1 Receptor Agonists",
- "Counseling",
- "Caloric Restriction",
- "Arthralgia",
- "Pain Measurement"
- ]
- },
- {
- "PMID": "39476330",
- "Title": "Clinical transplantation",
- "ArticleTitle": "Survey of Post-Prophylaxis Delayed-Onset Cytomegalovirus Management Strategies Among Transplant Providers.",
- "Abstract": "Management of PPDOC was highly variable among providers and strategies differed based on patient risk profile. These findings could help shape future studies and guidelines to harmonize CMV management.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Cytomegalovirus Infections",
- "Organ Transplantation",
- "Cytomegalovirus",
- "Surveys and Questionnaires",
- "Antiviral Agents",
- "Prognosis",
- "Disease Management",
- "Practice Patterns, Physicians'",
- "Follow-Up Studies",
- "Postoperative Complications",
- "Graft Rejection",
- "Female",
- "Male",
- "Post-Exposure Prophylaxis"
- ]
- },
- {
- "PMID": "39476327",
- "Title": "United European gastroenterology journal",
- "ArticleTitle": "Variation in the detection of lymphovascular invasion in T1 colorectal cancer and its impact on treatment: A nationwide Dutch study.",
- "Abstract": "These findings suggest that a high detection rate of LVI does not improve oncological outcomes and may expose more patients to unnecessary oncological surgery, emphasizing the need for standardization of LVI diagnosis.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Colorectal Neoplasms",
- "Netherlands",
- "Female",
- "Male",
- "Lymphatic Metastasis",
- "Aged",
- "Middle Aged",
- "Neoplasm Invasiveness",
- "Neoplasm Staging",
- "Neoplasm Recurrence, Local",
- "Lymph Nodes"
- ]
- },
- {
- "PMID": "39476322",
- "Title": "Nursing open",
- "ArticleTitle": "Setting national nursing research priorities in Qatar: A Delphi survey.",
- "Abstract": "Not applicable.",
- "Predictions": [
- "Male"
- ],
- "MeshTerms": [
- "Qatar",
- "Humans",
- "Delphi Technique",
- "Nursing Research",
- "Surveys and Questionnaires",
- "Male",
- "Female",
- "Adult",
- "Consensus"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/mental_health.json b/model/data/mental_health.json
deleted file mode 100644
index 68d2da50836a2344c998e0bc99037153bb4b97b8..0000000000000000000000000000000000000000
--- a/model/data/mental_health.json
+++ /dev/null
@@ -1,489 +0,0 @@
-[
- {
- "PMID": "39738254",
- "Title": "Scientific reports",
- "ArticleTitle": "Cross sectional associations of physical activity and sleep with mental health among Chinese university students.",
- "Abstract": "The intensity of PA among university students is predominantly light, and the reported rate of insufficient sleep is relatively high. Moderate to high-intensity PA and sufficient high-quality sleep may alleviate MH issues among college students, with an interaction effect observed among PA, sleep, and depression symptoms. Future studies should further explore targeted interventions combining PA and sleep behaviors to enhance the MH of university students.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Students",
- "Female",
- "Exercise",
- "Universities",
- "China",
- "Mental Health",
- "Young Adult",
- "Depression",
- "Cross-Sectional Studies",
- "Anxiety",
- "Sleep",
- "Surveys and Questionnaires",
- "Adult",
- "Adolescent",
- "Sleep Quality",
- "Prevalence"
- ]
- },
- {
- "PMID": "39737457",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Impact of COVID-19 vaccination on adolescent and youth students' mental health and bullying behaviors after the lifting of COVID-19 restrictions in China.",
- "Abstract": "This study suggests that COVID-19 vaccination will not only protect students' physical health, but also improve mental health. It is crucial to explore the mechanism between vaccination and mental health problems and bullying behaviors in further studies.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Adolescent",
- "China",
- "COVID-19",
- "Male",
- "Female",
- "Students",
- "Bullying",
- "COVID-19 Vaccines",
- "Surveys and Questionnaires",
- "Mental Health",
- "Vaccination",
- "Depression",
- "Anxiety",
- "SARS-CoV-2",
- "Stress Disorders, Post-Traumatic"
- ]
- },
- {
- "PMID": "39735766",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Unemployment and mental health: a global study of unemployment's influence on diverse mental disorders.",
- "Abstract": "These findings underscore the critical interplay between socio-economic factors and mental health, highlighting the need for proactive strategies to address the dual burden of unemployment and mental health disorders. Targeted interventions, such as employment support programs and accessible mental health services, are essential to improve global mental health outcomes. These initiatives can also alleviate the economic burden of unemployment by boosting workforce participation and productivity. Long-term economic gains may offset the increased healthcare expenditures associated with mental health support.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Unemployment",
- "Mental Disorders",
- "Female",
- "Male",
- "Adult",
- "Middle Aged",
- "Global Health",
- "Mental Health",
- "Young Adult",
- "Socioeconomic Factors"
- ]
- },
- {
- "PMID": "39735765",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Public perceptions of digital mental health awareness campaign in the Arab Gulf states: a qualitative thematic analysis.",
- "Abstract": "Mental illness is a significant public health concern and a leading cause of disability worldwide. Research shows a lack of mental health knowledge and inappropriate practices in the Gulf Cooperation Council (GCC) states. Our study aimed to evaluate individuals' perspectives on mental health by analyzing their responses to a digital campaign directed at GCC adolescents. We conducted a qualitative thematic analysis of comments in response to the Gulf Health Council's mental health campaign. The campaign content was shared on four social media platforms: TikTok, YouTube, Instagram, and X. A total of 2,146 comments were included in the analysis. There was a widespread denial of the existence of mental illness. The comments revealed a lack of understanding and insufficient support for individuals dealing with mental health issues. Stigma and discrimination against people with mental illness were evident in the comments. The general perception was that individuals have control over their mental health, often associating mental illness with weakness and lack of willpower. Mental illness was believed to be caused by religious and moral shortcomings, and religion was viewed as the solution. Some comments highlighted the need to acknowledge mental illness and urged the development of strategies to promote mental health. Our research shows a lack of awareness, stigma, and inadequate resources for individuals dealing with mental health issues. It highlights the importance of addressing barriers to mental healthcare and increasing access to support. Interventions focusing on stigma reduction and promoting acceptance of mental health disorders are crucial and require collaborative efforts from various stakeholders.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Mental Disorders",
- "Qualitative Research",
- "Adolescent",
- "Female",
- "Health Promotion",
- "Male",
- "Social Media",
- "Social Stigma",
- "Health Knowledge, Attitudes, Practice",
- "Middle East",
- "Mental Health",
- "Public Opinion"
- ]
- },
- {
- "PMID": "39735755",
- "Title": "Frontiers in public health",
- "ArticleTitle": "A study of the impact of internet use on the mental health of rural older adults-empirical analysis based on China General Social Survey 2021 data.",
- "Abstract": "Internet use, social participation, and friend-gathering type participation all have an effect on the mental health of rural older adults. The research results reveal the impact of Internet use on the mental health of rural older adults and its mechanism, which is helpful to provide useful enlightenment for improving the mental health of rural older adults in the Internet era.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "China",
- "Aged",
- "Rural Population",
- "Mental Health",
- "Male",
- "Female",
- "Social Participation",
- "Internet Use",
- "Surveys and Questionnaires",
- "Middle Aged",
- "Aged, 80 and over",
- "Internet"
- ]
- },
- {
- "PMID": "39735753",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Chronic impacts of natural infrastructure on the physical and psychological health of university students during and after COVID-19: a case study of Chengdu, China.",
- "Abstract": "The study emphasizes the importance of incorporating natural elements into urban planning to enhance outdoor activity and well-being, especially in post-pandemic settings. Recommendations are provided for future urban design to address the therapeutic needs of specific populations.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "China",
- "Students",
- "Universities",
- "Male",
- "Female",
- "Mental Health",
- "Young Adult",
- "Adult",
- "SARS-CoV-2",
- "City Planning"
- ]
- },
- {
- "PMID": "39735752",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Effects of a flexibly delivered group-based acceptance and commitment therapy on reducing stress and enhancing psychological wellbeing in parents of school-age children during the COVID-19 pandemic: a quasi-experimental study.",
- "Abstract": "The findings highlight the potential of group-based Acceptance and Commitment Therapy to alleviate stress and improve psychological well-being in parents of school-age children, regardless of the delivery method, especially during crises such as the COVID-19 pandemic. However, due to limitations in the study design, caution is warranted when interpreting the overall effects of group-based ACT on parent outcomes and the moderating role of delivery methods. Further research is needed to validate these findings and explore the nuances of delivery methods in similar real-world situations.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Acceptance and Commitment Therapy",
- "Female",
- "Male",
- "Parents",
- "Stress, Psychological",
- "Adult",
- "Child",
- "Hong Kong",
- "Middle Aged",
- "SARS-CoV-2",
- "Psychotherapy, Group",
- "Pandemics",
- "Mental Health"
- ]
- },
- {
- "PMID": "39735743",
- "Title": "Frontiers in public health",
- "ArticleTitle": "The impact of university freshmen's mental health on academic performance: an empirical study based on M University in Fujian Province, China.",
- "Abstract": "University officials should strengthen mental health surveillance and intervention during the first few years of student enrollment to mitigate the harmful impact of mental health issues on academic performance. The moderate to strong effect sizes for variables like somatization, depression, and anxiety indicate that early interventions could be crucial in reducing their negative impact on both short-and long-term academic outcomes. Furthermore, the study discovered disparities in mental health and academic performance across students of different genders and enrollment years, emphasizing that educational personnel should design more tailored mental health support methods that consider these differences.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Universities",
- "Male",
- "Female",
- "China",
- "Students",
- "Academic Performance",
- "Mental Health",
- "Young Adult",
- "Depression",
- "Anxiety",
- "Adolescent",
- "Adult"
- ]
- },
- {
- "PMID": "39735742",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Effects of volcanic eruptions on the mental health of exposed populations: a systematic review.",
- "Abstract": "The negative influence of experiencing volcanic activity on mental health was confirmed. Clearly, there is a need for more research to improve the mental health of the populations highly exposed to volcanic eruptions. Recommendations for future research are also included.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Volcanic Eruptions",
- "Humans",
- "Mental Health",
- "Mental Disorders",
- "Environmental Exposure"
- ]
- },
- {
- "PMID": "39734104",
- "Title": "Journal of research on adolescence : the official journal of the Society for Research on Adolescence",
- "ArticleTitle": "LGBTQ+ youth policy and mental health: Indirect effects through school experiences.",
- "Abstract": "The link between state policies and LGBTQ+ youth mental health is well-established, yet less well-understood are the mechanisms that drive these associations. We used a sample from the LGBTQ+ National Teen Survey (n\u2009=\u20098368) collected in 2022 to examine whether and to what degree LGBTQ+ inclusive school strategies, student perceptions of school safety, and experiences with bias-based bullying and peer victimization explain the association between state LGBTQ+ youth-focused policies and LGBTQ+ youth mental health symptomology. We observed significant indirect effects between policy and LGBTQ+ youth mental health through all four constructs, suggesting that each of these more proximal school experiences was independently implicated in this association. Findings underscore how state policies shape LGBTQ+ youth mental health symptomology via more proximal contexts and emphasize the importance of policy implementation following enactment.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Adolescent",
- "Male",
- "Sexual and Gender Minorities",
- "Female",
- "Schools",
- "Bullying",
- "Mental Health",
- "Crime Victims",
- "United States",
- "Surveys and Questionnaires",
- "Students",
- "Peer Group"
- ]
- },
- {
- "PMID": "39734100",
- "Title": "Journal of research on adolescence : the official journal of the Society for Research on Adolescence",
- "ArticleTitle": "Adolescents in various contexts during the COVID-19 pandemic: A commentary.",
- "Abstract": "This commentary provides a reflection on the impact of the COVID-19 pandemic on adolescents in the context of family dynamics, school environments, peer relationships, and civic engagement. Drawing from four systematic literature reviews, the commentary highlights key findings, such as the long-term effects of COVID-19 on adolescent development, mental health, and academic well-being. The need for future research is emphasized to assess how these cohort effects will evolve over time. Cultural context and socioeconomic disparities emerge as crucial considerations, with the pandemic exacerbating existing inequalities, especially in access to education and digital resources. This commentary also underscores the importance of adopting a socio-ecological perspective to understand the multifaceted impact of COVID-19 on adolescents globally. In conclusion, it calls for targeted policies to support adolescents' mental health and academic recovery post-pandemic, particularly in underserved communities. Governments, educators, and civic organizations are encouraged to create inclusive policies that address these disparities while fostering resilience and well-being among young people. These reviews may also inform translational research that could aid in the development of evidence-based interventions and policies aimed at helping adolescents thrive in a post-pandemic world.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Adolescent",
- "Mental Health",
- "SARS-CoV-2",
- "Adolescent Development",
- "Pandemics",
- "Peer Group",
- "Socioeconomic Factors"
- ]
- },
- {
- "PMID": "39732736",
- "Title": "BMC psychology",
- "ArticleTitle": "Factorial validation and invariance of the Academic Procrastination Scale in Colombian students.",
- "Abstract": "The Modified Academic Procrastination Scale (EPA-C) demonstrates adequate psychometric properties and is gender-invariant for assessing academic procrastination among Colombian university students. Moreover, it has an impact on the mental health and life satisfaction of these students.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Colombia",
- "Students",
- "Young Adult",
- "Adult",
- "Adolescent",
- "Psychometrics",
- "Personal Satisfaction",
- "Universities",
- "Procrastination",
- "Reproducibility of Results",
- "Mental Health",
- "Surveys and Questionnaires",
- "Factor Analysis, Statistical"
- ]
- },
- {
- "PMID": "39732545",
- "Title": "Endocrinologia, diabetes y nutricion",
- "ArticleTitle": "Nurse-led therapeutic patient education program on glycemic control and emotional wellbeing in adolescents with type 1 diabetes mellitus during hospital transition.",
- "Abstract": "The structured therapeutic education program for adolescents with T1DM transitioning from pediatric to adult care maintains glycemic control and emotional wellbeing.",
- "Predictions": [
- "Mental Health",
- "Diabetes type 1"
- ],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Adolescent",
- "Male",
- "Female",
- "Patient Education as Topic",
- "Glycemic Control",
- "Transition to Adult Care",
- "Self Care",
- "Emotions",
- "Mental Health",
- "Feeding and Eating Disorders"
- ]
- },
- {
- "PMID": "39731523",
- "Title": "Sociology of health & illness",
- "ArticleTitle": "Extending Fundamental Cause Theory to Holistic Health.",
- "Abstract": "Fundamental Cause Theory (FCT) offers a unique middle range and longitudinal understanding of the lasting social causational relationships between certain social conditions and disease/death. In this research note, I argue that FCT should extend its outcome measures beyond physical disease and death into holistic health. I briefly review how FCT is evaluated, explore the proposed extension and discuss some operational and conceptual challenges using mental illness and positive mental health outcomes as exemplars. I conclude by discussing the benefits of extending FCT for 1) the theory's own validity, 2) social health inequalities research more broadly, and 3) public health policy.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Holistic Health",
- "Mental Disorders",
- "Health Policy",
- "Social Theory",
- "Mental Health",
- "Health Status Disparities"
- ]
- },
- {
- "PMID": "39731316",
- "Title": "Nordic journal of psychiatry",
- "ArticleTitle": "Gender-stratified national mental health norms of BSI-53, BSI-18, SCL-10, ADHD-9, and ADHD-6 for Denmark.",
- "Abstract": "This study provides gender-stratified Danish mental health norms for multiple symptom scales. The considerable gender differences in the SCL-10 underscore the importance of gender-specific norms. The 2020 SCL-10 norms are biased by COVID-19 distress. Until new normative data is available, the gender-specific norms provided here are recommended.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Denmark",
- "Female",
- "Male",
- "Attention Deficit Disorder with Hyperactivity",
- "Adult",
- "Middle Aged",
- "Adolescent",
- "Young Adult",
- "Aged",
- "COVID-19",
- "Sex Factors",
- "Aged, 80 and over",
- "Reference Values",
- "Brief Psychiatric Rating Scale",
- "Mental Health"
- ]
- },
- {
- "PMID": "39730730",
- "Title": "Scientific reports",
- "ArticleTitle": "Insights into adolescent sleep and mental health in rural area of Northwestern China.",
- "Abstract": "Adolescents in affluent nations have experienced a decline in sleep duration, associated with adverse outcomes such as behavioral issues and health concerns. However, the connection between sleep and mental well-being during adolescence, particularly in developing regions like rural China, remains underexplored. A cross-sectional study of 18,516 adolescents in 124 junior high schools in Ningxia, China, utilized the strengths and difficulties questionnaire to assess mental health. The findings highlighted a complex, nonlinear link between sleep duration and mental health, with a U-shaped trend for overall difficulties and an inverse U-shape for prosocial behavior. The study also explored potential mechanisms behind these relationships, suggesting that time allocation to activities such as screen time and outdoor activities could mediate the effects of sleep duration on mental health. Longer sleep durations could lead to less screen time and more outdoor engagement, both of which positively affect mental well-being. Balanced sleep duration is crucial for adolescent mental health. The study calls for interventions to improve sleep hygiene and mental health services in rural areas, emphasizing the need for policy support to address sleep deprivation and its impact on mental well-being.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Adolescent",
- "China",
- "Male",
- "Mental Health",
- "Female",
- "Rural Population",
- "Sleep",
- "Cross-Sectional Studies",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39730531",
- "Title": "Scientific reports",
- "ArticleTitle": "A chain-mediated model of the effect of physical exercise on loneliness.",
- "Abstract": "The physical and mental health development of college students has gradually become an important topic of social concern. The academic community focuses on different ways of physical exercise to improve the mental health of college students. On the basis of sports psychology, this paper discusses the interaction mechanism between physical activity and social support, interpersonal relationship quality and loneliness of college students, that is, physical and mental health effects of physical activities to promote the psychological level of college students. By random sampling, 784 college students were investigated and analyzed with physical exercise scale, loneliness scale, interpersonal relationship scale and social support scale, based on the general characteristics of the demographics variables, and through the analysis of multiple regression path model, this paper further explored the mechanism of the effects of physical activity, social support, loneliness and interpersonal relationship quality of college students. The results showed that physical exercise had a negative predictive effect on loneliness(\u03b2 = -\u00a00.246, p<0.01) and a positive predictive effect on interpersonal relationship quality and social support(\u03b2\u2009=\u20090.186, p<0.01; \u03b2\u2009=\u20090.156, p<0.01).In addition, social support and interpersonal relationship quality play a mediating role between physical exercise and loneliness, including three mediating paths, namely, social support and interpersonal relationship quality play an independent mediating role, the link mediating effect of social support and interpersonal relationship quality. According to the theory of psychological needs, the results show that physical exercise has an indirect effect on loneliness of college students through the chain mediating effect of interpersonal relationship quality and social support. College students can improve the level of social support and the quality of interpersonal relationships, and reduce the sense of loneliness.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Loneliness",
- "Humans",
- "Exercise",
- "Male",
- "Female",
- "Social Support",
- "Students",
- "Young Adult",
- "Interpersonal Relations",
- "Adult",
- "Adolescent",
- "Universities",
- "Mental Health",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39730236",
- "Title": "Sleep medicine",
- "ArticleTitle": "Mental health and sleep routines: Uttarkashi, India tunnel collapse workers' experience.",
- "Abstract": "Among the mental health outcomes and disaster types (determined by damage to life, property, long-term consequences, displacement, and unpredictability), floods are associated with anxiety and sleep problems, mudslides with anxiety and mood disturbance, volcanic eruptions with acute stress reactions, and earthquakes with anxiety, depression, and physical complaints. Disasters such as tunnel collapse are unique as it involves the healthy, without loss of personal property or displacement; hence, they can have very different health-related outcomes. In this study, we explore mental health and sleep-related issues in workers rescued from an under-construction collapsed tunnel trapped for 17 days. After the initial triage and stabilization and a detailed evaluation of their physical and mental health status, the participants responded to self-administered scales for assessing anxiety [Generalized Anxiety Disorder-7], depression [Patient Health Questionnaire-9], and insomnia [Insomnia Severity Index] in the local language (Hindi). A separate research team conducted open-ended interviews to explore daily routines and concerns, circadian rhythm, orientation to time and day of tunnel collapse to day of rescue events, and sleep routine (and other nuances such as sleep quality and daytime napping) during the 17 days of entrapment. Thirty-three workers consented and hailed from the northern and eastern states of India. They report a mix of hope and worry in the initial days. On the assessment of anxiety, depression, and sleep, only 2-5 scored above the cut-off value, and scales correlated with each other, though clinically it had no bearing. One-third were disoriented to the passage of time, which was related to difficulty falling asleep and more napping. Daytime napping was associated with delayed waketime. Those depressed had more difficulty in the onset, maintinance, and termination of sleep, and reduced total sleep time. Victims of tunnel collapse experience a different set of mental health and sleep problems compared to those reported in other disasters. The findings can partly be attributed to the disruption of light-dark cycles. As only a fraction develops these problems, there is a need for triaging while providing mental health and sleep-related interventions in such circumstances. Lastly, there is a need to establish a light-dark cycle to prevent disorientation among victims.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "India",
- "Male",
- "Adult",
- "Female",
- "Anxiety",
- "Mental Health",
- "Middle Aged",
- "Disasters",
- "Depression",
- "Sleep Initiation and Maintenance Disorders",
- "Sleep",
- "Surveys and Questionnaires",
- "Circadian Rhythm"
- ]
- },
- {
- "PMID": "39729870",
- "Title": "Environment international",
- "ArticleTitle": "Life in green: Associations between greenspace availability and mental health over the lifecourse - A 40-year prospective birth cohort study.",
- "Abstract": "This study supports the protective effects of greenspace on adult depressive symptoms, highlighting the significance of employing a spatial lifecourse epidemiology framework to examine the long-term effects of environmental factors on health over the lifecourse.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Adolescent",
- "New Zealand",
- "Prospective Studies",
- "Adult",
- "Mental Health",
- "Male",
- "Female",
- "Child",
- "Young Adult",
- "Infant",
- "Child, Preschool",
- "Birth Cohort",
- "Parks, Recreational",
- "Infant, Newborn",
- "Depression"
- ]
- },
- {
- "PMID": "39729805",
- "Title": "Drug and alcohol dependence",
- "ArticleTitle": "Tobacco cessation, mental health, and substance use in a community pharmacist-linked cessation program for people experiencing homelessness.",
- "Abstract": "A community pharmacist-linked cessation program in homeless shelters was associated with reduced consumption and increased weekly quit attempts, highlighting its potential for scalability among people experiencing homelessness with high rates of co-occurring behavioral health conditions.",
- "Predictions": [
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Adult",
- "Community Pharmacy Services",
- "Community-Based Participatory Research",
- "Ill-Housed Persons",
- "Tobacco Use Cessation",
- "Mental Health",
- "Substance-Related Disorders",
- "Program Evaluation",
- "San Francisco",
- "Counseling",
- "Nicotine Replacement Therapy",
- "Mentoring",
- "Tobacco Products",
- "Tobacco Use",
- "Odds Ratio",
- "Poisson Distribution",
- "Logistic Models",
- "Time Factors",
- "Diagnosis, Dual (Psychiatry)",
- "Mental Disorders"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/neoplasms.json b/model/data/neoplasms.json
deleted file mode 100644
index 94d29c40f2937cfa6eab27688154e34a5f7ef556..0000000000000000000000000000000000000000
--- a/model/data/neoplasms.json
+++ /dev/null
@@ -1,489 +0,0 @@
-[
- {
- "PMID": "39476057",
- "Title": "Cancer research",
- "ArticleTitle": "H4K20me3-Mediated Repression of Inflammatory Genes Is a Characteristic and Targetable Vulnerability of Persister Cancer Cells.",
- "Abstract": "Anticancer therapies can induce cellular senescence or drug-tolerant persistence, two types of proliferative arrest that differ in their stability. While senescence is highly stable, persister cells efficiently resume proliferation upon therapy termination, resulting in tumor relapse. Here, we used an ATP-competitive mTOR inhibitor to induce and characterize persistence in human cancer cells of various origins. Using this model and previously described models of senescence, we compared the same cancer cell lines under the two types of proliferative arrest. Persister and senescent cancer cells shared an expanded lysosomal compartment and hypersensitivity to BCL-XL inhibition. However, persister cells lacked other features of senescence, such as loss of lamin B1, senescence-associated \u03b2-galactosidase activity, upregulation of MHC-I, and an inflammatory and secretory phenotype (senescence-associated secretory phenotype or SASP). A genome-wide CRISPR/Cas9 screening for genes required for the survival of persister cells revealed that they are hypersensitive to the inhibition of one-carbon (1C) metabolism, which was validated by the pharmacologic inhibition of serine hydroxymethyltransferase, a key enzyme that feeds methyl groups from serine into 1C metabolism. Investigation into the relationship between 1C metabolism and the epigenetic regulation of transcription uncovered the presence of the repressive heterochromatic mark H4K20me3 at the promoters of SASP and IFN response genes in persister cells, whereas it was absent in senescent cells. Moreover, persister cells overexpressed the H4K20 methyltransferases KMT5B/C, and their downregulation unleashed inflammatory programs and compromised the survival of persister cells. In summary, this study identifies distinctive features and actionable vulnerabilities of persister cancer cells and provides mechanistic insight into their low inflammatory activity. Significance: Cell persistence and senescence are distinct states of proliferative arrest induced by cancer therapy, with persister cells being characterized by the silencing of inflammatory genes through the heterochromatic mark H4K20me3. See related commentary by Schmitt, p. 7.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Humans",
- "Cellular Senescence",
- "Histones",
- "Cell Line, Tumor",
- "Inflammation",
- "Gene Expression Regulation, Neoplastic",
- "Cell Proliferation",
- "Neoplasms",
- "TOR Serine-Threonine Kinases",
- "Epigenesis, Genetic",
- "Histone-Lysine N-Methyltransferase",
- "Senescence-Associated Secretory Phenotype",
- "Drug Resistance, Neoplasm",
- "Glycine Hydroxymethyltransferase"
- ]
- },
- {
- "PMID": "39475993",
- "Title": "Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer",
- "ArticleTitle": "Exploring disparities in healthcare utilization, cancer care experience, and beliefs about cancer among asian and hispanic cancer survivors.",
- "Abstract": "The findings suggest tailored approaches to improve healthcare utilization rates among racial/ethnic minoritized groups and highlight the need for increased research and clinical practice efforts to address racial/ethnic disparities in the cancer care continuum.",
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Adult",
- "Aged",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Young Adult",
- "Asian",
- "Cancer Survivors",
- "Health Knowledge, Attitudes, Practice",
- "Healthcare Disparities",
- "Hispanic or Latino",
- "Neoplasms",
- "Patient Acceptance of Health Care",
- "SEER Program",
- "United States"
- ]
- },
- {
- "PMID": "39475987",
- "Title": "Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer",
- "ArticleTitle": "The potential characteristics of the sense of coherence in cancer radiotherapy patients and its correlation with coping strategies.",
- "Abstract": "The SOC among cancer radiotherapy patients can be divided into three potential profiles. Younger patients with side effect have lower levels of the SOC. Adopting a acceptance-resignation coping strategies is related to a lower SOC, suggesting that enhancing the level of the SOC plays a positive role in helping patients cope with stressful events.",
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Adaptation, Psychological",
- "Female",
- "Male",
- "Sense of Coherence",
- "Middle Aged",
- "Neoplasms",
- "Surveys and Questionnaires",
- "China",
- "Adult",
- "Aged",
- "Radiotherapy",
- "Coping Skills"
- ]
- },
- {
- "PMID": "39475848",
- "Title": "JMIR cancer",
- "ArticleTitle": "Impact of Patient Personality on Adherence to Oral Anticancer Medications: An Opportunity?",
- "Abstract": "Adherence to prescribed oral anticancer therapy is an important determinant of patient outcomes, including progression-free and overall survival. While many factors (eg, medication side effects and out-of-pocket costs, problems with insurance authorization, and timely medication refills) can affect adherence, one that is relatively unexplored is the impact of a patient's attitude and personality. Patient personality influences medication adherence and persistence in nonmalignant chronic conditions such as cardiovascular disease and diabetes. In breast cancer and chronic myeloid leukemia, studies suggest that personality also affects adherence to oral chemotherapy which can be targeted to improve adherence. In this viewpoint, we highlight the opportunity of incorporating patient personality as interventions to oral cancer therapy adherence and discuss current barriers to implementation.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Humans",
- "Administration, Oral",
- "Antineoplastic Agents",
- "Medication Adherence",
- "Neoplasms",
- "Personality"
- ]
- },
- {
- "PMID": "39475661",
- "Title": "JCO precision oncology",
- "ArticleTitle": "Expert-Guided Large Language Models for Clinical Decision Support in Precision Oncology.",
- "Abstract": "Expert feedback and domain-specific data augment LLM performance. Future research should investigate responsible LLM integration into real-world clinical workflows.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Humans",
- "Precision Medicine",
- "Decision Support Systems, Clinical",
- "Medical Oncology",
- "Neoplasms"
- ]
- },
- {
- "PMID": "39475656",
- "Title": "JCO clinical cancer informatics",
- "ArticleTitle": "Identifying Oncology Patients at High Risk for Potentially Preventable Emergency Department Visits Using a Novel Definition.",
- "Abstract": "Our novel definition of PPEDs appears promising in identifying oncology patients who could avoid the ED with targeted interventions. This work demonstrated that patients with early-stage disease, those with breast cancer, and those on systemic therapy are at the highest risk for PPEDs and may benefit from proactive interventions to avoid the ED. Although our definition requires validation, using ML models for more robust predictive modeling appears promising.",
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Emergency Service, Hospital",
- "Female",
- "Male",
- "Neoplasms",
- "Middle Aged",
- "Retrospective Studies",
- "Aged",
- "Adult",
- "Machine Learning",
- "Risk Assessment",
- "Emergency Room Visits"
- ]
- },
- {
- "PMID": "39475618",
- "Title": "Science advances",
- "ArticleTitle": "Metabolic programs drive function of therapeutic NK cells in hypoxic tumor environments.",
- "Abstract": "Limited oxygen (hypoxia) in solid tumors poses a challenge to successful immunotherapy with natural killer (NK) cells. NK cells have impaired cytotoxicity when cultured in hypoxia (1% oxygen) but not physiologic (>5%) or atmospheric oxygen (20%). We found that changes to cytotoxicity were regulated at the transcriptional level and accompanied by metabolic dysregulation. Dosing with interleukin-15 (IL-15) enhanced NK cell cytotoxicity in hypoxia, but preactivation with feeder cells bearing IL-21 and 4-1BBL was even better. Preactivation resulted in less perturbed metabolism in hypoxia; greater resistance to oxidative stress; and no hypoxia-induced loss of transcription factors (T-bet and Eomes), activating receptors, adhesion molecules (CD2), and cytotoxic proteins (TRAIL and FasL). There remained a deficit in CD122/IL-2R\u03b2 when exposed to hypoxia, which affected IL-15 signaling. However, tri-specific killer engager molecules that deliver IL-15 in the context of anti-CD16/Fc\u03b3RIII were able to bypass this deficit, enhancing cytotoxicity of both fresh and preactivated NK cells in hypoxia.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Killer Cells, Natural",
- "Humans",
- "Tumor Microenvironment",
- "Interleukin-15",
- "Neoplasms",
- "Cytotoxicity, Immunologic",
- "Cell Line, Tumor",
- "Signal Transduction",
- "Cell Hypoxia"
- ]
- },
- {
- "PMID": "39475601",
- "Title": "Science advances",
- "ArticleTitle": "Hybridized and engineered microbe for catalytic generation of peroxynitrite and cancer immunotherapy under sonopiezo initiation.",
- "Abstract": "Living therapeutics is an emerging antitumor modality by living microorganisms capable of selective tropism and effective therapeutics. Nevertheless, primitive microbes could only present limited therapeutic functionalities against tumors. Hybridization of the microbes with multifunctional nanocatalysts is of great significance to achieve enhanced tumor catalytic therapy. In the present work, nitric oxide synthase (NOS)-engineered ",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Peroxynitrous Acid",
- "Animals",
- "Escherichia coli",
- "Immunotherapy",
- "Mice",
- "Neoplasms",
- "Catalysis",
- "Nanoparticles",
- "Cell Line, Tumor",
- "Humans",
- "Nitric Oxide Synthase",
- "Nitric Oxide"
- ]
- },
- {
- "PMID": "39475568",
- "Title": "Science translational medicine",
- "ArticleTitle": "Bayesian modeling for analyzing heterogeneous response in preclinical mouse tumor models.",
- "Abstract": "In anticancer research, tumor growth measured in mouse models is important for assessing treatment efficacy for a treatment to progress to human clinical trials. Statistical analysis of time-to-event tumor volume data is complex because of heterogeneity in response and welfare-related data loss. Traditional statistical methods of testing the mean difference between groups are not robust because they assume common responses across a population. Heterogeneity in response is also seen in the clinic, and consequently, the assessment of the treatment considers the diversity through classification of the individual's response using the RECIST (Response Evaluation Criteria in Solid Tumors). To provide a comparable and translatable assessment of in vivo tumor response, we developed a statistical method called INSPECT (IN vivo reSPonsE Classification of Tumors) for analyzing heterogeneous responses through Bayesian modeling. This method can classify individual tumor behaviors into the categories of nonresponder, modest responder, stable responder, and regressing responder. Using both published and simulated data, we show that INSPECT methodology is more accurate and sensitive than existing methods with respect to balancing false-negative and false-positive rates. A case study demonstrates the value of INSPECT in drug projects for supporting the translation of drug efficacy from the preclinical phase into clinical trials. We also provide a package, \"INSPECTumours,\" that launches a web interface to enable users to conduct the analysis and generate reports.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Bayes Theorem",
- "Animals",
- "Mice",
- "Disease Models, Animal",
- "Neoplasms",
- "Humans",
- "Treatment Outcome",
- "Computer Simulation",
- "Antineoplastic Agents"
- ]
- },
- {
- "PMID": "39475554",
- "Title": "ACS nano",
- "ArticleTitle": "Dual-Mode Reactive Oxygen Species-Stimulated Carbon Monoxide Release for Synergistic Photodynamic and Gas Tumor Therapy.",
- "Abstract": "Controllable carbon monoxide (CO) release simulated by light-generated reactive oxygen species (ROS) represents a promising approach for cancer therapy but is hampered by low CO release rate and low ROS generation of conventional photosensitizers in hypoxia tumor microenvironments. In this study, we developed a highly efficient nanoplatform (TPyNO",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Reactive Oxygen Species",
- "Carbon Monoxide",
- "Photochemotherapy",
- "Humans",
- "Photosensitizing Agents",
- "Animals",
- "Mice",
- "Prodrugs",
- "Antineoplastic Agents",
- "Neoplasms",
- "Gases",
- "Nanoparticles"
- ]
- },
- {
- "PMID": "39475524",
- "Title": "Biochemistry",
- "ArticleTitle": "Sugar Highs: Recent Notable Breakthroughs in Glycobiology.",
- "Abstract": "Glycosylation is biochemically complex and functionally critical to a wide range of processes and disease states, making it a vibrant area of contemporary research. Here, we highlight a selection of notable recent advances in the glycobiology of SARS-CoV-2 infection and immunity, cancer biology and immunotherapy, and newly discovered glycosylated RNAs. Together, these studies illustrate the significance of glycosylation in normal biology and the great promise of manipulating glycosylation for therapeutic benefit in disease.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Glycomics",
- "Glycosylation",
- "Immunotherapy",
- "Neoplasms",
- "SARS-CoV-2"
- ]
- },
- {
- "PMID": "39475511",
- "Title": "Cell reports",
- "ArticleTitle": "Muscle inflammation is regulated by NF-\u03baB from multiple cells to control distinct states of wasting in cancer cachexia.",
- "Abstract": "Although cancer cachexia is classically characterized as a systemic inflammatory disorder, emerging evidence indicates that weight loss also associates with local tissue inflammation. We queried the regulation of this inflammation and its causality to cachexia by exploring skeletal muscle, whose atrophy strongly associates with poor outcomes. Using multiple mouse models and patient samples, we show that cachectic muscle is marked by enhanced innate immunity. Nuclear factor \u03baB (NF-\u03baB) activity in multiple cells, including satellite cells, myofibers, and fibro-adipogenic progenitors, promotes macrophage expansion equally derived from infiltrating monocytes and resident cells. Moreover, NF-\u03baB-activated cells and macrophages undergo crosstalk; NF-\u03baB",
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Cachexia",
- "Animals",
- "NF-kappa B",
- "Macrophages",
- "Inflammation",
- "Neoplasms",
- "Humans",
- "Mice",
- "Muscle, Skeletal",
- "Mice, Inbred C57BL",
- "Muscular Atrophy",
- "Male"
- ]
- },
- {
- "PMID": "39475510",
- "Title": "Cell reports",
- "ArticleTitle": "Deciphering the regulatory mechanisms and biological implications of ARID1A missense mutations in cancer.",
- "Abstract": "ARID1A is a key component of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex and functions as a critical tumor suppressor in various cancers. In this study, we find that tumor cells with hotspot missense mutations in ARID1A (AT-rich interactive domain-containing protein 1A) exhibit a malignant phenotype. Mechanistically, these mutations facilitate the translocation of ARID1A mutant proteins to the cytoplasm by the nucleocytoplasmic shuttler XPO1 (exportin 1). Subsequently, the E3 ubiquitin ligase STUB1 ubiquitinates the ARID1A mutant protein, marking it for degradation. Knocking down STUB1 or inhibiting XPO1 stabilizes the ARID1A mutant protein, retaining it in the nucleus, which restores the assembly of the cBAF complex, the chromatin remodeling function, and the normal expression of genes related to the MAPK and anti-apoptotic pathways, thereby decreasing the tumor burden. Our research shows that nuclear-localized mutated ARID1A proteins retain tumor-suppressive function. We identify promising strategies to treat cancers harboring missense mutations in the BAF complex.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Humans",
- "DNA-Binding Proteins",
- "Mutation, Missense",
- "Transcription Factors",
- "Animals",
- "Neoplasms",
- "Cell Line, Tumor",
- "Exportin 1 Protein",
- "Karyopherins",
- "Mice",
- "Chromatin Assembly and Disassembly",
- "Ubiquitin-Protein Ligases",
- "Ubiquitination",
- "Mice, Nude",
- "Gene Expression Regulation, Neoplastic",
- "Cell Nucleus"
- ]
- },
- {
- "PMID": "39475356",
- "Title": "Cancer immunology research",
- "ArticleTitle": "BTN2A1: A Novel Target to Boost Tumor Killing Capacity of Human \u03b3\u03b4 T Cells.",
- "Abstract": "\u03b3\u03b4 T cells have recently raised great interest as effector cells in cancer immunotherapy because of their HLA-independent mode of action and their broad tumor reactivity. To translate the application of \u03b3\u03b4 T cells into clinically effective immunotherapies, specific tumor targeting and/or boosting of \u03b3\u03b4 T-cell activation in vivo seem to be a critical step. In this issue, Le Floch and colleagues report a new strategy for enabling \u03b3\u03b4 T cells to be specifically activated to kill acute lymphoblastic leukemia cells and solid tumor cells using agonistic BTN2A1 antibodies. See related article by Le Floch et al., p. 1677.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Humans",
- "Receptors, Antigen, T-Cell, gamma-delta",
- "Butyrophilins",
- "Neoplasms",
- "Immunotherapy",
- "Lymphocyte Activation",
- "Animals",
- "Cytotoxicity, Immunologic",
- "T-Lymphocytes"
- ]
- },
- {
- "PMID": "39475167",
- "Title": "Cancer medicine",
- "ArticleTitle": "Treatment of obstructive sleep apnea with CPAP improves daytime sleepiness and fatigue in cancer patients.",
- "Abstract": "PAP therapy for OSA in cancer patients improves EDS and fatigue. Larger studies are necessary to evaluate the efficacy of PAP in improving fatigue in this population.",
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Sleep Apnea, Obstructive",
- "Continuous Positive Airway Pressure",
- "Male",
- "Female",
- "Neoplasms",
- "Middle Aged",
- "Fatigue",
- "Retrospective Studies",
- "Aged",
- "Treatment Outcome",
- "Disorders of Excessive Somnolence",
- "Adult",
- "Sleepiness",
- "Patient Compliance"
- ]
- },
- {
- "PMID": "39475101",
- "Title": "Cancer medicine",
- "ArticleTitle": "Perceptions of Multicancer Detection Tests Among Primary Care Physicians and Laypersons: A Qualitative Study.",
- "Abstract": "There is a major need for more rigorous data regarding MCDs to inform the development of guidelines for use as cancer screening tools.",
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Physicians, Primary Care",
- "Female",
- "Male",
- "Early Detection of Cancer",
- "Middle Aged",
- "Neoplasms",
- "Qualitative Research",
- "Adult",
- "Focus Groups",
- "Health Knowledge, Attitudes, Practice",
- "Aged"
- ]
- },
- {
- "PMID": "39475053",
- "Title": "Advanced science (Weinheim, Baden-Wurttemberg, Germany)",
- "ArticleTitle": "Targeting BRIX1 via Engineered Exosomes Induces Nucleolar Stress to Suppress Cancer Progression.",
- "Abstract": "Elevated ribosome biogenesis correlates with the rapid growth and progression of cancer. Targeted blockade of ribosome biogenesis induces nucleolar stress, which preferentially leads to the elimination of malignant cells. In this study, it is reported that the nucleolar protein BRIX1 is a critical regulator for the homeostasis between ribosome biogenesis and p53 activation. BRIX1 facilitated the processing of pre-rRNA by supporting the formation of the PeBoW complex. In addition, BRIX1 prevented p53 activation in response to nucleolar stress by impairing the interactions between MDM2 and the ribosomal proteins, RPL5, and RPL11, thereby triggering the resistance of cancer cells to chemotherapy. Conversely, depletion of BRIX1 induced nucleolar stress, which in turn activated p53 through RPL5 and RPL11, consequently inhibiting the growth of tumors. Moreover, engineered exosomes are developed, which are surface-decorated with iRGD, a tumor-homing peptide, and loaded with siRNAs specific to BRIX1, for the treatment of cancer. iRGD-Exo-siBRIX1 significantly suppressed the growth of colorectal cancer and enhanced the efficacy of 5-FU chemotherapy in vivo. Overall, the study uncovers that BRIX1 functions as an oncoprotein to promote rRNA synthesis and dampen p53 activity, and also implies that targeted inhibition of BRIX1 via engineered exosomes can be a potent approach for cancer therapy.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Humans",
- "Exosomes",
- "Mice",
- "Animals",
- "Cell Line, Tumor",
- "Disease Progression",
- "Disease Models, Animal",
- "Tumor Suppressor Protein p53",
- "Neoplasms",
- "Cell Nucleolus",
- "Nuclear Proteins",
- "Ribosomal Proteins"
- ]
- },
- {
- "PMID": "39475021",
- "Title": "British journal of hospital medicine (London, England : 2005)",
- "ArticleTitle": "Analysis of Risk Factors for Multidrug-Resistant Organism (MDRO) Infections and Construction of a Risk Prediction Model in a Cancer Specialty Hospital.",
- "Abstract": {
- "b": "Conclusion",
- "i": "p"
- },
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Risk Factors",
- "Middle Aged",
- "Drug Resistance, Multiple, Bacterial",
- "Nomograms",
- "Aged",
- "Anti-Bacterial Agents",
- "Risk Assessment",
- "ROC Curve",
- "Cross Infection",
- "Cancer Care Facilities",
- "Neoplasms",
- "Retrospective Studies",
- "Bacterial Infections",
- "Adult"
- ]
- },
- {
- "PMID": "39474936",
- "Title": "International journal of cancer",
- "ArticleTitle": "Engineered exosomes in service of tumor immunotherapy: From optimizing tumor-derived exosomes to delivering CRISPR/Cas9 system.",
- "Abstract": "Exosomes can be modified and designed for various therapeutic goals because of their unique physical and chemical characteristics. Researchers have identified tumor-derived exosomes (TEXs) as significant players in cancer by influencing tumor growth, immune response evasion, angiogeneis, and drug resistance. TEXs promote the production of specific proteins important for cancer progression. Due to their easy accessibility, TEXs are being modified through genetic, drug delivery, membrane, immune system, and chemical alterations to be repurposed as vehicles for delivering drugs to improve cancer treatment outcomes. In the complex in vivo environment, the clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9 (CRISPR/Cas9) system encounters challenges from degradation, neutralization, and immune responses, emphasizing the need for strategic distribution strategies for effective genome editing. Engineered exosomes present a promising avenue for delivering CRISPR/Cas9 in vivo. In this review, we will explore different techniques for enhancing TEXs using various engineering strategies. Additionally, we will discuss how these exosomes can be incorporated into advanced genetic engineering systems like CRISPR/Cas9 for possible therapeutic uses.",
- "Predictions": [
- "Neoplasms"
- ],
- "MeshTerms": [
- "Animals",
- "Humans",
- "CRISPR-Cas Systems",
- "Exosomes",
- "Gene Editing",
- "Immunotherapy",
- "Neoplasms"
- ]
- },
- {
- "PMID": "39474868",
- "Title": "Open biology",
- "ArticleTitle": "The post-translational modification O-GlcNAc is a sensor and regulator of metabolism.",
- "Abstract": "Cells must rapidly adapt to changes in nutrient conditions through responsive signalling cascades to maintain homeostasis. One of these adaptive pathways results in the post-translational modification of proteins by O-GlcNAc. O-GlcNAc modifies thousands of nuclear and cytoplasmic proteins in response to nutrient availability through the hexosamine biosynthetic pathway. O-GlcNAc is highly dynamic and can be added and removed from proteins multiple times throughout their life cycle, setting it up to be an ideal regulator of cellular processes in response to metabolic changes. Here, we describe the link between cellular metabolism and O-GlcNAc, and we explore O-GlcNAc's role in regulating cellular processes in response to nutrient levels. Specifically, we discuss the mechanisms of elevated O-GlcNAc levels in contributing to diabetes and cancer, as well as the role of decreased O-GlcNAc levels in neurodegeneration. These studies form a foundational understanding of aberrant O-GlcNAc in human disease and provide an opportunity to further improve disease identification and treatment.",
- "Predictions": [
- "Neoplasms",
- "Diabetes Mellitus"
- ],
- "MeshTerms": [
- "Protein Processing, Post-Translational",
- "Humans",
- "Acetylglucosamine",
- "Animals",
- "Neoplasms",
- "Signal Transduction",
- "Glycosylation",
- "Diabetes Mellitus",
- "Neurodegenerative Diseases"
- ]
- },
- {
- "PMID": "39474469",
- "Title": "Pain research & management",
- "ArticleTitle": "Dexmedetomidine Combined With Patient-Controlled Analgesia for Palliative Sedation in Terminal-Stage Cancer Patients With Refractory Pain: A Retrospective Analysis of Nine Cases.",
- "Abstract": {
- "b": "Conclusion:",
- "i": "p"
- },
- "Predictions": [
- "Neoplasms",
- "Male"
- ],
- "MeshTerms": [
- "Humans",
- "Dexmedetomidine",
- "Male",
- "Retrospective Studies",
- "Female",
- "Palliative Care",
- "Aged",
- "Middle Aged",
- "Analgesia, Patient-Controlled",
- "Cancer Pain",
- "Pain, Intractable",
- "Hypnotics and Sedatives",
- "Neoplasms",
- "Analgesics, Non-Narcotic",
- "Pain Management",
- "Aged, 80 and over",
- "Adult"
- ]
- }
-]
\ No newline at end of file
diff --git a/model/data/noncommunicable_diseases.json b/model/data/noncommunicable_diseases.json
deleted file mode 100644
index 37ec530485eef820386d6656dd562011755b03e6..0000000000000000000000000000000000000000
--- a/model/data/noncommunicable_diseases.json
+++ /dev/null
@@ -1,463 +0,0 @@
-[
- {
- "PMID": "39737510",
- "Title": "The Indian journal of medical research",
- "ArticleTitle": "Prevalence of risk factors of non-communicable diseases among adults in urban slums of Burdwan municipality, West Bengal: A cross sectional study.",
- "Abstract": "Background & objectives Non communicable diseases (NCD) have emerged as one of the leading causes of mortality and morbidity in India in the past few decades. This study was undertaken to determine the prevalence of NCD risk factors among adults residing in urban slums of West Bengal, India. Methods A community based cross-sectional study was conducted among adult population aged 15-69 yr in urban slums of Purba Burdwan district, West Bengal over a period of two months. A total of with 180 study participants selected by simple random sampling. Data were collected using a semi-structured schedule, adopted from the WHO STEPS questionnaire. Analysis was done using Chi-square test and logistic analysis. P<0.05 was considered to be significant. Results The prevalence of alcohol intake, smoking, inadequate vegetable and fruit intake, reduced physical activity and overweight and/or obesity was 27.8, 15.6 , 93.3 , 32.8 and 15.5 per cent, respectively among the study population. A significant association of smoking was found among males [Adjusted odds ratio (AOR) 2.54 Confidence interval (CI):1.76-6.99], those living in joint families (AOR 1.24 CI:1.17-1.34) and without any formal education (AOR 3.22 CI:1.50-13.87). The odds of alcohol consumption alcohol, were higher among those aged >44 yr (AOR 1.98 CI:1.34-7.22), males (AOR 2.65 CI:1.89-8.76), those who had no formal education (AOR 1.43 CI:1.23-2.77) and those who were employed (AOR 1.34 CI:1.02-4.09). Again respondents aged 45-69 yr (AOR 4.45 CI:1.79-10.99) and married (AOR 3.77 CI:1.76-7.44) were associated with overweight and or/obesity. Furthermore, age AOR 5.04 CI:1.34-17.98) and employment status (AOR 1.78 CI:1.67-3.09) were significantly associated with raised blood pressure in multivariate analysis. Interpretation & conclusions The high prevalence of risk factors of NCD in the study population is suggestive of a need for health promotion by creating awareness about the dangers of smoking and alcohol consumption as well as educating the people about the benefits of physical activity and eating a healthy diet.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Adult",
- "Middle Aged",
- "India",
- "Male",
- "Female",
- "Noncommunicable Diseases",
- "Risk Factors",
- "Aged",
- "Poverty Areas",
- "Adolescent",
- "Prevalence",
- "Smoking",
- "Alcohol Drinking",
- "Obesity",
- "Cross-Sectional Studies",
- "Young Adult",
- "Urban Population"
- ]
- },
- {
- "PMID": "39737504",
- "Title": "The Indian journal of medical research",
- "ArticleTitle": "Stem cell therapy approaches for non-malignant diseases & non-haematological diseases in India: A systematic review.",
- "Abstract": "Background & objectives Our study aims to provide the diversity of stem cell use for non-malignant, non-haematological diseases in India through the lens of clinical trials. Methods A PRISMA approach was used to evaluate the safety and efficacy of stem cell use for the period 2001-2021 in India. The outcomes were measured using each disease category, types of stem cells, the origin of stem cells, safety, and efficacy. Results Of the 9206 studies screened, 61 studies that were relevant to stem cell use for non-malignant diseases were included for analysis. Autologous stem cells (75%) were used predominantly compared to allogenic stem cells (18.33%), followed by mixed type (6.67%). Use of bone marrow-derived stem cells (51%) was dominant, followed by melanocytes (19%), adipose (7%), haematopoietic (12%), and (11%) other types of stem cells. The study revealed 37 randomized clinical trial studies conducted in the government research hospital compared to the non-government. Interpretation & conclusions Maintaining the gold standard for stem cell therapy requires randomized clinical trials with large sample sizes, control groups, failures, adverse effects, etc. It is important to have a monitoring and regulation system in stem cell clinical research activities with enough preclinical data and repeated exchanges between the bench and the bedside.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "India",
- "Stem Cell Transplantation",
- "Cell- and Tissue-Based Therapy",
- "Noncommunicable Diseases"
- ]
- },
- {
- "PMID": "39736607",
- "Title": "International journal for equity in health",
- "ArticleTitle": "Social and economic impacts of non-communicable diseases by gender and its correlates: a literature review.",
- "Abstract": "NCDs pose a significant social and economic burden due to their impact on the health of the population, healthcare systems, and the economies of households and nations, which will likely increase over time. This impact is closely related to gender, although it has been scarcely documented. Public policies aimed at enhancing access and achieving UHC are essential to guarantee effective financial protection in health, especially for the most vulnerable sectors of the population.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Noncommunicable Diseases",
- "Female",
- "Male",
- "Sex Factors",
- "Employment",
- "Socioeconomic Factors",
- "Poverty",
- "Universal Health Insurance",
- "Cost of Illness"
- ]
- },
- {
- "PMID": "39732655",
- "Title": "BMC public health",
- "ArticleTitle": "Bias in machine learning applications to address non-communicable diseases at a population-level: a scoping review.",
- "Abstract": "This review examines current applications of ML in NCDs, highlighting potential biases and strategies for mitigation. Future research should focus on communicable diseases and the transferability of ML models in low and middle-income settings. Our findings can guide the development of guidelines for the equitable use of ML to improve population health outcomes.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Noncommunicable Diseases",
- "Machine Learning",
- "Bias",
- "Population Health",
- "Algorithms"
- ]
- },
- {
- "PMID": "39731009",
- "Title": "BMC public health",
- "ArticleTitle": "Investigating the influence of working status changes on physical activity and non-communicable diseases in Korean middle-aged and older adults: insights from a longitudinal panel study.",
- "Abstract": "This longitudinal study revealed that individuals engaged in or transitioning to employment displayed a reduced likelihood of regular PA. Moreover, those with work history, transitioning, or consistently working, exhibited increased vulnerability to all NCDs compared to those without work experience.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Republic of Korea",
- "Male",
- "Female",
- "Middle Aged",
- "Longitudinal Studies",
- "Noncommunicable Diseases",
- "Exercise",
- "Employment",
- "Aged",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39725416",
- "Title": "BMJ open",
- "ArticleTitle": "How does the level of functional impairment vary in individuals with non-communicable disease and comorbidity? Cross-sectional analysis of linked census and administrative data in Aotearoa New Zealand.",
- "Abstract": "Functional impairment was strongly patterned by NCD type. NCD prevention efforts and disability supports are needed to reduce the burden of disability experienced.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "New Zealand",
- "Cross-Sectional Studies",
- "Male",
- "Female",
- "Middle Aged",
- "Aged",
- "Noncommunicable Diseases",
- "Adult",
- "Comorbidity",
- "Censuses",
- "Adolescent",
- "Young Adult",
- "Aged, 80 and over",
- "Prevalence",
- "Child",
- "Child, Preschool"
- ]
- },
- {
- "PMID": "39722627",
- "Title": "Eastern Mediterranean health journal = La revue de sante de la Mediterranee orientale = al-Majallah al-sihhiyah li-sharq al-mutawassit",
- "ArticleTitle": "The impact of health taxes on consumption of tobacco and sugar-sweetened beverages in the Eastern Mediterranean Region.",
- "Abstract": "Consumption of tobacco, nicotine and sugar-sweetened beverages (SSBs) poses a significant risk to public health, contributing to increases in noncommunicable diseases (NCDs) such as cardiovascular disease, diabetes, cancer, and obesity. Globally, regular consumption of SSBs increases the risk of type 2 diabetes by 26%, and deaths related to tobacco and nicotine consumption exceed 8 million annually, including 1.3 million due to exposure to second-hand smoke. This loss of lives and the negative impact on health underscore the urgent need for effective public health interventions to curb the consumption of these harmful products.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Sugar-Sweetened Beverages",
- "Taxes",
- "Tobacco Products",
- "Mediterranean Region",
- "Noncommunicable Diseases"
- ]
- },
- {
- "PMID": "39709790",
- "Title": "Redox biology",
- "ArticleTitle": "Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases.",
- "Abstract": "Non-communicable chronic diseases (NCDs) are most commonly characterized by age-related loss of homeostasis and/or by cumulative exposures to environmental factors, which lead to low-grade sustained generation of reactive oxygen species (ROS), chronic inflammation and metabolic imbalance. Nuclear factor erythroid 2-like 2 (NRF2) is a basic leucine-zipper transcription factor that regulates the cellular redox homeostasis. NRF2 controls the expression of more than 250 human genes that share in their regulatory regions a cis-acting enhancer termed the antioxidant response element (ARE). The products of these genes participate in numerous functions including biotransformation and redox homeostasis, lipid and iron metabolism, inflammation, proteostasis, as well as mitochondrial dynamics and energetics. Thus, it is possible that a single pharmacological NRF2 modulator might mitigate the effect of the main hallmarks of NCDs, including oxidative, proteostatic, inflammatory and/or metabolic stress. Research on model organisms has provided tremendous knowledge of the molecular mechanisms by which NRF2 affects NCDs pathogenesis. This review is a comprehensive summary of the most commonly used model organisms of NCDs in which NRF2 has been genetically or pharmacologically modulated, paving the way for drug development to combat NCDs. We discuss the validity and use of these models and identify future challenges.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "NF-E2-Related Factor 2",
- "Humans",
- "Animals",
- "Noncommunicable Diseases",
- "Oxidative Stress",
- "Reactive Oxygen Species",
- "Oxidation-Reduction",
- "Disease Models, Animal",
- "Inflammation",
- "Gene Expression Regulation"
- ]
- },
- {
- "PMID": "39702198",
- "Title": "BMC geriatrics",
- "ArticleTitle": "Age- and sex-disaggregated disease burden among the older persons in India.",
- "Abstract": "This comprehensive assessment of the differentials in disease burden among older persons across age, sex and states of India, and the gaps identified in the service utilisation data capture by age and sex for the older persons in the national health programs can provide crucial inputs for strengthening the on-going public health policy and programmatic efforts aimed at improving the health and well-being of the growing older population in India.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Aged",
- "Female",
- "Male",
- "India",
- "Middle Aged",
- "Aged, 80 and over",
- "Noncommunicable Diseases",
- "Cost of Illness",
- "Disability-Adjusted Life Years",
- "Sex Factors",
- "Age Factors",
- "Global Burden of Disease",
- "Wounds and Injuries"
- ]
- },
- {
- "PMID": "39699459",
- "Title": "Revista brasileira de epidemiologia = Brazilian journal of epidemiology",
- "ArticleTitle": "Chronic noncommunicable diseases and absenteeism from work: National Survey of Health, 2019.",
- "Abstract": "The burden of disease and multimorbidity are highly prevalent among employed individuals and are strongly related to absenteeism from work, especially among women. In this sense, workers must be the target of interventions to reduce the impact of chronic noncommunicable diseases.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Absenteeism",
- "Male",
- "Female",
- "Brazil",
- "Cross-Sectional Studies",
- "Adult",
- "Middle Aged",
- "Chronic Disease",
- "Noncommunicable Diseases",
- "Prevalence",
- "Health Surveys",
- "Young Adult",
- "Adolescent",
- "Sex Distribution",
- "Socioeconomic Factors",
- "Cost of Illness",
- "Multimorbidity",
- "Sociodemographic Factors"
- ]
- },
- {
- "PMID": "39697299",
- "Title": "Frontiers in public health",
- "ArticleTitle": "Non-communicable diseases related multimorbidity, catastrophic health expenditure, and associated factors in Ernakulam district.",
- "Abstract": "The high prevalence of multimorbidity and associated CHE among individuals over 60\u202fyears highlights the urgent need for the National Programme for the Prevention and Control of Non-Communicable Diseases to prioritise multimorbidity and its management, especially above 60 years within this age group.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Middle Aged",
- "Male",
- "Female",
- "Cross-Sectional Studies",
- "Multimorbidity",
- "Noncommunicable Diseases",
- "Health Expenditures",
- "Prevalence",
- "Aged",
- "Adult",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39696316",
- "Title": "Health research policy and systems",
- "ArticleTitle": "Enhancing multi-sectoral collaborations for the prevention and control of NCDs in Thailand with a new approach.",
- "Abstract": "This new approach (middle-management oriented), if implemented, may encourage more commitment from the Ministries' representatives, policy-relevant knowledge generation and effective communications between ministries involved in an MSC. Ideally, it would complement the conventional approach (top-management oriented) in enhancing the MSC for controlling NCDs, and thereby bring hope for achieving the NCD-related SDGs for Thailand and possibly other countries as well.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Thailand",
- "Humans",
- "Noncommunicable Diseases",
- "Stakeholder Participation",
- "Health Policy",
- "Sustainable Development",
- "Intersectoral Collaboration",
- "Cooperative Behavior"
- ]
- },
- {
- "PMID": "39696309",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Prevalence of diabetes and its associated factors in Cape Verde: an analysis of the 2020 WHO STEPS survey on non-communicable diseases risk factors.",
- "Abstract": "Not applicable.",
- "Predictions": [
- "Noncommunicable Diseases",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Middle Aged",
- "Adult",
- "Male",
- "Female",
- "Diabetes Mellitus, Type 2",
- "Prevalence",
- "Aged",
- "Risk Factors",
- "Adolescent",
- "Young Adult",
- "Cabo Verde",
- "Prediabetic State",
- "Noncommunicable Diseases",
- "World Health Organization",
- "Cross-Sectional Studies",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39695503",
- "Title": "BMC public health",
- "ArticleTitle": "The relationship between non-communicable disease risk and mental wellbeing in adolescence: a cross-sectional study utilising objective measures in Indonesia.",
- "Abstract": "Our analysis also shows that these NCD risks (both individual risks and co-occurring risk count) are related to poorer profiles of mental wellbeing in adolescents, after adjusting for likely confounders.",
- "Predictions": [
- "Noncommunicable Diseases",
- "Mental Health"
- ],
- "MeshTerms": [
- "Humans",
- "Indonesia",
- "Adolescent",
- "Male",
- "Female",
- "Noncommunicable Diseases",
- "Cross-Sectional Studies",
- "Risk Factors",
- "Mental Health",
- "Quality of Life",
- "Prevalence"
- ]
- },
- {
- "PMID": "39693027",
- "Title": "Sub-cellular biochemistry",
- "ArticleTitle": "Melatonin as a Chronobiotic and Cytoprotector in Non-communicable Diseases: More than an Antioxidant.",
- "Abstract": "A circadian disruption, manifested by disturbed sleep and low-grade inflammation, is commonly seen in noncommunicable diseases (NCDs). Cardiovascular, respiratory and renal disorders, diabetes and the metabolic syndrome, cancer, and neurodegenerative diseases are among the most common NCDs prevalent in today's 24-h/7\u00a0days Society. The decline in plasma melatonin, which is a conserved phylogenetic molecule across all known aerobic creatures, is a constant feature in NCDs. The daily evening melatonin surge synchronizes both the central pacemaker located in the hypothalamic suprachiasmatic nuclei (SCN) and myriads of cellular clocks in the periphery (\"chronobiotic effect\"). Melatonin is the prototypical endogenous chronobiotic agent. Several meta-analyses and consensus studies support the use of melatonin to treat sleep/wake cycle disturbances associated with NCDs. Melatonin also has cytoprotective properties, acting primarily not only as an antioxidant by buffering free radicals, but also by regulating inflammation, down-regulating pro-inflammatory cytokines, suppressing low-grade inflammation, and preventing insulin resistance, among other effects. Melatonin's phylogenetic conservation is explained by its versatility of effects. In animal models of NCDs, melatonin treatment prevents a wide range of low-inflammation-linked alterations. As a result, the therapeutic efficacy of melatonin as a chronobiotic/cytoprotective drug has been proposed. Sirtuins 1 and 3 are at the heart of melatonin's chronobiotic and cytoprotective function, acting as accessory components or downstream elements of circadian oscillators and exhibiting properties such as mitochondrial protection. Allometric calculations based on animal research show that melatonin's cytoprotective benefits may require high doses in humans (in the 100\u00a0mg/day range). If melatonin is expected to improve health in NCDs, the low doses currently used in clinical trials (i.e., 2-10\u00a0mg) are unlikely to be beneficial. Multicentre double-blind studies are required to determine the potential utility of melatonin in health promotion. Moreover, melatonin dosage and levels used should be re-evaluated based on preclinical research information.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Melatonin",
- "Humans",
- "Animals",
- "Antioxidants",
- "Noncommunicable Diseases",
- "Circadian Rhythm",
- "Cytoprotection",
- "Inflammation"
- ]
- },
- {
- "PMID": "39683555",
- "Title": "Nutrients",
- "ArticleTitle": "Risky Behaviors for Non-Communicable Diseases: Italian Adolescents' Food Habits and Physical Activity.",
- "Abstract": "Many adolescents lead unhealthy lifestyles, but younger adolescents and girls appear to be at higher risk of unhealthy behaviors. Targeted initiatives promoting regular physical activity and balanced diets in schools, involving parents and teachers in a collaborative plan, are essential to improving adolescents' health and well-being.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Adolescent",
- "Male",
- "Female",
- "Italy",
- "Exercise",
- "Feeding Behavior",
- "Cross-Sectional Studies",
- "Noncommunicable Diseases",
- "Health Knowledge, Attitudes, Practice",
- "Young Adult",
- "Child",
- "Adolescent Behavior",
- "Surveys and Questionnaires",
- "Health Risk Behaviors",
- "Risk-Taking",
- "Diet"
- ]
- },
- {
- "PMID": "39678524",
- "Title": "Iranian journal of medical sciences",
- "ArticleTitle": "Clustering the Economic Status via Partitioning around Medoid and Its Association with Common Non-communicable Diseases.",
- "Abstract": "The findings of the present study showed that economic status was significantly associated with the majority of NCDs.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Noncommunicable Diseases",
- "Female",
- "Male",
- "Middle Aged",
- "Adult",
- "Aged",
- "Iran",
- "Economic Status",
- "Cluster Analysis",
- "Cohort Studies"
- ]
- },
- {
- "PMID": "39671524",
- "Title": "American journal of physical medicine & rehabilitation",
- "ArticleTitle": "Correlation Between Self-reported or Supervised Physical Activity in Noncommunicable Diseases and Comorbidities During COVID-19 Pandemic: A Systematic Review.",
- "Abstract": "There is evidence that exercise can protect people with noncommunicable diseases during the COVID-19 pandemic.Registration: Registered with Prospero registry.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Exercise",
- "Comorbidity",
- "Noncommunicable Diseases",
- "SARS-CoV-2",
- "Self Report",
- "Pandemics"
- ]
- },
- {
- "PMID": "39662975",
- "Title": "Global health, science and practice",
- "ArticleTitle": "Service Delivery Redesign for Noncommunicable Disease Management: Assessment of Needs and Solutions Through a Co-Creation Process in Argentina.",
- "Abstract": "Our research highlights the potential for Argentina's primary care system to initiate transformative, system-level changes aimed at improving health outcomes. We propose an innovative methodological assessment and co-design for improving primary care.",
- "Predictions": [
- "Noncommunicable Diseases",
- "Diabetes type 2"
- ],
- "MeshTerms": [
- "Humans",
- "Argentina",
- "Noncommunicable Diseases",
- "Primary Health Care",
- "Male",
- "Female",
- "Cross-Sectional Studies",
- "Middle Aged",
- "Delivery of Health Care",
- "Focus Groups",
- "Adult",
- "Aged",
- "Disease Management",
- "Health Services Accessibility",
- "Needs Assessment",
- "Diabetes Mellitus, Type 2",
- "Delphi Technique"
- ]
- },
- {
- "PMID": "39662129",
- "Title": "Public health",
- "ArticleTitle": "Non-communicable disease mortality and economic costs attributable to high body mass index in Argentina.",
- "Abstract": "The burden of NCD mortality and associated economic costs attributable to high BMI in Argentina are substantial, highlighting the urgent need for multi-sectoral interventions to address the increasing prevalence of overweight and obesity.",
- "Predictions": [
- "Noncommunicable Diseases"
- ],
- "MeshTerms": [
- "Humans",
- "Argentina",
- "Body Mass Index",
- "Male",
- "Female",
- "Noncommunicable Diseases",
- "Adult",
- "Middle Aged",
- "Obesity",
- "Aged",
- "Cost of Illness",
- "Risk Assessment",
- "Overweight"
- ]
- }
-]
\ No newline at end of file
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deleted file mode 100644
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@@ -1,6693 +0,0 @@
-[
- {
- "PMID": "39476387",
- "Title": "Current opinion in anaesthesiology",
- "ArticleTitle": "Caring for patients with diabetes in the outpatient surgical setting: current recommendations and controversies.",
- "Abstract": "Future research needs to specifically examine chronic blood glucose control, day of surgery targets, effective home medication management and the risk of perioperative hyperglycemia in ambulatory surgery. Education, protocols and resources to support the care of perioperative patients in the outpatient setting will aid providers on the day of surgery and provide optimal diabetes care leading up to surgery.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Ambulatory Surgical Procedures",
- "Hypoglycemic Agents",
- "Diabetes Mellitus",
- "Perioperative Care",
- "Blood Glucose",
- "Insulin",
- "Ambulatory Care",
- "Postoperative Care",
- "Practice Guidelines as Topic",
- "Hyperglycemia",
- "Preoperative Care"
- ]
- },
- {
- "PMID": "39476122",
- "Title": "PloS one",
- "ArticleTitle": "Burden of diabetes mellitus in Weifang: Changing trends in prevalence and deaths from 2010 to 2021.",
- "Abstract": "The city is faced with a significant challenge of diabetes, which is influenced by factors such as gender, age, cultural background, and marital status. Unspecified diabetes mellitus (DM) with ketoacidosis (10.03%) and T2DM with renal complications (0.23%) are identified as the primary direct and underlying causes of death among diabetic patients, respectively. This study serves as a valuable reference for other regions in terms of diabetes prevention, control, and the management of chronic diseases.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Aged",
- "Middle Aged",
- "Prevalence",
- "Diabetes Mellitus",
- "Adult",
- "China",
- "Cost of Illness",
- "Adolescent",
- "Aged, 80 and over",
- "Young Adult",
- "Disability-Adjusted Life Years",
- "Cause of Death",
- "Child"
- ]
- },
- {
- "PMID": "39474868",
- "Title": "Open biology",
- "ArticleTitle": "The post-translational modification O-GlcNAc is a sensor and regulator of metabolism.",
- "Abstract": "Cells must rapidly adapt to changes in nutrient conditions through responsive signalling cascades to maintain homeostasis. One of these adaptive pathways results in the post-translational modification of proteins by O-GlcNAc. O-GlcNAc modifies thousands of nuclear and cytoplasmic proteins in response to nutrient availability through the hexosamine biosynthetic pathway. O-GlcNAc is highly dynamic and can be added and removed from proteins multiple times throughout their life cycle, setting it up to be an ideal regulator of cellular processes in response to metabolic changes. Here, we describe the link between cellular metabolism and O-GlcNAc, and we explore O-GlcNAc's role in regulating cellular processes in response to nutrient levels. Specifically, we discuss the mechanisms of elevated O-GlcNAc levels in contributing to diabetes and cancer, as well as the role of decreased O-GlcNAc levels in neurodegeneration. These studies form a foundational understanding of aberrant O-GlcNAc in human disease and provide an opportunity to further improve disease identification and treatment.",
- "Predictions": [],
- "MeshTerms": [
- "Protein Processing, Post-Translational",
- "Humans",
- "Acetylglucosamine",
- "Animals",
- "Neoplasms",
- "Signal Transduction",
- "Glycosylation",
- "Diabetes Mellitus",
- "Neurodegenerative Diseases"
- ]
- },
- {
- "PMID": "39474832",
- "Title": "Medical decision making : an international journal of the Society for Medical Decision Making",
- "ArticleTitle": "Using QALYs as an Outcome for Assessing Global Prediction Accuracy in Diabetes Simulation Models.",
- "Abstract": "Diabetes simulation models are currently validated by examining their ability to predict the incidence of individual events (e.g., myocardial infarction, stroke, amputation) or composite events (e.g., first major adverse cardiovascular event).We introduce Q",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Quality-Adjusted Life Years",
- "Computer Simulation",
- "Hypoglycemic Agents",
- "Diabetes Mellitus, Type 2",
- "Cost-Benefit Analysis",
- "United Kingdom",
- "Technology Assessment, Biomedical",
- "Diabetes Mellitus",
- "Female",
- "Male"
- ]
- },
- {
- "PMID": "39472978",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Association between night blindness history and risk of diabetes in the Chinese population: a multi-center, cross sectional study.",
- "Abstract": "The results suggest that NB history might be associated with increased odds of diabetes in Chinese community-dwelling adults.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Cross-Sectional Studies",
- "Middle Aged",
- "Male",
- "Female",
- "Adult",
- "Aged",
- "China",
- "Diabetes Mellitus",
- "Adolescent",
- "Young Adult",
- "Night Blindness",
- "Risk Factors",
- "Aged, 80 and over",
- "East Asian People"
- ]
- },
- {
- "PMID": "39472915",
- "Title": "BMC health services research",
- "ArticleTitle": "Geographical Access to Point-of-care diagnostic tests for diabetes, anaemia, Hepatitis B, and human immunodeficiency virus in the Bono Region, Ghana.",
- "Abstract": "The findings revealed moderate access to all the tests in districts across the region. However, geographical access to glucose, Hb, Hep B, and HIV POC testing was poor (distance\u2009\u2265\u200910\u00a0km and travel time of \u2265\u200993\u00a0min), in the Banda district. This study showed the need to prioritise the Banda district for targeted improvement for all the tests. A further study is recommended to identify potential solutions to addressing the POC testing implementation in the BR, as demonstrated by this study.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Ghana",
- "HIV Infections",
- "Health Services Accessibility",
- "Anemia",
- "Hepatitis B",
- "Diabetes Mellitus",
- "Point-of-Care Testing",
- "Point-of-Care Systems"
- ]
- },
- {
- "PMID": "39471268",
- "Title": "Journal of managed care & specialty pharmacy",
- "ArticleTitle": "Potential benefits of incorporating social determinants of health screening on comprehensive medication management effectiveness.",
- "Abstract": "Although not statistically significant, the results of this pilot evaluation suggest the potential for meaningful clinical improvements from screening and referral of SDoH needs as a part of CMM encounters. These results should be corroborated using a larger, more robust study design.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Retrospective Studies",
- "Social Determinants of Health",
- "Female",
- "Male",
- "Middle Aged",
- "Medication Therapy Management",
- "Aged",
- "Pharmacists",
- "Referral and Consultation",
- "Mass Screening",
- "Adult",
- "Cohort Studies",
- "Hypertension",
- "Diabetes Mellitus",
- "Chronic Disease"
- ]
- },
- {
- "PMID": "39470899",
- "Title": "Current diabetes reports",
- "ArticleTitle": "Implementation Science and Pediatric Diabetes: A Scoping Review of the State of the Literature and Recommendations for Future Research.",
- "Abstract": "Of 23 papers identified, 19 were published since 2017 and 21 focused on type 1 diabetes. Most involved medical evidence-based practices (EBPs; n\u2009=\u200915), whereas fewer focused on psychosocial (n\u2009=\u20097) and diabetes education (n\u2009=\u20092). The majority either identified barriers and facilitators of implementing an EBP (n\u2009=\u200911) or were implementation trials (n\u2009=\u200911). Fewer studies documented gaps in EBP implementation in standard care (n\u2009=\u20097) or development of implementation strategies (n\u2009=\u20091). Five papers employed IS theories and two aimed to improve equity. There is a paucity of IS research in pediatric diabetes care literature. Few papers employed IS theory, used consistent IS terminology, or described IS strategies or outcomes. Guidance for future research to improve IS research in pediatric diabetes is offered.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Implementation Science",
- "Child",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus",
- "Pediatrics",
- "Evidence-Based Practice"
- ]
- },
- {
- "PMID": "39470889",
- "Title": "Biogerontology",
- "ArticleTitle": "A novel (-)-(2S)-7,4'-dihydroxyflavanone compound for treating age-related diabetes mellitus through immunoinformatics-guided activation of CISD3.",
- "Abstract": "The iron-sulfur domain (CISD) proteins of CDGSH are classified into three classes: CISD1, CISD2, and CISD3. During premature ageing, mutations that affect these proteins, namely their binding sites, could result in reduced protein production and an inability to preserve cellular integrity. Consequently, this leads to the development of conditions such as diabetes. Notably, CISD3 plays a crucial role in the management of age-related disorders such as Wolfram syndrome, which is often referred to as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness). Computational analyses have predicted that CISD3 regulates the redox state, safeguards the endoplasmic reticulum and mitochondria, and maintains intracellular calcium levels. CISD3, a member of a recently discovered gene family associated with the CDGSH iron protein apoptotic compensatory response, fulfils a crucial function in mitigating the effects of accelerated ageing. The compound \"(-)-(2S)-7,4'-Dihydroxyflavanone\" has been discovered by computational drug design as a possible activator of CISD3. It shows potential therapeutic benefits in ameliorating metabolic dysfunction and enhancing glucose regulation. The ligand binds to the binding pocket of the CISD3 protein, increasing the stability of the protein and enhancing its functionality. The current research investigates the binding processes of the molecule in various structures and its anticipated effects on these tissues, therefore providing valuable insights into the mitigation of age-related diabetes and metabolic dysfunction. The projected tripling of the worldwide population of individuals aged 50 and above by 2050 necessitates the urgent development of immunoinformatics-based approaches, including pharmaceutical therapies that target CISD3, to prevent age-related pathologies. The stimulation of CISD3, namely by compounds such as \"(-)-(2S)-7,4'-Dihydroxyflavanone\", has the potential to counteract telomere shortening and improve metabolic pathways.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus",
- "Aging",
- "Flavanones",
- "Hypoglycemic Agents",
- "Molecular Docking Simulation",
- "Computational Biology",
- "Drug Design",
- "Immunoinformatics"
- ]
- },
- {
- "PMID": "39470403",
- "Title": "The journals of gerontology. Series B, Psychological sciences and social sciences",
- "ArticleTitle": "Economic Disadvantage During Childhood, Obesity, and Diabetes Across Three Birth Cohorts of Older Mexicans.",
- "Abstract": "High body weight across Mexican birth cohorts seemed to offset the potential benefits from improvements in childhood conditions on adult diabetes risk.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Middle Aged",
- "Aged",
- "Mexico",
- "Diabetes Mellitus",
- "Prevalence",
- "Obesity",
- "Birth Cohort",
- "Body Mass Index",
- "Adverse Childhood Experiences",
- "Overweight",
- "Poverty",
- "North American People"
- ]
- },
- {
- "PMID": "39468609",
- "Title": "Stem cell research & therapy",
- "ArticleTitle": "Human mesenchymal stem/stromal cell based-therapy in diabetes mellitus: experimental and clinical perspectives.",
- "Abstract": "Diabetes mellitus (DM), a chronic metabolic disease, poses a significant global health challenge, with current treatments often fail to prevent the long-term disease complications. Mesenchymal stem/stromal cells (MSCs) are, adult progenitors, able to repair injured tissues, exhibiting regenerative effects and immunoregulatory and anti-inflammatory responses, so they have been emerged as a promising therapeutic approach in many immune-related and inflammatory diseases. This review summarizes the therapeutic mechanisms and outcomes of MSCs, derived from different human tissue sources (hMSCs), in the context of DM type 1 and type 2. Animal model studies and clinical trials indicate that hMSCs can facilitate pleiotropic actions in the diabetic milieu for improved metabolic indices. In addition to modulating abnormally active immune system, hMSCs can ameliorate peripheral insulin resistance, halt beta-cell destruction, preserve residual beta-cell mass, promote beta-cell regeneration and insulin production, support islet grafts, and correct lipid metabolism. Moreover, hMSC-free derivatives, importantly extracellular vesicles, have shown potent experimental anti-diabetic efficacy. Moreover, the review discusses the diverse priming strategies that are introduced to enhance the preclinical anti-diabetic actions of hMSCs. Such strategies are recommended to restore the characteristics and functions of MSCs isolated from patients with DM for autologous implications. Finally, limitations and merits for the wide spread clinical applications of MSCs in DM such as the challenge of autologous versus allogeneic MSCs, the optimal MSC tissue source and administration route, the necessity of larger clinical trials for longer evaluation duration to assess safety concerns, are briefly presented.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Mesenchymal Stem Cell Transplantation",
- "Mesenchymal Stem Cells",
- "Animals",
- "Insulin-Secreting Cells",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39468602",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Lipids as the link between central obesity and diabetes: perspectives from mediation analysis.",
- "Abstract": "In central obesity-related diabetes risk, most lipids, especially lipid ratio parameters, play a significant mediating role. Given these findings, we advocate for increased efforts in multifactorial risk monitoring and joint management of diabetes. The evaluation of lipids, particularly lipid ratio parameters, may be holds substantial value in the prevention and management of diabetes risk under close monitoring of central obesity.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Obesity, Abdominal",
- "Male",
- "Female",
- "Middle Aged",
- "Lipids",
- "Mediation Analysis",
- "Adult",
- "Risk Factors",
- "Waist Circumference",
- "Longitudinal Studies",
- "Diabetes Mellitus",
- "Biomarkers",
- "Diabetes Mellitus, Type 2",
- "Follow-Up Studies",
- "Aged",
- "Prognosis",
- "Triglycerides"
- ]
- },
- {
- "PMID": "39466432",
- "Title": "Applied microbiology and biotechnology",
- "ArticleTitle": "Gut microbiota predict retinopathy in patients with diabetes: A longitudinal cohort study.",
- "Abstract": "The gut microbiota has emerged as an independent risk factor for diabetes and its complications. This research aimed to delve into the intricate relationship between the gut microbiome and diabetic retinopathy (DR) through a dual approach of cross-sectional and prospective cohort studies. In our cross-sectional study cross-sectional investigation involving ninety-nine individuals with diabetes, distinct microbial signatures associated with DR were identified. Specifically, gut microbiome profiling revealed decreased levels of Butyricicoccus and Ruminococcus torques group, alongside upregulated methanogenesis pathways among DR patients. These individuals concurrently exhibited lower concentrations of short-chain fatty acids in their plasma. Leveraging machine learning models, including random forest classifiers, we constructed a panel of microbial genera and genes that robustly differentiated DR cases. Importantly, these genera also demonstrated significant correlations with dietary patterns and the molecular profiles of peripheral blood mononuclear cells. Building upon these findings, our prospective cohort study followed 62 diabetes patients over a 2-year period to assess the predictive value of these microbial markers. The results underlined the panel's efficacy in predicting DR incidence. By stratifying patients based on the predictive genera and metabolites identified in the cross-sectional phase, we established significant associations between reduced levels of Butyricicoccus, plasma acetate, and increased susceptibility to DR. This investigation not only deepens our understanding of how gut microbiota influences DR but also underscores the potential of microbial markers as early indicators of disease risk. These insights hold promise for developing targeted interventions aimed at mitigating the impact of diabetic complications. KEY POINTS: \u2022 Microbial signatures are differed in diabetic patients with and without retinopathy \u2022 DR-related taxa are linked to dietary habits and transcriptomic profiles \u2022 Lower abundances of Butyricicoccus and acetate were prospectively associated with DR.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Gastrointestinal Microbiome",
- "Cross-Sectional Studies",
- "Male",
- "Diabetic Retinopathy",
- "Middle Aged",
- "Longitudinal Studies",
- "Prospective Studies",
- "Female",
- "Fatty Acids, Volatile",
- "Aged",
- "Ruminococcus",
- "Clostridiales",
- "Acetates",
- "Adult",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39466337",
- "Title": "Current medical research and opinion",
- "ArticleTitle": "Technological advancements in glucose monitoring and artificial pancreas systems for shaping diabetes care.",
- "Abstract": "The management of diabetes mellitus has undergone remarkable progress with the introduction of cutting-edge technologies in glucose monitoring and artificial pancreas systems. These innovations have revolutionized diabetes care, offering patients more precise, convenient, and personalized management solutions that significantly improve their quality of life. This review aims to provide a comprehensive overview of recent technological advancements in glucose monitoring devices and artificial pancreas systems, focusing on their transformative impact on diabetes care. A detailed review of the literature was conducted to examine the evolution of glucose monitoring technologies, from traditional invasive methods to more advanced systems. The review explores minimally invasive techniques such as continuous glucose monitoring (CGM) systems and flash glucose monitoring (FGM) systems, which have already been proven to enhance glycemic control and reduce the risk of hypoglycemia. In addition, emerging non-invasive glucose monitoring technologies, including optical, electrochemical, and electro-mechanical methods, were evaluated. These techniques are paving the way for more patient-friendly options that eliminate the need for frequent finger-prick tests, thereby improving adherence and ease of use. Advancements in closed-loop artificial pancreas systems, which integrate CGM with automated insulin delivery, were also examined. These systems, often referred to as \"hybrid closed-loop\" or \"automated insulin delivery\" systems, represent a significant leap forward in diabetes care by automating the process of insulin dosing. Such advancements aim to mimic the natural function of the pancreas, allowing for better glucose regulation without the constant need for manual interventions by the patient. Technological breakthroughs in glucose monitoring and artificial pancreas systems have had a profound impact on diabetes management, providing patients with more accurate, reliable, and individualized treatment options. These innovations hold the potential to significantly improve glycemic control, reduce the incidence of diabetes-related complications, and ultimately enhance the quality of life for individuals living with diabetes. Researchers are continually exploring novel methods to measure glucose more effectively and with greater convenience, further refining the future of diabetes care. Researchers are also investigating the integration of artificial intelligence and machine learning algorithms to further enhance the precision and predictive capabilities of glucose monitoring and insulin delivery systems. With ongoing advancements in sensor technology, connectivity, and data analytics, the future of diabetes care promises to deliver even more seamless, real-time management, empowering patients with greater autonomy and improved health outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Pancreas, Artificial",
- "Blood Glucose Self-Monitoring",
- "Blood Glucose",
- "Diabetes Mellitus",
- "Insulin",
- "Insulin Infusion Systems",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39465859",
- "Title": "Medicine",
- "ArticleTitle": "Association of triglyceride-glucose index with diabetes or prediabetes in Chinese hypertensive patients: A retrospective cohort study.",
- "Abstract": "Insulin resistance is a key factor in diabetes development. This study aimed to investigate the association between baseline triglyceride-glucose (TyG) index, a surrogate marker of insulin resistance, and the onset of hyperglycemia in Chinese individuals with hypertension. Using the Rich Healthcare Group database, this retrospective cohort study included 28,687 hypertensive individuals without preexisting diabetes. A wide range of demographic information and baseline biochemical indicators was collected and rigorously analyzed. This study utilized the Cox proportional hazards model and smooth curve fitting to explore the link between TyG index and the risk of developing hyperglycemia. The robustness of the findings was validated by sensitivity and subgroup analyses. During longitudinal monitoring of hypertensive patients in our retrospective cohort study, we observed that 5.31% (1524/28,687) progressed to diabetes, while 21.66% (4620/21,326) developed prediabetes. After adjusting for confounding variables, a statistically significant positive association was observed between the TyG index and the risk of hyperglycemia. Subgroup and sensitivity analyses further supported these findings, demonstrating consistent outcomes and reinforcing the robustness of our conclusions. The TyG index, which is significantly linked to hyperglycemia in hypertensives, can aid early risk identification and intervention.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Retrospective Studies",
- "Male",
- "Female",
- "Prediabetic State",
- "Middle Aged",
- "Hypertension",
- "Triglycerides",
- "Blood Glucose",
- "China",
- "Aged",
- "Insulin Resistance",
- "Biomarkers",
- "Adult",
- "Diabetes Mellitus",
- "Proportional Hazards Models",
- "Hyperglycemia",
- "Risk Factors",
- "East Asian People"
- ]
- },
- {
- "PMID": "39465722",
- "Title": "Medicine",
- "ArticleTitle": "Association between serum globulins and diabetes mellitus in American latent tuberculosis infection patients: A cross-sectional study.",
- "Abstract": "Diabetes mellitus (DM) is predisposing to the development of latent tuberculosis infection (LTBI). An understanding of the underlying factors of LTBI-DM is important for tuberculosis prevention and control. This study aims to evaluate the association between LTBI and DM among the noninstitutionalized civilian population in the United States, focusing on the impact of serum globulins. We performed a cross-sectional study design using public data from 2011 to 2012 National Health and Nutrition Examination Survey, focusing on participants diagnosed with LTBI who were aged 20 and above. Weighted Wilcoxon rank-sum and weighted chi-square tests were used to compare group differences. A multivariable logistic regression model was constructed to assess the association between serum globulin and DM, with subgroup analyses and evaluations of nonlinear relationships. Receiver operating characteristic curves were used to assess the predictive power of the models. A total of 694 participants (512 DM and 182 nonDM) were included in our study and the incidence of DM was 22%. Higher serum globulin levels were significantly associated with an increased risk of DM, with a 21% increase in risk for each unit increase in serum globulin (odds ratio\u2005=\u20051.21, 95% confidence interval [1.03, 1.43], P\u2005<\u2005.001). The relationship between serum globulin and DM was linear, and higher serum globulin levels were associated with a higher risk of DM, particularly in males (P\u2005=\u2005.043) and obese individuals (P\u2005=\u2005.019). The area under the curve for serum globulin predicting DM was 0.795, with an optimal cutoff value of 2.9. Elevated serum globulin levels are significantly associated with an increased risk of DM among individuals with LTBI, highlighting the potential role of serum globulin as a predictive biomarker for DM in this population. However, the specific mechanism between globulin and LTBI-DM needs to be further investigated.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Cross-Sectional Studies",
- "Female",
- "Latent Tuberculosis",
- "Middle Aged",
- "Adult",
- "United States",
- "Diabetes Mellitus",
- "Nutrition Surveys",
- "Serum Globulins",
- "Risk Factors",
- "Aged",
- "Young Adult",
- "Incidence",
- "ROC Curve",
- "Biomarkers"
- ]
- },
- {
- "PMID": "39465638",
- "Title": "Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions",
- "ArticleTitle": "Drug-coated balloons in high-risk patients and diabetes mellitus: A meta-analysis of 10 studies.",
- "Abstract": "We confirmed a significant advantage of DCB versus DES in the treatment of de novo lesions in high-risk patients and mainly in DM, reducing overall mortality, MACE and target lesion revascularization.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Angioplasty, Balloon, Coronary",
- "Cardiac Catheters",
- "Cardiovascular Agents",
- "Coated Materials, Biocompatible",
- "Coronary Artery Disease",
- "Diabetes Mellitus",
- "Drug-Eluting Stents",
- "Equipment Design",
- "Odds Ratio",
- "Percutaneous Coronary Intervention",
- "Risk Assessment",
- "Risk Factors",
- "Time Factors",
- "Treatment Outcome"
- ]
- },
- {
- "PMID": "39465521",
- "Title": "Archives of Iranian medicine",
- "ArticleTitle": "Prevalence of Chronic Kidney Disease and Associated Factors among the Diabetic and Prediabetic Population in the Bandare-Kong Cohort Study; A Population-Based Study.",
- "Abstract": "The study emphasizes the importance of early detection and management of CKD risk factors, particularly among high-risk individuals, to mitigate CKD progression and associated complications. By addressing modifiable risk factors, proactive screening, and enhanced awareness, significant strides can be made in reducing CKD burden and improving patient outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Middle Aged",
- "Female",
- "Male",
- "Prediabetic State",
- "Renal Insufficiency, Chronic",
- "Adult",
- "Iran",
- "Aged",
- "Risk Factors",
- "Prevalence",
- "Glomerular Filtration Rate",
- "Prospective Studies",
- "Cohort Studies",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39464188",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "A mobile health application use among diabetes mellitus patients: a systematic review and meta-analysis.",
- "Abstract": "https://www.crd.york.ac.uk/prospero/, identifier 42024537917.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus",
- "Mobile Applications",
- "Self Care",
- "Telemedicine"
- ]
- },
- {
- "PMID": "39463812",
- "Title": "Ethnicity & disease",
- "ArticleTitle": "Racial Disparities in Foot Examination among People with Diabetes in Brazil: A Nationwide Survey, 2019.",
- "Abstract": "Black Brazilians with diabetes had higher negligence of foot examination by health care professionals. Strengthening primary care would help mitigate systemic racism in Brazil.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Brazil",
- "Female",
- "Male",
- "Adult",
- "Middle Aged",
- "Diabetic Foot",
- "Adolescent",
- "Young Adult",
- "Healthcare Disparities",
- "Aged",
- "White People",
- "Physical Examination",
- "Surveys and Questionnaires",
- "Diabetes Mellitus",
- "Black People",
- "Prevalence"
- ]
- },
- {
- "PMID": "39463434",
- "Title": "Scientific reports",
- "ArticleTitle": "Cystic fibrosis-related diabetes is associated with reduced islet protein expression of GLP-1 receptor and perturbation of cell-specific transcriptional programs.",
- "Abstract": "Insulin secretion is impaired in individuals with cystic fibrosis (CF), contributing to high rates of CF-related diabetes (CFRD) and substantially increasing disease burden. To develop improved therapies for CFRD, better knowledge of pancreatic pathology in CF is needed. Glucagon like peptide-1 (GLP-1) from islet \u03b1 cells potentiates insulin secretion by binding GLP-1 receptors (GLP-1Rs) on \u03b2 cells. We determined whether expression of GLP-1 and/or its signaling components are reduced in CFRD, thereby contributing to impaired insulin secretion. Immunohistochemistry of pancreas from humans with CFRD versus no-CF/no-diabetes revealed no difference in GLP-1 immunoreactivity per islet area, whereas GLP-1R immunoreactivity per islet area or per insulin-positive islet area was reduced in CFRD. Using spatial transcriptomics, we observed several differentially expressed \u03b1- and/or \u03b2-cell genes between CFRD and control pancreas. In CFRD, we found upregulation of \u03b1-cell PCSK1 which encodes the enzyme (PC1/3) that generates GLP-1, and downregulation of \u03b1-cell PCSK1N which inhibits PC1/3. Gene set enrichment analysis also revealed \u03b1 and \u03b2 cell-specific pathway dysregulation in CFRD. Together, our data suggest intra-islet GLP-1 is not limiting in CFRD, but its action may be restricted due to reduced GLP-1R protein levels. Thus, restoring \u03b2-cell GLP-1R protein expression may improve \u03b2-cell function in CFRD.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Cystic Fibrosis",
- "Glucagon-Like Peptide-1 Receptor",
- "Male",
- "Female",
- "Adult",
- "Diabetes Mellitus",
- "Insulin-Secreting Cells",
- "Islets of Langerhans",
- "Glucagon-Secreting Cells",
- "Glucagon-Like Peptide 1",
- "Young Adult",
- "Gene Expression Regulation",
- "Adolescent",
- "Insulin"
- ]
- },
- {
- "PMID": "39462457",
- "Title": "International journal of circumpolar health",
- "ArticleTitle": "Substance use and lifestyle risk factors for somatic disorders among psychiatric patients in Greenland.",
- "Abstract": "Patients with psychotic disorders exhibit elevated mortality and morbidity rates compared to the general population primarily due to comorbid somatic diseases. This study aims to describe the prevalence of selected risk factors and somatic disorders among psychiatric patients with a diagnosis of psychotic disorder. Material and methods: Data were retrieved from Greenland's nationwide electronic medical record. The study population consists of 104 patients diagnosed with a psychotic disorder, encompassing schizophrenia or schizotypal and delusional disorders, residing in Nuuk. The study population comprised 104 patients (68 males and 36 females) with a mean age of 40\u2009years. More than 80% were daily smokers, and 68% had harmful use of cannabis. More than half had dyslipidemia (any imbalance in lipids), while over a quarter were classified as obese with body mass index of 30\u2009kg/m2 or higher. Eighteen percent had hypertension, and six percent suffered from diabetes. This study revealed a notable prevalence of risk factors for somatic diseases, particularly smoking and cannabis use among patients with schizophrenia in Nuuk, indicating that a high prevalence of somatic diseases might be expected as the population gets older and the risk of developing somatic diseases becomes greater. Increased focus on monitoring and preventing those as part of the health care is recommended.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Greenland",
- "Male",
- "Female",
- "Adult",
- "Risk Factors",
- "Middle Aged",
- "Substance-Related Disorders",
- "Prevalence",
- "Psychotic Disorders",
- "Schizophrenia",
- "Life Style",
- "Smoking",
- "Young Adult",
- "Comorbidity",
- "Obesity",
- "Dyslipidemias",
- "Diabetes Mellitus",
- "Hypertension",
- "Arctic Regions",
- "Aged"
- ]
- },
- {
- "PMID": "39461240",
- "Title": "International immunopharmacology",
- "ArticleTitle": "Natural polysaccharides: The potential biomacromolecules for treating diabetes and its complications via AGEs-RAGE-oxidative stress axis.",
- "Abstract": "Diabetes mellitus, a chronic metabolic disorder, poses a significantly public health challenge. Extensive research highlights that contemporary dietary patterns, characterized by excessive intake of sugar, fat, and protein, are major contributors to the onset and progression of diabetes. The central element to this process is the aberrant activation of the advanced glycation end products (AGEs) - receptor for AGEs (RAGE) - oxidative stress axis, which plays a pivotal role in disrupting normal carbohydrate metabolism. This pathway presents a critical target for developing interventions aimed at mitigating diabetes and its complications. In recent years, natural polysaccharides have emerged as promising agents in the prevention and treatment of diabetes, due to their ability to inhibit AGE formation, regulate RAGE expression, and modulate the AGEs-RAGE-oxidative stress axis. In this paper, we explore the pathogenic mechanism of this axis and review the therapeutic potential of natural polysaccharides in managing diabetes and its complications. Our goal is to provide new insights for the effective management of diabetes and its associated health challenges.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Oxidative Stress",
- "Polysaccharides",
- "Animals",
- "Receptor for Advanced Glycation End Products",
- "Glycation End Products, Advanced",
- "Diabetes Mellitus",
- "Diabetes Complications",
- "Hypoglycemic Agents",
- "Biological Products",
- "Signal Transduction"
- ]
- },
- {
- "PMID": "39461229",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "Prevalence and clinical implications of diabetes mellitus in autoimmune nodopathies: A systematic review.",
- "Abstract": "DM patients fall under the typical clinical phenotype of autoimmune nodopathy, displaying predominantly paranodal antibodies. Early suspicion is crucial, as unlike DPN, diagnosis of autoimmune nodopathy unfolds therapeutic perspectives.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Prevalence",
- "Autoantibodies",
- "Diabetic Neuropathies",
- "Diabetes Mellitus",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39460855",
- "Title": "Investigational new drugs",
- "ArticleTitle": "A phase II study of ME2136 (Asenapine Maleate) plus standard antiemetic therapy for patients, including diabetic patients, receiving cisplatin-based chemotherapy.",
- "Abstract": "Olanzapine combined with the neurokinin-1 receptor antagonist, palonosetron and dexamethasone is the standard treatment for chemotherapy-induced nausea and vomiting (CINV) due to highly emetogenic chemotherapy (HEC). However, the use of olanzapine poses challenges in patients with diabetes mellitus (DM) due to the potential risk of hyperglycemia. ME2136, antipsychotic similar to olanzapine, is associated with a lower risk of hyperglycemia. This study investigated the antiemetic efficacy and safety of ME2136 for HEC. This single-arm phase 2 study examined the safety and efficacy of ME2136 5\u00a0mg for 4\u00a0days in combination with triplet-combination antiemetic therapy. Two cohorts were established for the safety assessment: DM and non-DM. Eligible patients had malignant tumors and were receiving cisplatin-based chemotherapy for the first time. The primary endpoint was the complete response (CR) rate, defined as the percentage of patients without vomiting and not requiring rescue medications in the delayed phase (24-120\u00a0h). Between December 2020 and January 2022, 40 patients were enrolled, with 20 in each cohort. All patients were included in the safety analysis and 35 in the efficacy analysis. The CR rate in the delayed phase was 71.4% [60% CI 63.1-78.6%] for all patients, 66.7% in the DM cohort, and 76.5% in the non-DM cohort. No treatment-related adverse events\u2009\u2265\u2009grade 3, including hyperglycemia, were reported. ME2136, when combined with standard triplet-combination antiemetic therapy, is expected to exert similar antiemetic effects to the standard treatment for CINV due to HEC. Currently, ME2136-02 trial is underway to examine the safety and efficacy of triplet-combination antiemetic therapy and a 5-day treatment with ME2136. This study was registered with the Japan Registry of Clinical Trials (jRCT2041200071) on 10 December 2020. Clinical trial registration: This study was registered with the Japan Registry of Clinical Trials (jRCT2041200071) on 10 December 2020.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Antiemetics",
- "Male",
- "Middle Aged",
- "Female",
- "Cisplatin",
- "Aged",
- "Vomiting",
- "Nausea",
- "Dibenzocycloheptenes",
- "Adult",
- "Dexamethasone",
- "Diabetes Mellitus",
- "Neoplasms",
- "Drug Therapy, Combination",
- "Antineoplastic Combined Chemotherapy Protocols",
- "Palonosetron"
- ]
- },
- {
- "PMID": "39460797",
- "Title": "Molecular biology reports",
- "ArticleTitle": "Molecular remodeling in comorbidities associated with heart failure: a current update.",
- "Abstract": "Recent advances in genomics and proteomics have helped in understanding the molecular mechanisms and pathways of comorbidities and heart failure. In this narrative review, we reviewed molecular alterations in common comorbidities associated with heart failure such as obesity, diabetes mellitus, systemic hypertension, pulmonary hypertension, coronary artery disease, hypercholesteremia and lipoprotein abnormalities, chronic kidney disease, and atrial fibrillation. We searched the electronic databases, PubMed, Ovid, EMBASE, Google Scholar, CINAHL, and PhysioNet for articles without time restriction. Although the association between comorbidities and heart failure is already well established, recent studies have explored the molecular pathways in much detail. These molecular pathways demonstrate how novels drugs for heart failure works with respect to the pathways associated with comorbidities. Understanding the altered molecular milieu in heart failure and associated comorbidities could help to develop newer medications and targeted therapies that incorporate these molecular alterations as well as key molecular variations across individuals to improve therapeutic outcomes. The molecular alterations described in this study could be targeted for novel and personalized therapeutic approaches in the future. This knowledge is also critical for developing precision medicine strategies to improve the outcomes for patients living with these conditions.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Heart Failure",
- "Comorbidity",
- "Obesity",
- "Hypertension",
- "Diabetes Mellitus",
- "Renal Insufficiency, Chronic",
- "Atrial Fibrillation"
- ]
- },
- {
- "PMID": "39460639",
- "Title": "Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery",
- "ArticleTitle": "The Effects of Metformin on Cisplatin-Induced Ototoxicity in Diabetic Patients.",
- "Abstract": "Contrary to expectations from preclinical data, metformin did not reduce the incidence of hearing loss in patients receiving cisplatin and may, in fact, be associated with an increased risk.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Cisplatin",
- "Metformin",
- "Male",
- "Retrospective Studies",
- "Female",
- "Middle Aged",
- "Ototoxicity",
- "Antineoplastic Agents",
- "Case-Control Studies",
- "Aged",
- "Hypoglycemic Agents",
- "Hearing Loss",
- "Diabetes Mellitus",
- "Adult"
- ]
- },
- {
- "PMID": "39459480",
- "Title": "Medicina (Kaunas, Lithuania)",
- "ArticleTitle": "Associations between Systemic and Dental Diseases in Elderly Korean Population.",
- "Abstract": {
- "i": "Conclusions"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Aged",
- "Republic of Korea",
- "Male",
- "Female",
- "Aged, 80 and over",
- "Prevalence",
- "Arthritis, Rheumatoid",
- "Osteoporosis",
- "Hypertension",
- "Periodontal Diseases",
- "Diabetes Mellitus",
- "Stomatognathic Diseases",
- "Tooth Loss"
- ]
- },
- {
- "PMID": "39458437",
- "Title": "Nutrients",
- "ArticleTitle": "Diet Quality and Eating Frequency Were Associated with Insulin-Taking Status among Adults.",
- "Abstract": "Evidence of the low diet quality and eating frequency of insulin takers may help inform and justify nutrition education to control and manage diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Adult",
- "Middle Aged",
- "Male",
- "Female",
- "Cross-Sectional Studies",
- "Insulin",
- "Feeding Behavior",
- "Young Adult",
- "Adolescent",
- "Diet, Healthy",
- "Diet",
- "Aged",
- "Pilot Projects",
- "Indiana",
- "Diabetes Mellitus",
- "Surveys and Questionnaires"
- ]
- },
- {
- "PMID": "39455937",
- "Title": "BMC nephrology",
- "ArticleTitle": "Efficacy of continuous glucose monitoring in people living with diabetes and end stage kidney disease on dialysis: a systematic review.",
- "Abstract": "PROSPERO registration number: CRD42023371635, https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=371635 .",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Kidney Failure, Chronic",
- "Renal Dialysis",
- "Blood Glucose Self-Monitoring",
- "Blood Glucose",
- "Treatment Outcome",
- "Diabetic Nephropathies",
- "Hypoglycemia",
- "Glycated Hemoglobin",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39455403",
- "Title": "Revista de gastroenterologia de Mexico (English)",
- "ArticleTitle": "Gastrointestinal adverse effects of old and new antidiabetics: How do we deal with them in real life?",
- "Abstract": "Diabetes is a public health problem with an estimated worldwide prevalence of 10% and a prevalence of 12% in Mexico. The costs resulting from this chronic-degenerative disease are significant. Treatment for diabetes involves different medication groups, some of which can cause significant gastrointestinal adverse effects, such as dyspepsia, nausea, vomiting, bloating, diarrhea, and constipation. The medications most frequently associated with said adverse effects are metformin, acarbose, and GLP-1 agonists. Gastrointestinal adverse effects negatively impact the quality of life and management of patients with diabetes. The factors of visceral neuropathy, acute dysglycemia, dysbiosis, and intestinal bacterial overgrowth contribute to the gastrointestinal symptoms in patients with diabetes, making it necessary to consider multiple etiologic factors in the presence of gastrointestinal symptoms, and not exclusively attribute them to the use of antidiabetics. Personalized treatment, considering gastrointestinal comorbidity and the type of drug utilized, is essential for mitigating the adverse effects and improving the quality of life in patients with diabetes. The aim of the present narrative review was to describe the gastrointestinal adverse effects of the antidiabetic drugs, their pathophysiologic mechanisms, and the corresponding therapeutic measures.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus",
- "Gastrointestinal Diseases",
- "Hypoglycemic Agents",
- "Quality of Life"
- ]
- },
- {
- "PMID": "39455264",
- "Title": "Journal of the American Board of Family Medicine : JABFM",
- "ArticleTitle": "Impact of Point of Care Hemoglobin A1c Testing on Time to Therapeutic Intervention.",
- "Abstract": "Without compromising accuracy, point of care testing (POCT) provides immediate results at the time of in person patient consultation. The purpose of this study was to evaluate time until therapeutic intervention with POCT HbA1c versus venipuncture, where venipuncture was considered standard of care.The primary outcome was time (hours) to implementation of a therapeutic intervention based on POCT HbA1c result, as compared with most recent venipuncture HbA1c before the study and its associated therapeutic intervention. A total of 94 POCT HbA1c tests were included in the primary analysis.For the POCT HbA1c, the mean time to therapeutic intervention was 1.6\u2009\u00b1\u20093.14\u2009hours. For the previous venipuncture HbA1c, the mean time to therapeutic intervention was 1376.66\u2009\u00b1\u20093356.6\u2009hours (",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Glycated Hemoglobin",
- "Female",
- "Point-of-Care Testing",
- "Male",
- "Middle Aged",
- "Phlebotomy",
- "Time Factors",
- "Point-of-Care Systems",
- "Primary Health Care",
- "Aged",
- "Adult",
- "Time-to-Treatment",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39454827",
- "Title": "Molecular metabolism",
- "ArticleTitle": "PET imaging of sodium-glucose cotransporters (SGLTs): Unveiling metabolic dynamics in diabetes and oncology.",
- "Abstract": "SGLT-targeted PET imaging offers promising improvements in diagnostic accuracy and therapeutic planning. The findings underscore the physiological and pathological significance of SGLTs, indicating that this imaging approach could shape future diagnostic and therapeutic strategies in metabolic and oncologic fields.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Humans",
- "Diabetes Mellitus",
- "Fluorodeoxyglucose F18",
- "Glucose",
- "Neoplasms",
- "Positron-Emission Tomography",
- "Radiopharmaceuticals",
- "Sodium-Glucose Transport Proteins"
- ]
- },
- {
- "PMID": "39454697",
- "Title": "The American journal of cardiology",
- "ArticleTitle": "Impact of Diabetes Mellitus on Bifurcation Percutaneous Coronary Intervention: Insights from the Prospective Global Registry for the Study of Bifurcation Lesion Interventions Registry.",
- "Abstract": "The impact of diabetes mellitus (DM) on the outcomes of bifurcation percutaneous coronary intervention (PCI) has received limited study. We compared the procedural characteristics and outcomes of patients with and without DM in 1,302 bifurcation PCIs (1,147 patients) performed at 5 centers between 2013 and 2024. The prevalence of DM was 33.8% (n = 388). Patients with diabetes were younger and had more cardiovascular risk factors and greater angiographic complexity, including more main vessel calcification and more frequent stenoses in the left main, proximal left anterior descending, and right coronary artery. There was no difference in technical (95.5% vs 94.9%, p = 0.613) or procedural success (90.2% vs 91.3%, p = 0.540); provisional stenting was used less frequently in patients with diabetes (64.5% vs 71.1%, p = 0.015). Patients with diabetes had higher rates of repeat in-hospital PCI and acute kidney injury. Other in-hospital outcomes were similar after adjusting for confounders. During a median follow-up of 1,095 days, diabetes was independently associated with greater incidence of major adverse cardiovascular events (hazard ratio [HR] 2.04, 95% confidence intervals [CI] 1.52 to 2.72, p <0.001), myocardial infarction (HR 1.94, 95% CI 1.05 to 3.25, p = 0.033), death (HR 2.26, 95% CI 1.46 to 3.51, p <0.001), and target (HR 1.6, 95% CI 1.01 to 2.66, p = 0.045) and nontarget (HR 2.00, CI 1.06 to 3.78, p = 0.032) vessel revascularization. Patients with DM who underwent bifurcation PCI had greater risk of in-hospital repeat-PCI and major adverse cardiac events during follow-up than did those without diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Percutaneous Coronary Intervention",
- "Male",
- "Female",
- "Registries",
- "Middle Aged",
- "Prospective Studies",
- "Aged",
- "Diabetes Mellitus",
- "Coronary Angiography",
- "Coronary Artery Disease",
- "Risk Factors",
- "Treatment Outcome",
- "Follow-Up Studies",
- "Incidence",
- "Drug-Eluting Stents"
- ]
- },
- {
- "PMID": "39453822",
- "Title": "Diabetes care",
- "ArticleTitle": "Relationship of Plasma Apolipoprotein C-I Truncation With Risk of Diabetes in the Multi-Ethnic Study of Atherosclerosis and the Actos Now for the Prevention of Diabetes Study.",
- "Abstract": "Our results indicate that apoC-I truncation may contribute to changes in glucose levels, IR, and risk of diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Aged",
- "Atherosclerosis",
- "Apolipoprotein C-I",
- "Insulin Resistance",
- "Diabetes Mellitus",
- "Blood Glucose",
- "Glucose Tolerance Test",
- "Prediabetic State",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39453429",
- "Title": "American journal of physiology. Heart and circulatory physiology",
- "ArticleTitle": "Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.",
- "Abstract": "Diabetes mellitus (DM) is characterized by chronic hyperglycemia, and despite intensive glycemic control, the risk of heart failure in patients with diabetes remains high. Diabetes-induced heart failure (DHF) presents a unique metabolic challenge, driven by significant alterations in cardiac substrate metabolism, including increased reliance on fatty acid oxidation, reduced glucose utilization, and impaired mitochondrial function. These metabolic alterations lead to oxidative stress, lipotoxicity, and energy deficits, contributing to the progression of heart failure. Emerging research has identified novel mechanisms involved in the metabolic remodeling of diabetic hearts, such as autophagy dysregulation, epigenetic modifications, polyamine regulation, and branched-chain amino acid (BCAA) metabolism. These processes exacerbate mitochondrial dysfunction and metabolic inflexibility, further impairing cardiac function. Therapeutic interventions targeting these pathways-such as enhancing glucose oxidation, modulating fatty acid metabolism, and optimizing ketone body utilization-show promise in restoring metabolic homeostasis and improving cardiac outcomes. This review explores the key molecular mechanisms driving metabolic remodeling in diabetic hearts, highlights advanced methodologies, and presents the latest therapeutic strategies for mitigating the progression of DHF. Understanding these emerging pathways offers new opportunities to develop targeted therapies that address the root metabolic causes of heart failure in diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Heart Failure",
- "Animals",
- "Energy Metabolism",
- "Diabetic Cardiomyopathies",
- "Mitochondria, Heart",
- "Oxidative Stress",
- "Autophagy",
- "Epigenesis, Genetic",
- "Myocardium",
- "Diabetes Mellitus",
- "Fatty Acids"
- ]
- },
- {
- "PMID": "39452893",
- "Title": "Diabetes care",
- "ArticleTitle": "Consensus Considerations and Good Practice Points for Use of Continuous Glucose Monitoring Systems in Hospital Settings.",
- "Abstract": "Continuous glucose monitoring (CGM) systems provide frequent glucose measurements in interstitial fluid and have been used widely in ambulatory settings for diabetes management. During the coronavirus disease 2019 (COVID-19) pandemic, regulators in the U.S. and Canada temporarily allowed for CGM systems to be used in hospitals with the aim of reducing health care professional COVID-19 exposure and limiting use of personal protective equipment. As such, studies on hospital CGM system use have been possible. With improved sensor accuracy, there is increased interest in CGM usage for diabetes management in hospitals. Laboratorians and health care professionals must determine how to integrate CGM usage into practice. The aim of this consensus guidance document is to provide an update on the application of CGM systems in hospital, with insights and opinions from laboratory medicine, endocrinology, and nursing.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Consensus",
- "Blood Glucose",
- "Pandemics",
- "SARS-CoV-2",
- "Blood Glucose Self-Monitoring",
- "Hospitals",
- "Diabetes Mellitus",
- "Coronavirus Infections",
- "Pneumonia, Viral",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39451699",
- "Title": "Biosensors",
- "ArticleTitle": "Noninvasive Monitoring of Glycemia Level in Diabetic Patients by Wearable Advanced Biosensors.",
- "Abstract": "We report on the possibility of noninvasive diabetes monitoring through continuous analysis of sweat. The prediction of the blood glucose level in diabetic patients is possible on the basis of their sweat glucose content due to the positive correlation discovered. The ratio between the blood glucose and sweat glucose concentrations for a certain diabetic subject is stable within weeks, excluding requirements for frequent blood probing. The glucose variations in sweat display allometric (non-linear) dependence on those in blood, allowing more precise blood glucose estimation. Selective (avoiding false-positive responses) and sensitive (sweat glucose is on average 30-50 times lower) detection is possible with biosensors based on the glucose oxidase enzyme coupled with a Prussian Blue transducer. Reliable glucose detection in just secreted sweat would allow noninvasive monitoring of the glycemia level in diabetic patients.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Biosensing Techniques",
- "Wearable Electronic Devices",
- "Blood Glucose",
- "Diabetes Mellitus",
- "Glucose Oxidase",
- "Sweat",
- "Blood Glucose Self-Monitoring",
- "Monitoring, Physiologic"
- ]
- },
- {
- "PMID": "39450816",
- "Title": "Revista medica de Chile",
- "ArticleTitle": "[Characteristics of Depressed Individuals with Hypertension and/ or Diabetes Mellitus in Primary Health Care in Santiago de Chile].",
- "Abstract": "These are people with depressive episode, hypertension and/or diabetes who, having a personal and family history of depression, are not receiving pharmacological treatment for depression, which probably affects their quality of life. Better adherence to clinical guidelines for the treatment of depression is required.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Primary Health Care",
- "Hypertension",
- "Chile",
- "Middle Aged",
- "Adult",
- "Diabetes Mellitus",
- "Depression",
- "Aged",
- "Comorbidity",
- "Antidepressive Agents",
- "Socioeconomic Factors"
- ]
- },
- {
- "PMID": "39450814",
- "Title": "Revista medica de Chile",
- "ArticleTitle": "[Decline in Renal Function with Age in Chile: Gender Differences and the Impact of Comorbidities].",
- "Abstract": "eGFR progressively decreased with age in the Chilean population, showing an early decline starting from 18 years, more pronounced in women, and in the presence of chronic diseases. Our findings provide relevant population-based information for interpreting eGFR across different age groups and risk categories.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Chile",
- "Female",
- "Male",
- "Cross-Sectional Studies",
- "Middle Aged",
- "Glomerular Filtration Rate",
- "Adult",
- "Sex Factors",
- "Age Factors",
- "Aged",
- "Young Adult",
- "Adolescent",
- "Comorbidity",
- "Renal Insufficiency, Chronic",
- "Creatinine",
- "Hypertension",
- "Risk Factors",
- "Sex Distribution",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39448967",
- "Title": "BMC public health",
- "ArticleTitle": "Longitudinal assessment of the impact of prevalent diabetes on hospital admissions and mortality in the general population: a prospective population-based study with 19 years of follow-up.",
- "Abstract": "Source: Pixabay.com. No permission or acknowledgement is required.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Middle Aged",
- "Male",
- "Female",
- "Adult",
- "Hospitalization",
- "Prospective Studies",
- "Sweden",
- "Aged",
- "Diabetes Mellitus",
- "Follow-Up Studies",
- "Prevalence",
- "Longitudinal Studies",
- "Registries"
- ]
- },
- {
- "PMID": "39448732",
- "Title": "Scientific reports",
- "ArticleTitle": "International dietary quality index and its association with diabetes in RaNCD cohort study.",
- "Abstract": "Diabetes and its complications pose a significant threat to global health. Various factors contribute to the development of diabetes, with diet being an important trigger. The Dietary Quality Index-International (DQI-I) serves as an indicator of changes in diet and its association with chronic diseases, including diabetes. The aim of this study is to examine the association between DQI-I and diabetes in adults. Data from the first phase of the Ravansar Non-Communicable Disease Cohort Study (RaNCD) were used for this cross-sectional study. The study included individuals from western Iran aged between 35 and 65 years. The DQI-I was used to assess diet quality and the essential aspects of a healthy diet. Multiple logistic regression analyses were performed to compare DQI-I total score and diabetes. A total of 7,079 individuals were included, including 608 diabetic and 6,471 healthy individuals. The mean DQI-I score was 60.51\u2009\u00b1\u20098.47 in healthy individuals and 63.12\u2009\u00b1\u20098.64 in diabetics. The odds of developing diabetes were higher in individuals with a higher DQI-I (adjusted odds ratio: 1.49, 95% CI: 1.30-1.73). The variety was 13.43\u2009\u00b1\u20094.47 in diabetics and 12.59\u2009\u00b1\u20094.79 in healthy individuals. Adequacy was 33.23\u2009\u00b1\u20093.71 in diabetics and 33.79\u2009\u00b1\u20093.37 in healthy individuals. Moderation was 13.27\u2009\u00b1\u20096.05 in diabetics and 11.79\u2009\u00b1\u20095.47 in healthy individuals. The overall balance was 2.88\u2009\u00b1\u20092.21 in the healthy group and 2.61\u2009\u00b1\u20092.13 in the diabetics. The macronutrient ratio was 2.15\u2009\u00b1\u20091.88 in the healthy group and 2.04\u2009\u00b1\u20091.84 in the diabetics. The fatty acid ratio was 0.72\u2009\u00b1\u20091.29 in the healthy group and 0.56\u2009\u00b1\u20091.17 in the diabetic group. The overall balance score was higher in the healthy subjects. The DQI-I total score was higher in diabetics, indicating a positive association between diabetes and the DQI-I. Therefore, the importance of continuous dietary management and education of diabetic patients should be emphasized.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Middle Aged",
- "Male",
- "Female",
- "Adult",
- "Cross-Sectional Studies",
- "Iran",
- "Aged",
- "Diabetes Mellitus",
- "Cohort Studies",
- "Diet",
- "Diet, Healthy"
- ]
- },
- {
- "PMID": "39448700",
- "Title": "Scientific reports",
- "ArticleTitle": "Impaired glomerular filtration rate and associated factors among diabetic mellitus patients with hypertension in referral hospitals, Amhara Regional State, Ethiopia.",
- "Abstract": "Impaired glomerular filtration rate is common health problem in diabetic mellitus patients (DM) with hypertension (HTN). It is a major cause of morbidity, mortality, and poor quality of life. There is limited data on the prevalence and associated factors of impaired glomerular filtration among diabetic mellitus patients with hypertension in Ethiopia. Therefore, this study aimed to determine the prevalence of impaired glomerular filtration rate and associated factors among diabetic patients with hypertension in referral hospitals in Amhara Regional State, Ethiopia, 2020. An institution-based cross-sectional study was conducted in Amhara Regional referral hospitals from February 20 to April 30, 2020. Systemic sampling techniques were used to select diabetic mellitus patients with hypertension. Epi data version 3.0 was used to enter the coded data and then exported to STATA 14 for analysis. Glomerular filtration rate was estimated using the equations of collaboration with chronic kidney disease (CKD-EPI), diet modification in renal disease (MDRD-4), and creatinine clearance (CrCl). In bi-variable logistic regression, variables with a p-value of <\u20090.25 were included in multi-variable logistic regression. Using a 95% confidence interval, variables having a p-value\u2009\u2264\u20090.05 in multi-variable logistic regression were declared as statistically significant variables. In this study, a total of 326 study participants were involved, with a 100% response rate. The prevalence of an impaired glomerular filtration rate among diabetic patients with hypertension was 30.1% (95% CI 25.1%-35.1%), 36.6% (95% CI 30.1%-40.8%) and 45.4% (95% CI 39.9%-50.8%), using the equations CKD-EPI, MDRD-4, and CrCl, respectively. Being \u2265\u200955 years old (CKD-EPI AOR\u2009=\u20092.9, 95%: 1.5-5.5, MDRD-4 AOR\u2009=\u20092.1, 95% CI: 1.2-3.7, CrCl AOR\u2009=\u20095.9, 95% CI: 3.5-10.1), proteinuria (CKD-EPI AOR\u2009=\u20092.7, 95% CI: 1.4-5.3, MDRD-4 AOR\u2009=\u20091.9, 95% CI: 1.1-3.4, CrCl AOR\u2009=\u20091.7, 95% CI: 1.0-2.9), duration of the disease (\u2265\u20095 years) (CKD-EPI AOR\u2009=\u20097.9, 95% CI: 4.2-13.0, MDRD-4 AOR\u2009=\u20097.4, 95% CI: 4.2-13.0, CrCl AOR\u2009=\u20091.9, 95% CI: 1.2-3.3), a glucose level of \u2265\u2009150\u00a0mg/dl (CKD-EPI AOR\u2009=\u20092.3, 95% CI: 1.3-4.4, MDRD-4 AOR\u2009=\u20092.1, 95% CI: 1.2-3.8) were variables significantly associated with impaired glomerular filtration rate. The prevalence of impaired glomerular filtration rate among diabetic mellitus patients with hypertension was high. Independent predictors of impaired glomerular filtration rate were older age, duration of the disease, proteinuria, and higher blood glucose levels.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Ethiopia",
- "Male",
- "Glomerular Filtration Rate",
- "Female",
- "Middle Aged",
- "Hypertension",
- "Cross-Sectional Studies",
- "Adult",
- "Prevalence",
- "Risk Factors",
- "Aged",
- "Referral and Consultation",
- "Diabetes Mellitus",
- "Renal Insufficiency, Chronic",
- "Creatinine"
- ]
- },
- {
- "PMID": "39447788",
- "Title": "International journal of biological macromolecules",
- "ArticleTitle": "Natural polymer nanofiber dressings for effective management of chronic diabetic wounds: A comprehensive review.",
- "Abstract": "Diabetic wounds present a chronic challenge in effective treatment. Natural polymer nanofiber dressings have emerged as a promising solution due to their impressive biocompatibility, biodegradability, safety, high specific surface area, and resemblance to the extracellular matrix. These qualities make them ideal materials with excellent biological properties and cost-effectiveness. Additionally, they can effectively deliver therapeutic agents, enabling diverse treatment effects. This review offers a comprehensive overview of natural polymer-based nanofibers in diabetic wound dressings. It examines the characteristics and challenges associated with diabetic wounds and the role of natural polymers in facilitating wound healing. The review highlights the preparation, mechanism, and applications of various functional dressings composed of natural polymer nanofibers. Furthermore, it addresses the main challenges and future directions in utilizing natural polymer nanofibers for diabetic wound treatment, providing valuable insights into effective wound management for diabetic patients.",
- "Predictions": [],
- "MeshTerms": [
- "Nanofibers",
- "Humans",
- "Wound Healing",
- "Bandages",
- "Polymers",
- "Animals",
- "Diabetes Mellitus",
- "Chronic Disease"
- ]
- },
- {
- "PMID": "39447680",
- "Title": "Diabetes research and clinical practice",
- "ArticleTitle": "Salivary glycated albumin could be as reliable a marker of glycemic control as blood glycated albumin in people with diabetes.",
- "Abstract": "This exploratory research revealed that the salivary GA levels by this method were accurate and might be able to replace blood GA measurement. The home salivary GA measurement is expected to be developed that may reduce the burden and complications in people with diabetes mellitus and improve the quality of life.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Glycation End Products, Advanced",
- "Saliva",
- "Male",
- "Glycated Serum Albumin",
- "Female",
- "Middle Aged",
- "Biomarkers",
- "Serum Albumin",
- "Aged",
- "Glycated Hemoglobin",
- "Blood Glucose",
- "Glycemic Control",
- "Diabetes Mellitus",
- "Chromatography, High Pressure Liquid",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39446913",
- "Title": "PloS one",
- "ArticleTitle": "Accuracy of ankle-brachial index in screening for peripheral arterial disease in people with diabetes.",
- "Abstract": "Although the ankle-brachial index (ABI) presents overall satisfactory accuracy, its sensitivity in the context of screening strategies does not ensure the detection of all individuals with peripheral arterial disease (PAD), especially in clinical situations where there is calcification of the arterial media layer. This study evaluated the accuracy of ABI in screening PAD among individuals with diabetes mellitus (DM) in a community setting. An observational study included only individuals with DM. ABI measurement was performed, and the lower limb duplex ultrasound (DU) was used as the reference standard for PAD diagnosis. Sensitivity, specificity, positive and negative predictive values (PPV and NPV), and positive and negative likelihood ratios (LR+ and LR-) of ABI were assessed. The analysis included 194 limbs from 99 participants, with a PAD prevalence identified by DU of 15.98%. ABI demonstrated an accuracy of 87.63%, with a sensitivity of 35.48%, specificity of 97.55%, PPV of 73.33%, NPV of 89.83%, LR+ of 14.46, and LR- of 0.66. ABI showed high specificity but limited sensitivity in detecting PAD among individuals with DM in a community setting. An LR- of 0.66 suggests that a normal ABI result reduces but does not eliminate the possibility of PAD, highlighting the importance of complementary diagnostic approaches to enhance accuracy in identifying PAD in high-risk patients, such as those with DM. Incorporating additional diagnostic methods may be necessary to improve the effectiveness of PAD screening in this group.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Ankle Brachial Index",
- "Peripheral Arterial Disease",
- "Male",
- "Female",
- "Aged",
- "Middle Aged",
- "Mass Screening",
- "Sensitivity and Specificity",
- "Diabetes Mellitus",
- "Aged, 80 and over"
- ]
- },
- {
- "PMID": "39446189",
- "Title": "International journal of implant dentistry",
- "ArticleTitle": "Correlation between marginal bone loss around dental implants and various systemic diseases: a cross-sectional study.",
- "Abstract": "Within the limitations of the present investigation, patients diagnosed with hyperlipidemia and hypertension were more likely to exhibit MBL surrounding dental implants.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Dental Implants",
- "Middle Aged",
- "Cross-Sectional Studies",
- "Male",
- "Female",
- "Alveolar Bone Loss",
- "Hyperlipidemias",
- "Hypertension",
- "Aged",
- "Adult",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39445809",
- "Title": "Cancer medicine",
- "ArticleTitle": "The association of diabetes mellitus and routinely collected patient-reported outcomes in patients with cancer. A real-world cohort study.",
- "Abstract": "The results of this study suggest that patients with cancer and diabetes may be at greater risk for anxiety, depression, fatigue, higher pain interference, and reduced physical function. Strengthening diabetes management is imperative to address the negative impact of diabetes on PROs. In particular, this may be true for patients with skin, breast, prostate, and kidney cancer.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Middle Aged",
- "Patient Reported Outcome Measures",
- "Neoplasms",
- "Diabetes Mellitus",
- "Aged",
- "Anxiety",
- "Depression",
- "Fatigue",
- "Cohort Studies",
- "Registries",
- "Surveys and Questionnaires",
- "Adult",
- "Quality of Life"
- ]
- },
- {
- "PMID": "39445800",
- "Title": "Journal of diabetes investigation",
- "ArticleTitle": "Association of impaired fasting glucose with cardiometabolic multimorbidity: The\u00a0Kailuan study.",
- "Abstract": "IFG was a risk factor for CMM. The effect of IFG on diabetes mellitus was stronger than that on other cardiometabolic diseases. The effects of IFG for CMM differed by sex.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Multimorbidity",
- "Blood Glucose",
- "Middle Aged",
- "Fasting",
- "China",
- "Adult",
- "Cardiovascular Diseases",
- "Diabetes Mellitus",
- "Follow-Up Studies",
- "Aged",
- "Risk Factors",
- "Proportional Hazards Models",
- "Glucose Intolerance"
- ]
- },
- {
- "PMID": "39444992",
- "Title": "Middle East African journal of ophthalmology",
- "ArticleTitle": "Status of Health-care Systems for Diabetes Mellitus and Diabetic Retinopathy in Jordan: Stakeholders and Health-care Providers Survey.",
- "Abstract": "Advanced DM and DR care is not accessible to most people. Programmatic efforts from the government and NGOs must formulate a national action plan to reduce the human and financial impact of the disease in Jordan.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Jordan",
- "Diabetic Retinopathy",
- "Male",
- "Surveys and Questionnaires",
- "Diabetes Mellitus",
- "Female",
- "Delivery of Health Care",
- "Health Personnel",
- "Qualitative Research",
- "Health Services Accessibility"
- ]
- },
- {
- "PMID": "39444141",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Graded association of muscle strength with all-cause and cause-specific mortality in older adults with diabetes: Prospective cohort study across 28 countries.",
- "Abstract": "Muscle strength is gradually and inversely associated with all-cause and cause-specific mortality risk in older adults with diabetes. As muscle strength is highly adaptable to resistance training at all ages, the present findings highlight the importance of improving muscle strength in older adults with diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Aged",
- "Male",
- "Female",
- "Prospective Studies",
- "Middle Aged",
- "Europe",
- "Muscle Strength",
- "Hand Strength",
- "Diabetes Mellitus",
- "Cause of Death",
- "Cardiovascular Diseases",
- "Aged, 80 and over",
- "Proportional Hazards Models"
- ]
- },
- {
- "PMID": "39443983",
- "Title": "Cardiovascular diabetology",
- "ArticleTitle": "Impact of diabetes mellitus on right ventricular dysfunction and ventricular interdependence in hypertensive patients with heart failure with reduced ejection fraction assessed via 3.0 T cardiac MRI.",
- "Abstract": "In hypertensive HFrEF patients, comorbid DM may have aggravated RV dysfunction and was an independent determinant of impaired RV strain. RV dysfunction might be directly affected by DM and partially mediated by LV strain through unfavorable ventricular independence.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Stroke Volume",
- "Heart Failure",
- "Ventricular Dysfunction, Right",
- "Hypertension",
- "Aged",
- "Ventricular Function, Right",
- "Ventricular Function, Left",
- "Predictive Value of Tests",
- "Magnetic Resonance Imaging, Cine",
- "Risk Factors",
- "Comorbidity",
- "Diabetes Mellitus",
- "Retrospective Studies",
- "Magnetic Resonance Imaging"
- ]
- },
- {
- "PMID": "39443972",
- "Title": "BMC medicine",
- "ArticleTitle": "Unhealthy plant-based diet is associated with a higher cardiovascular disease risk in patients with prediabetes and diabetes: a large-scale population-based study.",
- "Abstract": "Adherence to an unhealthy plant-based diet is associated with a higher CVD risk in people with prediabetes or diabetes, which may be partially attributed to low consumption of whole grains, high intake of SSB, and high blood cystatin C levels.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Prediabetic State",
- "Cardiovascular Diseases",
- "Male",
- "Female",
- "Middle Aged",
- "Diet, Vegetarian",
- "Aged",
- "Adult",
- "Diabetes Mellitus",
- "United Kingdom",
- "Risk Factors",
- "Diet, Plant-Based"
- ]
- },
- {
- "PMID": "39443848",
- "Title": "BMC primary care",
- "ArticleTitle": "Redesigning telemedicine: preliminary findings from an innovative assisted telemedicine healthcare model.",
- "Abstract": "The 'Digisahayam' model demonstrated feasibility in enhancing healthcare accessibility and quality by bridging healthcare gaps, diagnosing chronic conditions, and improving patient outcomes. The model presents a scalable and sustainable approach to revolutionising patient care and achieving digital health equity, with the potential for adaptation in similar settings worldwide.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Telemedicine",
- "Female",
- "Male",
- "Middle Aged",
- "India",
- "Hypertension",
- "Adult",
- "Diabetes Mellitus",
- "Electronic Health Records",
- "Decision Support Systems, Clinical",
- "Chronic Disease",
- "Delivery of Health Care"
- ]
- },
- {
- "PMID": "39442772",
- "Title": "Annals of epidemiology",
- "ArticleTitle": "\u200eThe association between cumulative exposure to neighborhood walkability (NW) and diabetes risk, a prospective cohort study.",
- "Abstract": "Long-term residence in more walkable neighborhoods may be protective against diabetes in women, especially postmenopausal women.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Walking",
- "Prospective Studies",
- "Middle Aged",
- "Adult",
- "Residence Characteristics",
- "Neighborhood Characteristics",
- "Environment Design",
- "Diabetes Mellitus",
- "Risk Factors",
- "Proportional Hazards Models",
- "Diabetes Mellitus, Type 2",
- "Incidence"
- ]
- },
- {
- "PMID": "39442756",
- "Title": "The Journal of nutrition",
- "ArticleTitle": "Betaine and B",
- "Abstract": "Our findings suggest that higher GSH level and higher intake of betaine, B",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Betaine",
- "Adult",
- "Poland",
- "Female",
- "Male",
- "Methylenetetrahydrofolate Reductase (NADPH2)",
- "Vitamin B 12",
- "Methylenetetrahydrofolate Dehydrogenase (NADP)",
- "Glutathione",
- "Genotype",
- "Phosphatidylethanolamine N-Methyltransferase",
- "Folic Acid",
- "Young Adult",
- "Choline",
- "Minor Histocompatibility Antigens",
- "Diabetes Mellitus",
- "Insulin",
- "Blood Glucose",
- "Methylamines",
- "Polymorphism, Single Nucleotide"
- ]
- },
- {
- "PMID": "39442645",
- "Title": "Brain research",
- "ArticleTitle": "In-depth investigation of the complex pathophysiological mechanisms between diabetes and ischemic stroke through gene expression and regulatory network analysis.",
- "Abstract": "This study explores the intricate relationship between diabetes and ischemic stroke (IS) through gene expression analysis and regulatory network investigation to identify potential biomarkers and therapeutic targets. Using datasets from the Gene Expression Omnibus (GEO) database, differential gene analysis was conducted on GSE43950 (diabetes) and GSE16561 (IS), revealing overlapping differentially expressed genes (DEGs). Functional enrichment analysis, Protein-Protein Interaction (PPI) network construction, and hub gene identification were performed, followed by validation in independent datasets (GSE156035 and GSE58294). The analysis identified 307 upregulated and 156 downregulated overlapping DEGs with significant enrichment in GO and KEGG pathways. Key hub genes (TLR2, TLR4, HDAC1, ITGAM) were identified through a PPI network (257 nodes, 456 interactions), with their roles in immune and inflammatory responses highlighted through GeneMANIA analysis. TRRUST-based transcription factor enrichment analysis revealed regulatory links involving RELA, SPI1, STAT3, and SP1. Differential expression analysis confirmed that RELA and SPI1 were upregulated in diabetes, while SPI1, STAT3, and SP1 were linked to IS. These transcription factors are involved in regulating immunity and inflammation, providing insights into the molecular mechanisms underlying diabetes-IS comorbidity. This bioinformatics-driven approach offers new understanding of the gene interactions and pathways involved, paving the way for potential therapeutic targets.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Gene Regulatory Networks",
- "Ischemic Stroke",
- "Protein Interaction Maps",
- "Diabetes Mellitus",
- "Gene Expression Profiling",
- "Gene Expression"
- ]
- },
- {
- "PMID": "39439869",
- "Title": "Farmaceuticos comunitarios",
- "ArticleTitle": "[Validation of the JH-SEFAC Questionnaire on Knowledge on Insulin Management by Patients with Diabetes in Community Pharmacies].",
- "Abstract": "The JH-SEFAC questionnaire was validated to evaluate the management of insulin injectables, providing community pharmacists with a valuable tool for therapeutic education.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Insulin",
- "Cross-Sectional Studies",
- "Male",
- "Female",
- "Middle Aged",
- "Reproducibility of Results",
- "Surveys and Questionnaires",
- "Health Knowledge, Attitudes, Practice",
- "Adult",
- "Diabetes Mellitus",
- "Hypoglycemic Agents",
- "Pharmacies",
- "Community Pharmacy Services",
- "Pharmacists",
- "Aged",
- "Spain"
- ]
- },
- {
- "PMID": "39439564",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "The emerging modulators of non-coding RNAs in diabetic wound healing.",
- "Abstract": "Diabetic wound healing is a complex physiological process often hindered by the underlying metabolic dysfunctions associated with diabetes. Despite existing treatments, there remains a critical need to explore innovative therapeutic strategies to improve patient outcomes. This article comprehensively examines the roles of non-coding RNAs (ncRNAs), specifically microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), in regulating key phases of the wound healing process: inflammation, angiogenesis, re-epithelialization, and tissue remodeling. Through a deep review of current literature, we discuss recent discoveries of ncRNAs that have been shown to either promote or impair the wound healing process in diabetic wound healing, which were not covered in earlier reviews. This review highlights the specific mechanisms by which these ncRNAs impact cellular behaviors and pathways critical to each healing stage. Our findings indicate that understanding these recently identified ncRNAs provides new insights into their potential roles in diabetic wound healing, thereby contributing valuable knowledge for future research directions in this field.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Wound Healing",
- "RNA, Untranslated",
- "Animals",
- "Diabetes Mellitus",
- "MicroRNAs",
- "RNA, Long Noncoding",
- "RNA, Circular",
- "Diabetes Complications"
- ]
- },
- {
- "PMID": "39439382",
- "Title": "Journal of primary care & community health",
- "ArticleTitle": "Longer Multimorbidity Intervals Are Associated With Lower Mortality in Diabetes: A Whole-Population Nested Case-Control Study.",
- "Abstract": "Delayed multimorbidity among patients living with diabetes may be related to a lower risk of mortality. This study suggests that we should focus on mitigating and lowering the risk of multimorbidity in clinical management of diabetes to reduce further complication and mortality.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Multimorbidity",
- "Female",
- "Case-Control Studies",
- "Middle Aged",
- "Aged",
- "Hong Kong",
- "Diabetes Mellitus",
- "Time Factors",
- "Adult",
- "Aged, 80 and over",
- "Logistic Models",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39439171",
- "Title": "Yonsei medical journal",
- "ArticleTitle": "Association of the COVID-19 Pandemic with HbA1c Testing and Complication Screening in Patients with Diabetes Mellitus.",
- "Abstract": "A high level of COVID-19 transmission was associated with a decrease in undergoing fundus examination and kidney disease screening. To fully realize the potential benefit of diabetes complication screenings, further effort is required to identify and address challenges to obtaining these screenings, especially in outbreak regions.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Glycated Hemoglobin",
- "Male",
- "Female",
- "Middle Aged",
- "Republic of Korea",
- "Aged",
- "Diabetes Complications",
- "Adult",
- "Diabetes Mellitus",
- "Mass Screening",
- "SARS-CoV-2",
- "Pandemics",
- "Logistic Models"
- ]
- },
- {
- "PMID": "39438414",
- "Title": "Digestive diseases and sciences",
- "ArticleTitle": "Association Between Body Composition Measured by Artificial Intelligence and Long-Term Sequelae After Acute Pancreatitis.",
- "Abstract": "Body composition was not associated with having a recurrent AP. At follow-up, 30% and 25% of evaluated patients developed CP and DM, respectively. A higher SAT and IMAT were associated with a lower incidence of CP and higher incidence of DM, respectively.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Retrospective Studies",
- "Body Composition",
- "Pancreatitis",
- "Adult",
- "Recurrence",
- "Artificial Intelligence",
- "Tomography, X-Ray Computed",
- "Aged",
- "Pancreatitis, Chronic",
- "Acute Disease",
- "Diabetes Mellitus",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39437808",
- "Title": "Biomedical physics & engineering express",
- "ArticleTitle": "Pioneering diabetes screening tool: machine learning driven optical vascular signal analysis.",
- "Abstract": "The escalating prevalence of diabetes mellitus underscores the critical need for non-invasive screening tools capable of early disease detection. Present diagnostic techniques depend on invasive procedures, which highlights the need for advancement of non-invasive alternatives for initial disease detection. Machine learning in integration with the optical sensing technology can effectively analyze the signal patterns associated with diabetes. The objective of this research is to develop and evaluate a non-invasive optical-based method combined with machine learning algorithms for the classification of individuals into normal, prediabetic, and diabetic categories. A novel device was engineered to capture real-time optical vascular signals from participants representing the three glycemic states. The signals were then subjected to quality assessment and preprocessing to ensure data reliability. Subsequently, feature extraction was performed using time-domain analysis and wavelet scattering techniques to derive meaningful characteristics from the optical signals. The extracted features were subsequently employed to train and validate a suite of machine learning algorithms. An ensemble bagged trees classifier with wavelet scattering features and random forest classifier with time-domain features demonstrated superior performance, achieving an overall accuracy of 86.6% and 80.0% in differentiating between normal, prediabetic, and diabetic individuals based on the optical vascular signals. The proposed non-invasive optical-based approach, coupled with advanced machine learning techniques, holds promise as a potential screening tool for diabetes mellitus. The classification accuracy achieved in this study warrants further investigation and validation in larger and more diverse populations.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Machine Learning",
- "Algorithms",
- "Diabetes Mellitus",
- "Mass Screening",
- "Reproducibility of Results",
- "Prediabetic State",
- "Signal Processing, Computer-Assisted",
- "Male",
- "Wavelet Analysis",
- "Female",
- "Blood Glucose",
- "Adult",
- "Middle Aged"
- ]
- },
- {
- "PMID": "39437577",
- "Title": "The journal of nutrition, health & aging",
- "ArticleTitle": "Impact of diabetes on the association between serum urate levels and incident dementia: a cohort study in the UK biobank.",
- "Abstract": "Appropriately higher urate levels within the threshold of hyperuricemia can reduce the adverse health effects of excessively high urate levels and better protect the cognitive health of people with varying diabetes status.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Uric Acid",
- "Female",
- "Dementia",
- "United Kingdom",
- "Middle Aged",
- "Incidence",
- "Biological Specimen Banks",
- "Diabetes Mellitus",
- "Cohort Studies",
- "Aged",
- "Risk Factors",
- "Dementia, Vascular",
- "UK Biobank"
- ]
- },
- {
- "PMID": "39437357",
- "Title": "North Carolina medical journal",
- "ArticleTitle": "\"It Takes a Village\"- A Conversation with the Interprofessional Diabetes Clinic at the ECU Health Family Medicine Center.",
- "Abstract": "Interprofessional collaboration and shared understanding positively impact both patients and providers. Current recommendations from the CDC and experts agree that collaboration between diverse professions is necessary to improve patient outcomes and empower patients to selfmanage their chronic conditions.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus",
- "Interprofessional Relations",
- "North Carolina",
- "Patient Care Team",
- "Cooperative Behavior",
- "Family Practice"
- ]
- },
- {
- "PMID": "39436167",
- "Title": "Medical gas research",
- "ArticleTitle": "Nitric oxide-based treatments improve wound healing associated with diabetes mellitus.",
- "Abstract": "Non-healing wounds are long-term complications of diabetes mellitus (DM) that increase mortality risk and amputation-related disability and decrease the quality of life. Nitric oxide (NO\u00b7)-based treatments (i.e., use of both systemic and topical NO\u00b7 donors, NO\u00b7 precursors, and NO\u00b7 inducers) have received more attention as complementary approaches in treatments of DM wounds. Here, we aimed to highlight the potential benefits of NO\u00b7-based treatments on DM wounds through a literature review of experimental and clinical evidence. Various topical NO\u00b7-based treatments have been used. In rodents, topical NO\u00b7-based therapy facilitates wound healing, manifested as an increased healing rate and a decreased half-closure time. The wound healing effect of NO\u00b7-based treatments is attributed to increasing local blood flow, angiogenesis induction, collagen synthesis and deposition, re-epithelization, anti-inflammatory and anti-oxidative properties, and potent broad-spectrum antibacterial effects. The existing literature lacks human clinical evidence on the safety and efficacy of NO\u00b7-based treatments for DM wounds. Translating experimental favors of NO\u00b7-based treatments of DM wounds into human clinical practice needs conducting clinical trials with well-predefined effect sizes, i.e., wound reduction area, rate of wound healing, and hospital length of stay.",
- "Predictions": [],
- "MeshTerms": [
- "Wound Healing",
- "Humans",
- "Nitric Oxide",
- "Animals",
- "Diabetes Mellitus",
- "Diabetes Complications",
- "Nitric Oxide Donors"
- ]
- },
- {
- "PMID": "39436016",
- "Title": "Journal of diabetes",
- "ArticleTitle": "Chronic glycemic control influences the relationship between acute perioperative dysglycemia and perioperative outcome.",
- "Abstract": "In surgical patients with diabetes, prior exposure to hyperglycemia attenuates the impact of perioperative hyperglycemia and glycemic variability on inpatient mortality and ICU admission. In patients without diabetes mellitus, all absolute thresholds of dysglycemia are associated with ICU admission, unlike those with diabetes, suggesting the need to use more relative measures such as the SHR.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Glycemic Control",
- "Middle Aged",
- "Blood Glucose",
- "Aged",
- "Hyperglycemia",
- "Hospital Mortality",
- "Hypoglycemia",
- "Perioperative Period",
- "Diabetes Mellitus",
- "South Australia",
- "Postoperative Complications",
- "Retrospective Studies",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39435468",
- "Title": "Global health action",
- "ArticleTitle": "Hypertension, diabetes, and cardiovascular disease nexus: investigating the role of urbanization and lifestyle in Cabo Verde.",
- "Abstract": "These findings add to the toolset of public health practitioners and policymakers in formulating policies and interventions aimed at managing cardiovascular diseases, particularly in developing nations.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Cardiovascular Diseases",
- "Male",
- "Hypertension",
- "Female",
- "Urbanization",
- "Middle Aged",
- "Diabetes Mellitus",
- "Life Style",
- "Adult",
- "Aged",
- "Risk Factors",
- "Waist Circumference"
- ]
- },
- {
- "PMID": "39434602",
- "Title": "The Korean journal of internal medicine",
- "ArticleTitle": "Current status of modifiable risk factors for cardiovascular disease in Korean women.",
- "Abstract": "Hypertension, diabetes mellitus, dyslipidemia, obesity, and smoking are the primary modifiable risk factors contributing to the increasing morbidity and mortality rates from cardiovascular disease (CVD) among Korean women. Significant sex-related differences exist in the prevalence, awareness, treatment, and control of these risk factors, highlighting the importance of age- and sex-specific approaches to the management and prevention of CVD. Notably, the prevalence of hypertension and diabetes mellitus increases with age, with a higher prevalence in elderly women compared to men. Dyslipidemia and obesity are also trending upward, particularly in postmenopausal women, highlighting the impact of menopause on cardiovascular risk. The present review advocates for improved diagnostic, therapeutic, and educational efforts to mitigate the risk of CVD among Korean women, with the goals of reducing the overall burden of the disease and promoting better cardiovascular health outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Adult",
- "Aged",
- "Female",
- "Humans",
- "Middle Aged",
- "Age Factors",
- "Cardiovascular Diseases",
- "Diabetes Mellitus",
- "Dyslipidemias",
- "Heart Disease Risk Factors",
- "Hypertension",
- "Obesity",
- "Prevalence",
- "Republic of Korea",
- "Risk Assessment",
- "Risk Factors",
- "Sex Factors",
- "Smoking",
- "Women's Health"
- ]
- },
- {
- "PMID": "39434446",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Synergies between diabetes and hyperhomocysteinaemia: New insights to predict and prevent adverse cardiovascular effects.",
- "Abstract": "The findings highlight the synergistic impact of diabetes and HHcy on CVD. Joint assessments of diabetes and Hcy levels should be emphasized for risk stratification and primary prevention of CVD.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Hyperhomocysteinemia",
- "Cardiovascular Diseases",
- "China",
- "Diabetes Mellitus",
- "Aged",
- "Adult",
- "Homocysteine",
- "Risk Factors",
- "Stroke"
- ]
- },
- {
- "PMID": "39434107",
- "Title": "Trials",
- "ArticleTitle": "Effects of an Exercise and Lifestyle Education Program in Brazilians living with prediabetes or diabetes: study protocol for a multicenter randomized controlled trial.",
- "Abstract": "ClinicalTrials.gov, NCT03914924 . Registered on April 16, 2019.",
- "Predictions": [],
- "MeshTerms": [
- "Male",
- "Patient Education as Topic",
- "Time Factors",
- "Health Knowledge, Attitudes, Practice",
- "Diabetes Mellitus",
- "South American People",
- "Humans",
- "Brazil",
- "Quality of Life",
- "Health Behavior",
- "Prediabetic State",
- "Middle Aged",
- "Treatment Outcome",
- "Healthy Lifestyle",
- "Risk Reduction Behavior",
- "Adult",
- "Multicenter Studies as Topic",
- "Exercise Therapy",
- "Female",
- "Randomized Controlled Trials as Topic",
- "Double-Blind Method"
- ]
- },
- {
- "PMID": "39433999",
- "Title": "BMC primary care",
- "ArticleTitle": "Perceptions of the 2D short animated videos for literacy against chronic diseases among adults with diabetes and/or hypertension: a qualitative study in primary care clinics.",
- "Abstract": "Animated videos are acceptable for delivering health information. Pilot testing animated videos for promoting literacy against chronic diseases in adults with diabetes and hypertension is needed for optimal utility.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Middle Aged",
- "Male",
- "Adult",
- "Female",
- "Hypertension",
- "Diabetes Mellitus",
- "Health Literacy",
- "Qualitative Research",
- "Aged",
- "Primary Health Care",
- "Chronic Disease",
- "Focus Groups",
- "Video Recording",
- "Thailand",
- "Smartphone"
- ]
- },
- {
- "PMID": "39433782",
- "Title": "Scientific data",
- "ArticleTitle": "The Journey to a FAIR CORE DATA SET for Diabetes Research in Germany.",
- "Abstract": "The German Center for Diabetes Research (DZD) established a core data set (CDS) of clinical parameters relevant for diabetes research in 2021. The CDS is central to the design of current and future DZD studies. Here, we describe the process and outcomes of FAIRifying the initial version of the CDS. We first did a baseline evaluation of the FAIRness using the FAIR Data Maturity Model. The FAIRification process and the results of this assessment led us to convert the CDS into the recommended format for spreadsheets, annotating the parameters with standardized medical codes, licensing the data set, enriching the data set with metadata, and indexing the metadata. The FAIRified version of the CDS is more suitable for data sharing in diabetes research across DZD sites and beyond. It contributes to the reusability of health research studies.",
- "Predictions": [],
- "MeshTerms": [
- "Germany",
- "Diabetes Mellitus",
- "Humans",
- "Metadata",
- "Information Dissemination",
- "Biomedical Research",
- "Datasets as Topic"
- ]
- },
- {
- "PMID": "39433450",
- "Title": "Primary care diabetes",
- "ArticleTitle": "Understanding primary care provider's knowledge and perceptions of diabetes self-management education and support.",
- "Abstract": "Providers have limited knowledge of the appropriate time to refer to DSMES but expressed a willingness to refer. They emphasized the importance of providing their patients with appropriate self-management education and support.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Health Knowledge, Attitudes, Practice",
- "Attitude of Health Personnel",
- "Primary Health Care",
- "Female",
- "Male",
- "Patient Education as Topic",
- "Diabetes Mellitus",
- "Perception",
- "Referral and Consultation",
- "Middle Aged",
- "Self Care",
- "Self-Management",
- "Health Care Surveys",
- "Physicians, Primary Care",
- "Interviews as Topic",
- "Adult"
- ]
- },
- {
- "PMID": "39432771",
- "Title": "Diabetes care",
- "ArticleTitle": "Diabetes and Driving: A Statement of the American Diabetes Association.",
- "Abstract": "Many people with diabetes in the U.S. will seek or currently hold a license to drive. For many, a driver's license is essential for everyday life. Considerable discussion has focused on whether, and the extent to which, diabetes may be a relevant factor in determining driver ability and eligibility for a license. This statement addresses such issues in relation to current scientific and medical evidence. A diagnosis of diabetes on its own is not sufficient to make judgments about an individual driver's ability or safety. This statement provides an overview of existing licensing rules for people with diabetes in the U.S., addresses the factors that affect driving ability, identifies general guidelines for assessing driver fitness and determining appropriately tailored licensing restrictions, and provides practical guidance for health care professionals regarding clinical interventions and education for people with diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Automobile Driving",
- "Humans",
- "Diabetes Mellitus",
- "United States",
- "Licensure"
- ]
- },
- {
- "PMID": "39432645",
- "Title": "Medicine",
- "ArticleTitle": "Mitochondrial diabetes presenting with spontaneous abortion and ketoacidosis onset: A case report and literature review.",
- "Abstract": "MDM presents with atypical clinical manifestations, and thorough physical examinations are crucial for its diagnosis. This case underscores the significance of genetic testing and family history in diagnosing MDM and the need for increased awareness among clinicians to prevent misdiagnosis.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Pregnancy",
- "Abortion, Spontaneous",
- "Adult",
- "Mitochondrial Diseases",
- "Diabetes Mellitus",
- "Hearing Loss, Sensorineural",
- "DNA, Mitochondrial",
- "Ketosis"
- ]
- },
- {
- "PMID": "39432605",
- "Title": "Medicine",
- "ArticleTitle": "Female and diabetes are risk factors for alpha-fetoprotein and protein induced by vitamin K absence or antagonist-II negative in hepatocellular carcinoma.",
- "Abstract": "Hepatocellular carcinoma (HCC) is a common type of tumor with a high incidence. Alpha-fetoprotein (AFP) and protein induced by vitamin K absence or antagonist-II (PIVKA-II or des-gamma-carboxy prothrombin) are proven effective biomarkers for HCC. Combining them can enhance detection rates. However, when both AFP and PIVKA-II are negative, clinical diagnosis may be missed. This study aims to explore the risk factors for AFP and PIVKA-II negativity in HCC, thereby reducing missed diagnoses. A retrospective study enrolled 609 HCC patients at Shandong Public Health Clinical Center Affiliated with Shandong University from January 2010 to March 2022. Patients with negative AFP and PIVKA-II were the observed group, and others with at least 1 positive were controls. Epidemiological, clinical, laboratory, and radiological data were collected and analyzed to identify the frequency and factors influencing AFP and PIVKA-II negativity. Receiver operating characteristic (ROC) curves were used to assess the prediction model's ability to detect negative AFP and PIVKA-II in HCC. Gender (P\u2005=\u2005.045, 95% confidence interval [95%CI]\u2005=\u20051.013-3.277), diabetes mellitus (P\u2005=\u2005.018, 95%CI\u2005=\u20051.151-4.422), tumor size (P\u2005=\u2005.000, 95%CI\u2005=\u20050.677-0.841), glutamate transpeptidase (P\u2005=\u2005.003, 95%CI\u2005=\u20050.239-0.737), total bilirubin (P\u2005=\u2005.001, 95%CI\u2005=\u20050.235-0.705), and hepatitis B virus-associated infections (P\u2005=\u2005.007, 95%CI\u2005=\u20050.077-0.661) were significantly associated with AFP and PIVKA-II negativity in HCC. The prediction model had an area under curve of 0.832 (P\u2005<\u2005.001, 95%CI\u2005=\u20050.786-0.877), with a sensitivity of 81.2% and specificity of 75.5% in all HCC patients. Female diabetic patients with levels closer to normal for glutamate transpeptidase and total bilirubin are more likely to develop AFP and PIVKA-II-negative HCC. Imaging is crucial for screening liver cancer in these patients.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Prothrombin",
- "Carcinoma, Hepatocellular",
- "Liver Neoplasms",
- "Female",
- "alpha-Fetoproteins",
- "Middle Aged",
- "Retrospective Studies",
- "Protein Precursors",
- "Male",
- "Risk Factors",
- "Biomarkers",
- "Sex Factors",
- "Adult",
- "ROC Curve",
- "Aged",
- "Diabetes Mellitus",
- "Biomarkers, Tumor"
- ]
- },
- {
- "PMID": "39431381",
- "Title": "Epidemiologia e prevenzione",
- "ArticleTitle": "[The study of migrant and immigrant population from the syndemic point of view].",
- "Abstract": "The study of health of migrant and immigrant populations is of particular interest and actual in recent years, and there is a lack of research assessing aspects of aging of permanently resident immigrants, chronic non-communicable diseases, multimorbidity, and study of second generations. This contribution proposes to describe the relationship between health and immigration and their association with frailty through the anthropological concept of syndemics. Syndemics represents a set of closely interconnected and mutually enhancing health problems, significantly influencing the overall health status of a population. This occurs within the context of a perpetual pattern of harmful social conditions. Among the syndemics described in the literature, the most interesting in this area is the one concerning the increased frailty due to the interaction among diabetes, depression, immigration, and social distress, called VIDDA (Violence, Immigration, Depression, Diabetes, and Abuse), first identified in Mexican immigrant women in the United States. The main limitation of using the syndemic approach to study the health of immigrant populations is the difficulty in moving from the anthropological, primarily qualitative approach to the epidemiological-quantitative approach. Despite this, the epidemiological study of immigrant populations could benefit from the syndemic approach, because it can better describe complex causal relationships and provide evidence for modification of the clinical approach.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Emigrants and Immigrants",
- "Syndemic",
- "Diabetes Mellitus",
- "Female",
- "Depression",
- "Transients and Migrants",
- "Mexico",
- "Italy",
- "Health Status",
- "Male",
- "United States"
- ]
- },
- {
- "PMID": "39431295",
- "Title": "Journal of diabetes science and technology",
- "ArticleTitle": "Psychosocial Aspects of Diabetes Technologies: Commentary on the Current Status of the Evidence and Suggestions for Future Directions.",
- "Abstract": "Diabetes technologies, including continuous glucose monitors, insulin pumps, and automated insulin delivery systems offer the possibility of improving glycemic outcomes, including reduced hemoglobin A1c, increased time in range, and reduced hypoglycemia. Given the rapid expansion in the use of diabetes technology over the past few years, and touted promise of these devices for improving both clinical and psychosocial outcomes, it is critically important to understand issues in technology adoption, equity in access, maintaining long-term usage, opportunities for expanded device benefit, and limitations of the existing evidence base. We provide a brief overview of the status of the literature-with a focus on psychosocial outcomes-and provide recommendations for future work and considerations in clinical applications. Despite the wealth of the existing literature exploring psychosocial outcomes, there is substantial room to expand our current knowledge base to more comprehensively address reasons for differential effects, with increased attention to issues of health equity and data harmonization around patient-reported outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Blood Glucose",
- "Blood Glucose Self-Monitoring",
- "Diabetes Mellitus",
- "Diabetes Mellitus, Type 1",
- "Glycemic Control",
- "Hypoglycemic Agents",
- "Insulin",
- "Insulin Infusion Systems"
- ]
- },
- {
- "PMID": "39430987",
- "Title": "Journal of preventive medicine and hygiene",
- "ArticleTitle": "Longitudinal trends in physical activity levels and lifetime cardiovascular disease risk: insights from the ATTICA cohort study (2002-2022).",
- "Abstract": "Promoting and maintaining regular physical activity throughout lifespan is crucial for reducing lifetime CVD risk and related risk factors. Tailored interventions addressing demographic and socioeconomic factors may help enhance cardiovascular health outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Cardiovascular Diseases",
- "Exercise",
- "Longitudinal Studies",
- "Adult",
- "Hypercholesterolemia",
- "Incidence",
- "Hypertension",
- "Cohort Studies",
- "Risk Factors",
- "Israel",
- "Diabetes Mellitus",
- "Heart Disease Risk Factors"
- ]
- },
- {
- "PMID": "39429548",
- "Title": "The Pan African medical journal",
- "ArticleTitle": "Knowledge, attitudes, and practices regarding diabetic retinopathy among patients with diabetes in Dongola, Northern State, Sudan, 2022: a cross-sectional study.",
- "Abstract": "despite the good knowledge, favorable attitude and good practices, the regular eye check-up practice was significantly low. Urban residence was significantly associated with knowledge. Similarly, knowledge was found to be significantly associated with practice level. The most common barrier to regular eye check-up was the misconception that it is not important.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Cross-Sectional Studies",
- "Sudan",
- "Female",
- "Health Knowledge, Attitudes, Practice",
- "Male",
- "Diabetic Retinopathy",
- "Middle Aged",
- "Adult",
- "Surveys and Questionnaires",
- "Young Adult",
- "Aged",
- "Diabetes Mellitus",
- "Urban Population"
- ]
- },
- {
- "PMID": "39427318",
- "Title": "Cell reports",
- "ArticleTitle": "A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes.",
- "Abstract": "In a patient with permanent neonatal syndromic diabetes clinically similar to cases with ONECUT1 biallelic mutations, we identified a disease-causing deletion located upstream of ONECUT1. Through genetic, genomic, and functional studies, we identified a crucial regulatory region acting as an enhancer of ONECUT1 specifically during pancreatic development. This enhancer region contains a low-frequency variant showing a strong association with type 2 diabetes and other glycemic traits, thus extending the contribution of this region to common forms of diabetes. Clinical relevance is provided by experimentally tailored therapy options for patients carrying ONECUT1 coding or regulatory mutations.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Pancreas",
- "Diabetes Mellitus",
- "Animals",
- "Diabetes Mellitus, Type 2",
- "Enhancer Elements, Genetic",
- "Mice",
- "Male",
- "Mutation",
- "Regulatory Sequences, Nucleic Acid",
- "Female"
- ]
- },
- {
- "PMID": "39427132",
- "Title": "BMC oral health",
- "ArticleTitle": "Association between total functional tooth unit score and hemoglobin A1c levels in Japanese community-dwelling individuals: the Nagasaki Islands study.",
- "Abstract": "In this community-based cross-sectional study, total FTU was significantly associated with HbA1c levels, independent of other risk factors. This suggests that reconstructed occlusal support areas, including dentures, are associated with glycemic control in the older population.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Glycated Hemoglobin",
- "Female",
- "Cross-Sectional Studies",
- "Male",
- "Aged",
- "Japan",
- "Middle Aged",
- "Adult",
- "Aged, 80 and over",
- "Independent Living",
- "Periodontal Index",
- "Periodontal Diseases",
- "Diabetes Mellitus",
- "East Asian People"
- ]
- },
- {
- "PMID": "39425574",
- "Title": "The science of diabetes self-management and care",
- "ArticleTitle": "Participants' Perspectives on Diabetes Self-Management Programming at Church: Faith-Placed Versus Faith-Based Approach.",
- "Abstract": "Church holds promise as a setting for DSMES program delivery in Hispanic communities. Church-based DSMES programs using a FB approach may further facilitate program adoption and sustainability.",
- "Predictions": [],
- "MeshTerms": [
- "Adult",
- "Aged",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Diabetes Mellitus",
- "Focus Groups",
- "Health Knowledge, Attitudes, Practice",
- "Hispanic or Latino",
- "Patient Education as Topic",
- "Self-Management",
- "Texas"
- ]
- },
- {
- "PMID": "39425096",
- "Title": "Cardiovascular diabetology",
- "ArticleTitle": "Altered RBC deformability in diabetes: clinical characteristics and RBC pathophysiology.",
- "Abstract": "NCT00071526.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Erythrocyte Deformability",
- "Cross-Sectional Studies",
- "Erythrocytes",
- "Aged",
- "Case-Control Studies",
- "Adult",
- "Diabetes Mellitus",
- "Risk Factors",
- "Osmotic Fragility",
- "Diabetic Angiopathies"
- ]
- },
- {
- "PMID": "39424428",
- "Title": "Journal of the American Heart Association",
- "ArticleTitle": "Association of Prepregnancy Cardiometabolic Health With Hypertensive Disorders of Pregnancy Among Historically Underrepresented Groups in the United States.",
- "Abstract": "Prepregnancy diabetes and obesity are associated with HDP across all racial and ethnic groups. Diabetes and obesity have highest population attributable fractions among Native Hawaiian and Other Pacific Islander individuals and should be aggressively targeted during childhood, adolescence, and young adulthood to reduce risk of HDPs.",
- "Predictions": [],
- "MeshTerms": [
- "Adult",
- "Female",
- "Humans",
- "Pregnancy",
- "Young Adult",
- "Cross-Sectional Studies",
- "Diabetes Mellitus",
- "Hypertension, Pregnancy-Induced",
- "Native Hawaiian or Pacific Islander",
- "Obesity",
- "Prevalence",
- "Risk Factors",
- "United States",
- "American Indian or Alaska Native"
- ]
- },
- {
- "PMID": "39424393",
- "Title": "BMJ open",
- "ArticleTitle": "Diabetic health literacy and associated factors among patients with diabetes attending follow-up in public hospitals of Northeastern Ethiopia: a multicentre cross-sectional study.",
- "Abstract": "The study showed that less than a quarter of the patients have high DHL, with almost half having low levels of DHL. Tailoring health education programmes to diverse educational levels, incorporating multiple information sources and fostering social support networks could enhance DHL.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Ethiopia",
- "Health Literacy",
- "Cross-Sectional Studies",
- "Female",
- "Male",
- "Adult",
- "Hospitals, Public",
- "Middle Aged",
- "Diabetes Mellitus",
- "Young Adult",
- "Health Knowledge, Attitudes, Practice"
- ]
- },
- {
- "PMID": "39424392",
- "Title": "BMJ open",
- "ArticleTitle": "Treatments, medical expenses and complications of hospital outpatient healthcare associated with stroke in patients with diabetes in China: a retrospective analysis of the Beijing Municipal Medical Insurance Database.",
- "Abstract": "Stroke is associated with a significant increase in complications and medications for patients with diabetes and greatly adds to the economic burden of these patients. Early identification of stroke risk factors in patients with diabetes, as well as targeted poststroke diabetes management, is crucial from a socioeconomic perspective for a comprehensive management and treatment of stroke in patients with diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Retrospective Studies",
- "Female",
- "Stroke",
- "Aged",
- "Middle Aged",
- "Diabetes Mellitus",
- "China",
- "Ambulatory Care",
- "Health Care Costs",
- "Databases, Factual",
- "Diabetes Complications",
- "Beijing",
- "Adult",
- "Hypoglycemic Agents"
- ]
- },
- {
- "PMID": "39424381",
- "Title": "BMJ open",
- "ArticleTitle": "Exploring the decision-making experience of elderly diabetes patients regarding their health-seeking behaviour: a descriptive qualitative study.",
- "Abstract": "The health-seeking behavioural decision-making level of elderly diabetic patients is relatively low. Medical and healthcare professionals should formulate targeted intervention measures aimed at improving their disease cognition level, changing their coping styles and enhancing their health-seeking behavioural decision-making level to improve their health outcomes. Meanwhile, policymakers should plan and allocate medical resources in a targeted manner based on the needs and expectations of patients.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Aged",
- "Male",
- "Female",
- "Qualitative Research",
- "Patient Acceptance of Health Care",
- "Decision Making",
- "China",
- "Middle Aged",
- "Diabetes Mellitus",
- "Aged, 80 and over",
- "Adaptation, Psychological",
- "Interviews as Topic"
- ]
- },
- {
- "PMID": "39423367",
- "Title": "JMIR formative research",
- "ArticleTitle": "Oral Diabetes Medication Videos on Douyin: Analysis of Information Quality and User Comment Attitudes.",
- "Abstract": "Despite most videos on Douyin being posted by doctors, with generally acceptable information quality and positive user comment attitudes, some content inaccuracies and poor actionability remain. Users show more positive attitudes toward videos with high-quality information about treatment choices. This study suggests that health care providers should ensure the accuracy and actionability of video content, enhance the information quality of treatment choices of oral diabetes medications to foster positive user attitudes, help users access accurate health information, and promote medication adherence.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus",
- "Video Recording",
- "Administration, Oral",
- "Hypoglycemic Agents",
- "Patient Education as Topic",
- "China",
- "Male"
- ]
- },
- {
- "PMID": "39423235",
- "Title": "PloS one",
- "ArticleTitle": "Primary care physicians' perspectives on adults with diabetes and the recommended hepatitis B vaccine: A qualitative study.",
- "Abstract": "Our findings indicate that physicians are generally aware of the existence of the CDC guidelines, but not all physicians recommend the HepB vaccine to adults with diabetes. This is because of a wide variation in treatment concerning glucose monitoring or insulin injection due to varying opinions about actual risk. We also identified barriers adults with diabetes have in receiving the HepB vaccine and strategies to increase HepB vaccination.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Physicians, Primary Care",
- "Hepatitis B Vaccines",
- "Female",
- "Male",
- "Adult",
- "Hepatitis B",
- "Middle Aged",
- "Vaccination",
- "Qualitative Research",
- "Attitude of Health Personnel",
- "Diabetes Mellitus",
- "Health Knowledge, Attitudes, Practice"
- ]
- },
- {
- "PMID": "39422035",
- "Title": "Molecular medicine reports",
- "ArticleTitle": "Epigenetic regulatory mechanism of macrophage polarization in diabetic wound healing (Review).",
- "Abstract": "Diabetic wounds represent a significant complication of diabetes and present a substantial challenge to global public health. Macrophages are crucial effector cells that play a pivotal role in the pathogenesis of diabetic wounds, through their polarization into distinct functional phenotypes. The field of epigenetics has emerged as a rapidly advancing research area, as this phenomenon has the potential to markedly affect gene expression, cellular differentiation, tissue development and susceptibility to disease. Understanding epigenetic mechanisms is crucial to further exploring disease pathogenesis. A growing body of scientific evidence has highlighted the pivotal role of epigenetics in the regulation of macrophage phenotypes. Various epigenetic mechanisms, such as DNA methylation, histone modification and non\u2011coding RNAs, are involved in the modulation of macrophage phenotype differentiation in response to the various environmental stimuli present in diabetic wounds. The present review provided an overview of the various changes that take place in macrophage phenotypes and functions within diabetic wounds and discussed the emerging role of epigenetic modifications in terms of regulating macrophage plasticity in diabetic wounds. It is hoped that this synthesis of information will facilitate the elucidation of diabetic wound pathogenesis and the identification of potential therapeutic targets.",
- "Predictions": [],
- "MeshTerms": [
- "Epigenesis, Genetic",
- "Humans",
- "Wound Healing",
- "Macrophages",
- "Animals",
- "DNA Methylation",
- "Diabetes Mellitus",
- "Diabetes Complications",
- "Cell Differentiation",
- "Macrophage Activation"
- ]
- },
- {
- "PMID": "39420889",
- "Title": "Archives of endocrinology and metabolism",
- "ArticleTitle": "Phenotypic and molecular reanalysis of a cohort of patients with monogenic diabetes reveals a case of partial lipodystrophy due to the A8344G mutation in the mitochondrial DNA.",
- "Abstract": "Familial partial lipodystrophy (FPLD) is a very rare genetic disease characterized by insulin resistance due to a loss of subcutaneous fat from the extremities together with a progressive storage of fat around the face and neck and inside the abdomen. In over 50% of cases, molecular genetic testing reveals pathogenic variants in two nuclear genes, LMNA and PPARG. The case reported here refers to a woman phenotypically diagnosed with FPLD, who presented with diabetes and multiple cervical lipomatosis and in whom no variant had been found in the nuclear genes classically associated with this syndrome that could explain her phenotype. Genetic sequencing using a target panel containing 48 nuclear genes related to monogenic diabetes plus the whole mitochondrial genome revealed the mitochondrial variant m.A8344G in 84.1% heteroplasmy. Following molecular diagnosis, her phenotype was expanded with the recognition of additional clinical characteristics: mild sensorineural hearing loss, proximal myopathy, fatigue, cognitive impairment, sensory ataxia, cardiac abnormalities and, finally, muscle biopsy findings compatible with mitochondrial disease. Therefore, careful and detailed phenotypic and genotypic reanalysis proved crucial in improving molecular diagnosis in FPLD.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "DNA, Mitochondrial",
- "Female",
- "Lipodystrophy, Familial Partial",
- "Phenotype",
- "Mutation",
- "Adult",
- "Middle Aged",
- "Diabetes Mellitus",
- "Mitochondrial Diseases",
- "Cohort Studies",
- "Lamin Type A"
- ]
- },
- {
- "PMID": "39419119",
- "Title": "Diabetes research and clinical practice",
- "ArticleTitle": "Nasopharyngeal carriage and antibiotic susceptibility of Streptococcus pneumoniae among diabetes patients in western Kenya.",
- "Abstract": "Nasopharyngeal carriage of S. pneumoniae is higher in patients with diabetes, with significant resistance to common antibiotics, though macrolides remain effective.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Streptococcus pneumoniae",
- "Male",
- "Female",
- "Kenya",
- "Nasopharynx",
- "Cross-Sectional Studies",
- "Adult",
- "Anti-Bacterial Agents",
- "Middle Aged",
- "Pneumococcal Infections",
- "Carrier State",
- "Diabetes Mellitus",
- "Microbial Sensitivity Tests",
- "Adolescent",
- "Young Adult",
- "Drug Resistance, Bacterial",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39418939",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "Individual and joint effects of diabetes and depression on incident cardiovascular diseases and all-cause mortality: Results from a population-based cohort study.",
- "Abstract": "Individuals with both diabetes and depression had greater risk of CVD and all-cause mortality when compared to those with diabetes or depression alone, or those without either condition.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Middle Aged",
- "Female",
- "Cardiovascular Diseases",
- "Aged",
- "China",
- "Longitudinal Studies",
- "Cohort Studies",
- "Depression",
- "Diabetes Mellitus",
- "Incidence",
- "Cause of Death",
- "Risk Factors",
- "Diabetic Angiopathies"
- ]
- },
- {
- "PMID": "39418781",
- "Title": "Journal of occupational and environmental medicine",
- "ArticleTitle": "Developing a Job-Exposure Matrix for Sedentary Behavior: A Study Based on the Inpatient Clinico-Occupational Database of Rosai Hospital Group.",
- "Abstract": "The job-exposure matrix provides valuable insights into the health impacts of sedentary behavior in the workplace, underscoring significant disease risks associated with prolonged inactivity.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Sedentary Behavior",
- "Female",
- "Male",
- "Case-Control Studies",
- "Middle Aged",
- "Adult",
- "Occupations",
- "Databases, Factual",
- "Occupational Exposure",
- "Risk Factors",
- "Noncommunicable Diseases",
- "Myocardial Infarction",
- "Sitting Position",
- "Diabetes Mellitus",
- "Aged",
- "Workplace"
- ]
- },
- {
- "PMID": "39418333",
- "Title": "Diabetes",
- "ArticleTitle": "Functionally Separate Populations of Ventromedial Hypothalamic Neurons in Obesity and Diabetes: A Report on Research Supported by Pathway to Stop Diabetes.",
- "Abstract": "The ventromedial hypothalamic nucleus (VMN) maintains healthy metabolic function through several important roles. Collectively, homeostasis is maintained via intermingled cells within the VMN that raise blood glucose, lower blood glucose, and stimulate energy expenditure when needed. In this article I discuss the defining factors for the VMN cell types that govern distinct functions induced by the VMN, particularly in relation to energy balance and blood glucose levels. Special attention is given to distinct features of VMN cells responsible for these processes. Finally, these topics are reviewed in the context of research funded by the American Diabetes Association Pathway to Stop Diabetes initiative, with highlighting of key findings and current unresolved questions for future investigations.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Humans",
- "Blood Glucose",
- "Diabetes Mellitus",
- "Energy Metabolism",
- "Neurons",
- "Obesity",
- "Ventromedial Hypothalamic Nucleus"
- ]
- },
- {
- "PMID": "39418173",
- "Title": "Preventing chronic disease",
- "ArticleTitle": "Prevalence of Self-Reported Diagnosed Diabetes Among Adults, by County Metropolitan Status and Region, United States, 2019-2022.",
- "Abstract": "The association of metropolitan residence with diabetes prevalence differs across US regions. These findings can help to guide efforts in areas where diabetes prevention and care resources may be better directed.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "United States",
- "Prevalence",
- "Male",
- "Adult",
- "Female",
- "Middle Aged",
- "Diabetes Mellitus",
- "Self Report",
- "Urban Population",
- "Aged",
- "Health Surveys",
- "Young Adult",
- "Rural Population",
- "Adolescent",
- "Socioeconomic Factors",
- "Health Status Disparities"
- ]
- },
- {
- "PMID": "39417708",
- "Title": "International journal of epidemiology",
- "ArticleTitle": "Long-term exposure to PM2.5 and mortality: a national health insurance cohort study.",
- "Abstract": "This study identified the hypothesis that long-term exposure to PM2.5 is associated with mortality, and the association might be different by causes of death. Our result highlights a novel vulnerable population: the middle-aged population with risk factors related to heart failure.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Particulate Matter",
- "Male",
- "Female",
- "Aged",
- "Middle Aged",
- "Republic of Korea",
- "Environmental Exposure",
- "Longitudinal Studies",
- "Air Pollution",
- "Air Pollutants",
- "Cardiovascular Diseases",
- "National Health Programs",
- "Proportional Hazards Models",
- "Cause of Death",
- "Mortality",
- "Cohort Studies",
- "Neoplasms",
- "Diabetes Mellitus"
- ]
- },
- {
- "PMID": "39415790",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Potential pathogenic roles of ferroptosis and cuproptosis in cadmium-induced or exacerbated cardiovascular complications in individuals with diabetes.",
- "Abstract": "Diabetes and its complications are major diseases that affect human health. Diabetic cardiovascular complications such as cardiovascular diseases (CVDs) are the major complications of diabetes, which are associated with the loss of cardiovascular cells. Pathogenically the role of ferroptosis, an iron-dependent cell death, and cuproptosis, a copper-dependent cell death has recently been receiving attention for the pathogenesis of diabetes and its cardiovascular complications. How exposure to environmental metals affects these two metal-dependent cell deaths in cardiovascular pathogenesis under diabetic and nondiabetic conditions remains largely unknown. As an omnipresent environmental metal, cadmium exposure can cause oxidative stress in the diabetic cardiomyocytes, leading to iron accumulation, glutathione depletion, lipid peroxidation, and finally exacerbate ferroptosis and disrupt the cardiac. Moreover, cadmium-induced hyperglycemia can enhance the circulation of advanced glycation end products (AGEs). Excessive AGEs in diabetes promote the upregulation of copper importer solute carrier family 31 member 1 through activating transcription factor 3/transcription factor PU.1, thereby increasing intracellular Cu",
- "Predictions": [],
- "MeshTerms": [
- "Ferroptosis",
- "Humans",
- "Cadmium",
- "Cardiovascular Diseases",
- "Copper",
- "Animals",
- "Diabetes Mellitus",
- "Myocytes, Cardiac",
- "Oxidative Stress",
- "Diabetes Complications"
- ]
- },
- {
- "PMID": "39415660",
- "Title": "Primary health care research & development",
- "ArticleTitle": "Evaluating physical activities in clinical diabetes: lifestyle scores hypothesis.",
- "Abstract": "This report contributes to diabetes cardiovascular complications management. Sedentary ADL factors need integration in healthy lifestyle education especially among the elderly.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Aged",
- "Cross-Sectional Studies",
- "Adolescent",
- "Aged, 80 and over",
- "Life Style",
- "Young Adult",
- "Exercise",
- "Diabetes Mellitus",
- "Activities of Daily Living"
- ]
- },
- {
- "PMID": "39476053",
- "Title": "Brazilian dental journal",
- "ArticleTitle": "Atorvastatin Accelerates Alveolar Bone Loss in Type 1 Diabetic Rats Submitted to Periodontitis.",
- "Abstract": "Periodontal bone loss is potentiated by diabetes. Despite the beneficial anti-inflammatory and antiresorptive effects of Atorvastatin (ATV) on periodontitis, it has been reported to increase the risk of diabetes, which may modify the course of periodontal disease. Therefore, this study aimed to evaluate the effect of ATV on alveolar bone in rats with periodontitis and diabetes. For this, 72 Wistar rats were divided into groups: Na\u00efve (N) not submitted to any procedure; Experimental periodontitis (EP) group submitted to ligature-induced periodontitis; diabetes mellitus (DM), submitted to EP and receiving single dose of streptozotocin (60 mg/kg, i.p.) after 12 hours of fasting; and ATV DM, submitted to EP and DM and receiving orally 27 mg/kg of ATV, 30 minutes before ligature placement, and continued daily until the 11th day. Animals from EP and DM received saline solution 0.9% as placebo. Glycemic levels measured in all animals and then were euthanized. Maxillae were collected for macroscopic, micro-tomographic, and microscopic analyses. DM caused intense bone loss (60%), characterized by a reduction in trabecular thickness and bone volume. DM reduced osteoblasts, increasing osteoclast counts, and induced an inflammatory infiltrate in the periodontium. ATV was found ineffective in protecting bone in diabetic rats, exacerbating bone loss by 21%. Additionally, ATV significantly increased blood glucose levels. In summary, ATV did not prevent alveolar bone loss or modulate inflammation in DM animals undergoing EP. ATV also increased blood glucose levels in these animals. Therefore, the systemic use of ATV in uncontrolled diabetic conditions should be carefully evaluated.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Alveolar Bone Loss",
- "Rats, Wistar",
- "Periodontitis",
- "Atorvastatin",
- "Rats",
- "Diabetes Mellitus, Experimental",
- "Male",
- "Diabetes Mellitus, Type 1",
- "X-Ray Microtomography"
- ]
- },
- {
- "PMID": "39475830",
- "Title": "Current opinion in allergy and clinical immunology",
- "ArticleTitle": "Expanding the spectrum of IPEX: from new clinical findings to novel treatments.",
- "Abstract": "Further research is needed to fully understand the variable clinical presentations of IPEX and optimize tailored therapies, ensuring better management and outcomes for affected individuals.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Forkhead Transcription Factors",
- "Genetic Diseases, X-Linked",
- "T-Lymphocytes, Regulatory",
- "Immune System Diseases",
- "Genetic Therapy",
- "Animals",
- "Diarrhea",
- "Epigenesis, Genetic",
- "Biomarkers",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39475134",
- "Title": "Endokrynologia Polska",
- "ArticleTitle": "Falls in RAC-OST-POL Study: the results from 10-year prospective longitudinal observation.",
- "Abstract": "In long-term follow-up in postmenopausal women, falls were frequently observed, and their occurrence increased the fracture rate. Diabetes type 1 and depression increase the fall rate, which suggests the necessity of implementation of some preventive procedures.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Accidental Falls",
- "Female",
- "Aged",
- "Middle Aged",
- "Prospective Studies",
- "Longitudinal Studies",
- "Incidence",
- "Poland",
- "Osteoporotic Fractures",
- "Risk Factors",
- "Postmenopause",
- "Comorbidity",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39474860",
- "Title": "Journal of diabetes investigation",
- "ArticleTitle": "The benefits and accuracy of real-time continuous glucose monitoring in children and adolescents with type 1 diabetes attending a summer camp.",
- "Abstract": "Rt-CGM exhibited higher usability and recommendation scores in HCPs than those in campers. This may be related to relatively lower accuracy in rt-CGM. Overall usability and recommendation are clinically satisfactory, but due to relatively low accuracy, no decision should be made based on a single, non-verified SG value alone.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Blood Glucose Self-Monitoring",
- "Adolescent",
- "Child",
- "Female",
- "Male",
- "Blood Glucose",
- "Japan",
- "Patient Satisfaction",
- "Surveys and Questionnaires",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39473047",
- "Title": "Diabetic medicine : a journal of the British Diabetic Association",
- "ArticleTitle": "An audit and feedback-based intervention to improve diabetes management in the year after transfer to adult type 1 diabetes care: A multi-center quasi-experimental study.",
- "Abstract": "We found an effect of the intervention on glycaemic management one year following transfer to adult care. Future work will focus on refining and testing the effectiveness of the intervention in an expanded number of study sites and in collaboration with adult diabetes care providers.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Female",
- "Male",
- "Glycated Hemoglobin",
- "Adult",
- "Transition to Adult Care",
- "Ontario",
- "Adolescent",
- "Young Adult",
- "Feedback",
- "Glycemic Control",
- "Medical Audit",
- "Quality Improvement"
- ]
- },
- {
- "PMID": "39472884",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Association between the soluble receptor for advanced glycation end products and diabetes mellitus: systematic review and meta-analysis.",
- "Abstract": "CRD42024521252.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Biomarkers",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus, Type 2",
- "Receptor for Advanced Glycation End Products"
- ]
- },
- {
- "PMID": "39472875",
- "Title": "Cardiovascular diabetology",
- "ArticleTitle": "Excessive occupational sitting increases risk of cardiovascular events among working individuals with type 1 diabetes in the prospective Finnish Diabetic Nephropathy Study.",
- "Abstract": "Excessive occupational sitting is associated with a higher risk of cardiovascular events and all-cause mortality in individuals with type 1 diabetes. This association persists regardless of leisure-time physical activity, after adjusting for independently associated variables identified in our cross-sectional analyses. These findings underscore the need to update physical activity guidelines to better address sedentary behavior and improve outcomes for individuals with type 1 diabetes. Targeting occupational sitting should be considered a key focus for interventions aimed at reducing overall sedentary time.",
- "Predictions": [],
- "MeshTerms": [
- "Adult",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Cardiovascular Diseases",
- "Cause of Death",
- "Diabetes Mellitus, Type 1",
- "Diabetic Nephropathies",
- "Finland",
- "Heart Disease Risk Factors",
- "Occupational Health",
- "Occupations",
- "Prognosis",
- "Prospective Studies",
- "Registries",
- "Risk Assessment",
- "Risk Factors",
- "Sedentary Behavior",
- "Sitting Position",
- "Time Factors",
- "Follow-Up Studies"
- ]
- },
- {
- "PMID": "39472557",
- "Title": "Nature communications",
- "ArticleTitle": "Physiological and pathogenic T cell autoreactivity converge in type 1 diabetes.",
- "Abstract": "Autoimmune diseases result from autoantigen-mediated activation of adaptive immunity; intriguingly, autoantigen-specific T cells are also present in healthy donors. An assessment of dynamic changes of this autoreactive repertoire in both health and disease is thus warranted. Here we investigate the physiological versus pathogenic autoreactive processes in the context of Type 1 diabetes (T1D) and one of its landmark autoantigens, glutamic acid decarboxylase 65 (GAD65). Using single cell gene expression profiling and tandem T cell receptor (TCR) sequencing, we find that GAD65-specific true na\u00efve cells are present in both health and disease, with GAD65-specific effector and memory responses showing similar ratios in healthy donors and patients. Deeper assessment of phenotype and TCR repertoire uncover differential features in GAD65-specific TCRs, including lower clonal sizes of healthy donor-derived clonotypes in patients. We thus propose a model whereby physiological autoimmunity against GAD65 is needed during early life, and that alterations of these physiological autoimmune processes in predisposed individuals trigger overt Type 1 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 1",
- "Humans",
- "Glutamate Decarboxylase",
- "Receptors, Antigen, T-Cell",
- "Autoantigens",
- "Autoimmunity",
- "T-Lymphocytes",
- "Male",
- "Female",
- "Adult",
- "Single-Cell Analysis",
- "Adolescent",
- "Young Adult",
- "Child",
- "Gene Expression Profiling"
- ]
- },
- {
- "PMID": "39471704",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "Effects of probiotics and fibers on markers of nephropathy, inflammation, intestinal barrier dysfunction and endothelial dysfunction in individuals with type 1 diabetes and albuminuria. The ProFOS Study.",
- "Abstract": "Twelve weeks treatment with synbiotic mix had no effect on UACR or on any of the secondary endpoints in subjects with type 1 diabetes and albuminuria.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Albuminuria",
- "Male",
- "Female",
- "Diabetic Nephropathies",
- "Probiotics",
- "Middle Aged",
- "Cross-Over Studies",
- "Aged",
- "Biomarkers",
- "Dietary Fiber",
- "Glomerular Filtration Rate",
- "Inflammation",
- "Endothelium, Vascular",
- "Synbiotics",
- "Intestinal Mucosa",
- "Adult"
- ]
- },
- {
- "PMID": "39471271",
- "Title": "Journal of managed care & specialty pharmacy",
- "ArticleTitle": "Comorbid depression and anxiety and their association with health care resource utilization among individuals with type 1 diabetes in the United States.",
- "Abstract": "Comorbid depression/anxiety among individuals with T1DM results in significantly higher HCRU than T1DM alone. The findings underscore the importance of effective management of comorbid depression/anxiety in the T1DM population.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Female",
- "Adult",
- "United States",
- "Middle Aged",
- "Young Adult",
- "Adolescent",
- "Patient Acceptance of Health Care",
- "Comorbidity",
- "Anxiety",
- "Depression",
- "Retrospective Studies",
- "Health Resources"
- ]
- },
- {
- "PMID": "39470899",
- "Title": "Current diabetes reports",
- "ArticleTitle": "Implementation Science and Pediatric Diabetes: A Scoping Review of the State of the Literature and Recommendations for Future Research.",
- "Abstract": "Of 23 papers identified, 19 were published since 2017 and 21 focused on type 1 diabetes. Most involved medical evidence-based practices (EBPs; n\u2009=\u200915), whereas fewer focused on psychosocial (n\u2009=\u20097) and diabetes education (n\u2009=\u20092). The majority either identified barriers and facilitators of implementing an EBP (n\u2009=\u200911) or were implementation trials (n\u2009=\u200911). Fewer studies documented gaps in EBP implementation in standard care (n\u2009=\u20097) or development of implementation strategies (n\u2009=\u20091). Five papers employed IS theories and two aimed to improve equity. There is a paucity of IS research in pediatric diabetes care literature. Few papers employed IS theory, used consistent IS terminology, or described IS strategies or outcomes. Guidance for future research to improve IS research in pediatric diabetes is offered.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Implementation Science",
- "Child",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus",
- "Pediatrics",
- "Evidence-Based Practice"
- ]
- },
- {
- "PMID": "39470851",
- "Title": "Current diabetes reports",
- "ArticleTitle": "Impact of Digitally Enabled Peer Support Interventions on Diabetes Distress and Depressive Symptoms in People Living with Type 1 Diabetes: A Systematic Review.",
- "Abstract": "We synthesized the results of nine key studies from a review of 3,623 English-language articles published between January 2012 and January 2024. Three studies demonstrated significant reductions in diabetes distress, and two studies reported reductions in depression. Data were analyzed using a narrative approach, including thematic synthesis. This process was structured around the Behavior Change Wheel framework Effective interventions shared several common features such as (1) involved participatory development approaches, (2) included diabetes education, (3) lasted over a longer time, (4) designed with a psychological framework, and (5) utilized peer mentors. Studies showed that digitally-enabled peer support has the potential to improve diabetes distress and depression among people living with T1D despite heterogeneity in intervention approaches. Moreover, designing interventions with certain features may enhance key psychosocial outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Depression",
- "Diabetes Mellitus, Type 1",
- "Peer Group",
- "Psychological Distress",
- "Social Support",
- "Stress, Psychological",
- "Digital Health"
- ]
- },
- {
- "PMID": "39468682",
- "Title": "Trials",
- "ArticleTitle": "Hypoglycaemia Prevention, Awareness of Symptoms, and Treatment (HypoPAST): protocol for a 24-week hybrid type 1 randomised controlled trial of a fully online psycho-educational programme for adults with type 1 diabetes.",
- "Abstract": "Australian and New Zealand Clinical Trials Registry (ANZCTR): ACTRN12623000894695 (21 August 2023).",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Hypoglycemia",
- "Patient Education as Topic",
- "Randomized Controlled Trials as Topic",
- "Health Knowledge, Attitudes, Practice",
- "Time Factors",
- "Adult",
- "Fear",
- "Hypoglycemic Agents",
- "Treatment Outcome",
- "Awareness",
- "Blood Glucose",
- "Quality of Life",
- "Glycemic Control",
- "Insulin",
- "Internet-Based Intervention"
- ]
- },
- {
- "PMID": "39468384",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Body weight variability as a predictor of cardiovascular outcomes in type 1 diabetes: A nationwide cohort study.",
- "Abstract": "High BWV is associated with an increased risk of CVD and all-cause mortality in individuals with T1D, independently of canonical risk factors. Weight trends, sex and glycaemic control do not modify such association while older age attenuates it.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Female",
- "Male",
- "Sweden",
- "Adult",
- "Cardiovascular Diseases",
- "Middle Aged",
- "Body Weight",
- "Cohort Studies",
- "Registries",
- "Incidence",
- "Risk Factors",
- "Diabetic Angiopathies",
- "Young Adult"
- ]
- },
- {
- "PMID": "39467874",
- "Title": "Diabetologia",
- "ArticleTitle": "The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository in the AIRR Data Commons: a practical guide for access, use and contributions through the Type 1 Diabetes AIRR Consortium.",
- "Abstract": "Human molecular genetics has brought incredible insights into the variants that confer risk for the development of tissue-specific autoimmune diseases, including type 1 diabetes. The hallmark cell-mediated immune destruction that is characteristic of type 1 diabetes is closely linked with risk conferred by the HLA class II gene locus, in combination with a broad array of additional candidate genes influencing islet-resident beta cells within the pancreas, as well as function, phenotype and trafficking of immune cells to tissues. In addition to the well-studied germline SNP variants, there are critical contributions conferred by T cell receptor (TCR) and B cell receptor (BCR) genes that undergo somatic recombination to yield the Adaptive Immune Receptor Repertoire (AIRR) responsible for autoimmunity in type 1 diabetes. We therefore created the T1D TCR/BCR Repository (The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository) to study these highly variable and dynamic gene rearrangements. In addition to processed TCR and BCR sequences, the T1D TCR/BCR Repository includes detailed metadata (e.g. participant demographics, disease-associated parameters and tissue type). We introduce the Type 1 Diabetes AIRR Consortium goals and outline methods to use and deposit data to this comprehensive repository. Our ultimate goal is to facilitate research community access to rich, carefully annotated immune AIRR datasets to enable new scientific inquiry and insight into the natural history and pathogenesis of type 1 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 1",
- "Humans",
- "Receptors, Antigen, T-Cell",
- "Receptors, Antigen, B-Cell",
- "Autoimmunity"
- ]
- },
- {
- "PMID": "39467873",
- "Title": "Diabetologia",
- "ArticleTitle": "Autoimmune diseases and the risk and prognosis of latent autoimmune diabetes in adults.",
- "Abstract": "We confirm that several common ADs confer an excess risk of LADA, especially LADA with higher GADA levels, but having such a comorbidity does not appear to affect the risk of diabetic retinopathy.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Autoimmune Diseases",
- "Middle Aged",
- "Latent Autoimmune Diabetes in Adults",
- "Adult",
- "Prognosis",
- "Diabetes Mellitus, Type 2",
- "Sweden",
- "Diabetic Retinopathy",
- "Aged",
- "Autoantibodies",
- "Risk Factors",
- "Comorbidity",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39467872",
- "Title": "Diabetologia",
- "ArticleTitle": "Exposure to antibiotics and risk of latent autoimmune diabetes in adults and type 2 diabetes: results from a Swedish case-control study (ESTRID) and the Norwegian HUNT study.",
- "Abstract": "We found no evidence that exposure to broad-spectrum antibiotics up to 10 years prior to diagnosis increases the risk of LADA. There was some indication of increased LADA risk with exposure to narrow-spectrum antibiotics, which warrants further investigation.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Case-Control Studies",
- "Diabetes Mellitus, Type 2",
- "Sweden",
- "Norway",
- "Anti-Bacterial Agents",
- "Female",
- "Male",
- "Adult",
- "Middle Aged",
- "Aged",
- "Risk Factors",
- "Latent Autoimmune Diabetes in Adults",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39466337",
- "Title": "Current medical research and opinion",
- "ArticleTitle": "Technological advancements in glucose monitoring and artificial pancreas systems for shaping diabetes care.",
- "Abstract": "The management of diabetes mellitus has undergone remarkable progress with the introduction of cutting-edge technologies in glucose monitoring and artificial pancreas systems. These innovations have revolutionized diabetes care, offering patients more precise, convenient, and personalized management solutions that significantly improve their quality of life. This review aims to provide a comprehensive overview of recent technological advancements in glucose monitoring devices and artificial pancreas systems, focusing on their transformative impact on diabetes care. A detailed review of the literature was conducted to examine the evolution of glucose monitoring technologies, from traditional invasive methods to more advanced systems. The review explores minimally invasive techniques such as continuous glucose monitoring (CGM) systems and flash glucose monitoring (FGM) systems, which have already been proven to enhance glycemic control and reduce the risk of hypoglycemia. In addition, emerging non-invasive glucose monitoring technologies, including optical, electrochemical, and electro-mechanical methods, were evaluated. These techniques are paving the way for more patient-friendly options that eliminate the need for frequent finger-prick tests, thereby improving adherence and ease of use. Advancements in closed-loop artificial pancreas systems, which integrate CGM with automated insulin delivery, were also examined. These systems, often referred to as \"hybrid closed-loop\" or \"automated insulin delivery\" systems, represent a significant leap forward in diabetes care by automating the process of insulin dosing. Such advancements aim to mimic the natural function of the pancreas, allowing for better glucose regulation without the constant need for manual interventions by the patient. Technological breakthroughs in glucose monitoring and artificial pancreas systems have had a profound impact on diabetes management, providing patients with more accurate, reliable, and individualized treatment options. These innovations hold the potential to significantly improve glycemic control, reduce the incidence of diabetes-related complications, and ultimately enhance the quality of life for individuals living with diabetes. Researchers are continually exploring novel methods to measure glucose more effectively and with greater convenience, further refining the future of diabetes care. Researchers are also investigating the integration of artificial intelligence and machine learning algorithms to further enhance the precision and predictive capabilities of glucose monitoring and insulin delivery systems. With ongoing advancements in sensor technology, connectivity, and data analytics, the future of diabetes care promises to deliver even more seamless, real-time management, empowering patients with greater autonomy and improved health outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Pancreas, Artificial",
- "Blood Glucose Self-Monitoring",
- "Blood Glucose",
- "Diabetes Mellitus",
- "Insulin",
- "Insulin Infusion Systems",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39465858",
- "Title": "Medicine",
- "ArticleTitle": "Study on serum vitamin A level in patients with type 1 diabetes: A systematic review and meta-analysis.",
- "Abstract": "Serum VA levels seem to have decreased in T1DM patients. Further research is needed to strengthen this finding and clarify possible impact mechanisms.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Vitamin A",
- "Case-Control Studies",
- "Vitamin A Deficiency"
- ]
- },
- {
- "PMID": "39465325",
- "Title": "Swiss medical weekly",
- "ArticleTitle": "Recommendations for early identification of heart failure in patients with diabetes: Consensus statement of the Swiss Society of Endocrinology and Diabetology and the Heart Failure Working Group of the Swiss Society of Cardiology.",
- "Abstract": "Diabetes is a well-recognised risk factor for the development of heart failure, with a prevalence higher than 30% in patients with diabetes aged over 60 years. Heart failure often emerges as the primary cardiovascular manifestation in patients with type 2 diabetes and appears to be even more prevalent in type 1 diabetes. In Switzerland, there are approximately 500,000 individuals with diabetes, and the number of affected people has been steadily rising in recent years. Therefore, the consequences of heart failure will affect an increasing number of patients, further straining the Swiss healthcare system. Early lifestyle modification and initiation of appropriate treatment can prevent or at least significantly delay the onset of symptomatic heart failure by several years. These facts underscore the urgent need for early detection of individuals with subclinical heart failure, which often remains undiagnosed until the first episode of acute heart failure requiring hospital admission occurs. To address this issue, the European Society of Cardiology, the American Diabetes Association (ADA) and other international professional societies have published recommendations on heart failure screening, diagnosis and management. To address this issue in Switzerland, experts from the Swiss Society of Endocrinology and Diabetology, the Swiss Society of Cardiology and the General Internal Medicine specialty met and prepared a consensus report including a simple diagnostic algorithm for use in everyday practice.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Heart Failure",
- "Switzerland",
- "Early Diagnosis",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Consensus",
- "Risk Factors",
- "Societies, Medical",
- "Cardiology",
- "Endocrinology",
- "Mass Screening"
- ]
- },
- {
- "PMID": "39464889",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "Circulating hsa-miR-320a and its regulatory network in type 1 diabetes mellitus.",
- "Abstract": "Our study presents a novel link between hsa-miR-320a-3p and T1D, and highlights its key regulatory role in the network of mRNA markers and transcription factors involved in T1D pathogenesis.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "MicroRNAs",
- "Male",
- "Gene Regulatory Networks",
- "Female",
- "Child",
- "Adolescent",
- "Biomarkers",
- "Gene Expression Profiling",
- "Adult",
- "Signal Transduction",
- "Circulating MicroRNA",
- "Gene Expression Regulation",
- "Leukocytes, Mononuclear",
- "Child, Preschool"
- ]
- },
- {
- "PMID": "39463013",
- "Title": "Journal of diabetes",
- "ArticleTitle": "Gut microbiota, serum metabolites, and lipids related to blood glucose control and type 1 diabetes.",
- "Abstract": "We identified distinct characteristics of gut microbiota, metabolites, and lipids in T1D patients exhibiting different levels of glycemic control. Through comprehensive analysis, microbiota (Bacteroides_nordii, Bacteroides_coprocola), metabolites (D-fructose), and lipids (Monoglycerides) may serve as potential mediators that communicated the interaction between the gut, circulatory systems, and glucose fluctuations in T1D patients.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Gastrointestinal Microbiome",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Female",
- "Lipids",
- "Blood Glucose",
- "Adult",
- "Glycemic Control",
- "Feces",
- "Metabolomics",
- "Glycated Hemoglobin",
- "Young Adult",
- "Adolescent",
- "RNA, Ribosomal, 16S",
- "Middle Aged",
- "Machine Learning"
- ]
- },
- {
- "PMID": "39462556",
- "Title": "The journal of medical investigation : JMI",
- "ArticleTitle": "Difference in the accuracy of the third-generation algorithm and the first-generation algorithm of FreeStyle Libre continuous glucose monitoring device.",
- "Abstract": "No proportional bias in the measurements by Gen. 3 algorithm was observed, but in those by Gen. 1 algorithm. J. Med. Invest. 71 : 225-231, August, 2024.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Algorithms",
- "Blood Glucose Self-Monitoring",
- "Female",
- "Male",
- "Diabetes Mellitus, Type 1",
- "Adult",
- "Blood Glucose",
- "Middle Aged",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39462390",
- "Title": "BMC psychology",
- "ArticleTitle": "Changes in health, lifestyle, and wellbeing of children with type 1 diabetes and their parents during the pandemic.",
- "Abstract": "Our findings indicate that the COVID-19 lockdown has had a significant psychological and possibly physiological impact on children with Type 1 diabetes and their parents. We conclude that there is a need for mental health support services focusing on these groups. Although full lockdown restrictions will have stopped in the past year, post-pandemic stressors may be expected to continue to adversely affect this cohort.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "COVID-19",
- "Child",
- "Male",
- "Female",
- "Parents",
- "Life Style",
- "Prospective Studies",
- "Kuwait",
- "Mental Health",
- "Anxiety",
- "Surveys and Questionnaires",
- "Adult",
- "Exercise",
- "Stress, Psychological",
- "Depression",
- "Pandemics"
- ]
- },
- {
- "PMID": "39461229",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "Prevalence and clinical implications of diabetes mellitus in autoimmune nodopathies: A systematic review.",
- "Abstract": "DM patients fall under the typical clinical phenotype of autoimmune nodopathy, displaying predominantly paranodal antibodies. Early suspicion is crucial, as unlike DPN, diagnosis of autoimmune nodopathy unfolds therapeutic perspectives.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Prevalence",
- "Autoantibodies",
- "Diabetic Neuropathies",
- "Diabetes Mellitus",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39456927",
- "Title": "International journal of molecular sciences",
- "ArticleTitle": "Relationship Between C-Peptide Levels, Clinical Features, and Serum Data in a Brazilian Type 1 Diabetes Population with Large Variations in Genomic Ancestry.",
- "Abstract": "Type 1 diabetes (T1D) is a chronic disease characterized by the immune-mediated destruction of the pancreatic beta cells responsible for insulin production. The secreted insulin and C-peptide are equimolar. Due to its longer half-life, C-peptide has become a safer means of assessing the pancreatic reserve. C-peptide levels were evaluated in a population of patients with T1D, focusing on the relationship between this variable and other factors. In addition, the influence of C-peptide on metabolic control and microvascular complications was investigated. This cross-sectional study included 95 patients who had been diagnosed with T1D at least five years earlier. These patients were evaluated using a clinical demographic survey, anthropometric data, laboratory tests, and fundoscopy. This study showed that 29.5% of patients had residual insulin secretion, which correlated directly with their age at diagnosis. No statistically significant differences in metabolic control or microvascular complications were observed between the C-peptide level groups. In addition, our results indicate that ancestry does not influence the persistence of residual C-peptide function in our highly mixed population. It is recommended that future research consider incorporating new variables, such as HLA and pancreatic autoimmunity, as factors that may influence residual \u03b2-cell function.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "C-Peptide",
- "Female",
- "Male",
- "Brazil",
- "Adult",
- "Cross-Sectional Studies",
- "Adolescent",
- "Insulin",
- "Young Adult",
- "Child",
- "Middle Aged",
- "Insulin-Secreting Cells"
- ]
- },
- {
- "PMID": "39456025",
- "Title": "Journal of nanobiotechnology",
- "ArticleTitle": "Islet cell spheroids produced by a thermally sensitive scaffold: a new diabetes treatment.",
- "Abstract": "The primary issues in treating type 1 diabetes mellitus (T1DM) through the transplantation of healthy islets or islet \u03b2-cells are graft rejection and a lack of available donors. Currently, the majority of approaches use cell encapsulation technology and transplant replacement cells that can release insulin to address transplant rejection and donor shortages. However, existing encapsulation materials merely serve as carriers for islet cell growth. A new treatment approach for T1DM could be developed by creating a smart responsive material that encourages the formation of islet cell spheroids to replicate their 3D connections in vivo and controls the release of insulin aggregates. In this study, we used microfluidics to create thermally sensitive porous scaffolds made of poly(N-isopropyl acrylamide)/graphene oxide (PNIPAM/GO). The material was carefully shrunk under near-infrared light, enriched with mouse insulinoma pancreatic \u03b2 cells (\u03b2-TC-6 cells), encapsulated, and cultivated to form 3D cell spheroids. The controlled contraction of the thermally responsive porous scaffold regulated insulin release from the spheroids, demonstrated using the glucose-stimulated insulin release assay (GSIS), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence assay. Eventually, implantation of the spheroids into C57BL/6\u00a0N diabetic mice enhanced the therapeutic effect, potentially offering a novel approach to the management of T1DM.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Mice",
- "Spheroids, Cellular",
- "Mice, Inbred C57BL",
- "Insulin",
- "Tissue Scaffolds",
- "Diabetes Mellitus, Experimental",
- "Graphite",
- "Acrylic Resins",
- "Insulin-Secreting Cells",
- "Diabetes Mellitus, Type 1",
- "Porosity",
- "Islets of Langerhans",
- "Islets of Langerhans Transplantation",
- "Temperature",
- "Male",
- "Glucose"
- ]
- },
- {
- "PMID": "39455747",
- "Title": "Scientific reports",
- "ArticleTitle": "Causal relationships between allergic and autoimmune diseases with chronic rhinosinusitis.",
- "Abstract": "Chronic rhinosinusitis (CRS) is a prevalent inflammatory airway disease affecting over 10% of the global population, leading to considerable socio-economic impacts, especially in developing countries. The pathogenesis of CRS is multifactorial, involving potential contributions from both genetic and environmental factors. While the influence of allergic and autoimmune diseases on CRS has been observed, the causal relationships between these diseases and CRS remain unclear. We extracted data from large-scale genome-wide association studies (GWAS) and utilized a bidirectional two-sample Mendelian randomization (MR) analysis to explore the causal relationships between CRS and ten autoimmune and allergic diseases, including asthma, allergic rhinitis (AR), atopic dermatitis (AD), psoriasis, type 1 diabetes (T1D), hypothyroidism, celiac disease (CeD), multiple sclerosis (MS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). Additionally, we conducted colocalization analysis to determine whether the allergic/autoimmune diseases showing statistical causal relationships with CRS are driven by the same genetic variants. The MR analysis identified that AR (OR\u2009=\u20091.30; 95% CI\u2009=\u20091.21-1.40; P\u2009=\u20093.26E-13), asthma (OR\u2009=\u20091.35; 95% CI\u2009=\u20091.25-1.45; P\u2009=\u20091.35E-14), and AD (OR\u2009=\u20091.17; 95% CI\u2009=\u20091.06-1.30; P\u2009=\u20090.003) were significantly associated with an increased risk of developing CRS. Interestingly, psoriasis (OR\u2009=\u20090.05; 95% CI\u2009=\u20090.01-0.37; P\u2009=\u20090.004) appeared to have a protective effect against CRS. Associations for T1D and hypothyroidism were also suggestive as potential risk factors for CRS. No significant associations in the reverse MR analysis, suggesting a one-directional relationship. Colocalization analysis indicated that asthma (PP.H4\u2009=\u20090.99) shared the same genetic variant (IL-33 rs3939286) with CRS. In conclusion, our study confirmed the causal relationships between allergic and autoimmune diseases (AR, asthma, AD, and psoriasis) and CRS. Notably, we identified a shared genetic variant, rs3939286 in the IL-33 gene, between asthma and CRS, suggesting that targeting the IL-33 pathway may provide a therapeutic strategy for both diseases.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Autoimmune Diseases",
- "Sinusitis",
- "Genome-Wide Association Study",
- "Chronic Disease",
- "Asthma",
- "Psoriasis",
- "Hypersensitivity",
- "Mendelian Randomization Analysis",
- "Rhinitis",
- "Diabetes Mellitus, Type 1",
- "Dermatitis, Atopic",
- "Polymorphism, Single Nucleotide",
- "Rhinitis, Allergic",
- "Genetic Predisposition to Disease",
- "Lupus Erythematosus, Systemic",
- "Arthritis, Rheumatoid",
- "Multiple Sclerosis",
- "Celiac Disease",
- "Hypothyroidism",
- "Rhinosinusitis"
- ]
- },
- {
- "PMID": "39455273",
- "Title": "Journal of the American Board of Family Medicine : JABFM",
- "ArticleTitle": "Clinician-Reported Barriers and Needs for Implementation of Continuous Glucose Monitoring.",
- "Abstract": "Primary care clinicians face several challenges to prescribing CGM, but they are interested in learning more to help them offer it to their patients. This study reinforces the ongoing need for improved clinician education on CGM technology and continued expansion of insurance coverage for people with both type 1 and type 2 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Blood Glucose Self-Monitoring",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Qualitative Research",
- "Male",
- "Female",
- "Primary Health Care",
- "Middle Aged",
- "Adult",
- "United States",
- "Practice Patterns, Physicians'",
- "Interviews as Topic",
- "Attitude of Health Personnel",
- "Blood Glucose",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39451194",
- "Title": "Cells",
- "ArticleTitle": "Immunomodulatory Functions of TNF-Related Apoptosis-Inducing Ligand in Type 1 Diabetes.",
- "Abstract": "Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF protein superfamily and was initially identified as a protein capable of inducing apoptosis in cancer cells. In addition, TRAIL can promote pro-survival and proliferation signaling in various cell types. Subsequent studies have demonstrated that TRAIL plays several important roles in immunoregulation, immunosuppression, and immune effector functions. Type 1 diabetes (T1D) is an autoimmune disease characterized by hyperglycemia due to the loss of insulin-producing \u03b2-cells, primarily driven by T-cell-mediated pancreatic islet inflammation. Various genetic, epigenetic, and environmental factors, in conjunction with the immune system, contribute to the initiation, development, and progression of T1D. Recent reports have highlighted TRAIL as an important immunomodulatory molecule with protective effects on pancreatic islets. Experimental data suggest that TRAIL protects against T1D by reducing the proliferation of diabetogenic T cells and pancreatic islet inflammation and restoring normoglycemia in animal models. In this review, we aimed to summarize the consequences of TRAIL action in T1D, focusing on and discussing its signaling mechanisms, role in the immune system, and protective effects in T1D.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 1",
- "Humans",
- "Animals",
- "TNF-Related Apoptosis-Inducing Ligand",
- "Immunomodulation",
- "Signal Transduction",
- "Islets of Langerhans"
- ]
- },
- {
- "PMID": "39451186",
- "Title": "Pediatric endocrinology, diabetes, and metabolism",
- "ArticleTitle": "Guidelines of the Polish Society of Pediatric Endocrinology and Diabetology and Pediatric Section of Diabetes Poland on insulin therapy using hybrid closed-loop systems in children and adolescents with diabetes in Poland.",
- "Abstract": "Currently, hybrid closed loop (HCL) systems represent the most advantageous therapeutic option for people with diabetes requiring intensive insulin therapy. They make it possible to achieve optimal metabolic control of the disease in any age group while improving the quality of life of children and adolescents with diabetes and their families. Therefore, we present recommendations for the use of HCL systems in children and adolescents focusing on systems currently available in Poland. These systems should be the first choice in terms of method of insulin therapy in the paediatric population. They can be implemented at any stage of diabetes management. These recommendations are based on scientific evidence and experts' experience. They include principles for the initiation, optimisation, and ongoing management of HCL therapy, as well as the required HCL-related education.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Child",
- "Adolescent",
- "Poland",
- "Insulin Infusion Systems",
- "Diabetes Mellitus, Type 1",
- "Insulin",
- "Hypoglycemic Agents",
- "Endocrinology",
- "Societies, Medical",
- "Practice Guidelines as Topic"
- ]
- },
- {
- "PMID": "39449679",
- "Title": "Journal of pediatric psychology",
- "ArticleTitle": "Barriers to healthy behaviors: perspectives from teens with comorbid Type 1 diabetes and overweight/obesity, caregivers, and pediatric endocrinologists.",
- "Abstract": "Results identify perceived limitations to engaging in recommended healthy lifestyle behaviors and diabetes management concurrently. Results may assist research and clinical care in identifying supports and guidance needed to support adolescents in meeting behavioral recommendations for their health.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Adolescent",
- "Male",
- "Female",
- "Caregivers",
- "Health Behavior",
- "Pediatric Obesity",
- "Endocrinologists",
- "Comorbidity",
- "Qualitative Research",
- "Overweight",
- "Healthy Lifestyle",
- "Adult",
- "Child",
- "Adolescent Behavior"
- ]
- },
- {
- "PMID": "39448829",
- "Title": "Nature reviews. Endocrinology",
- "ArticleTitle": "The epidemiology of type 1 diabetes mellitus in older adults.",
- "Abstract": "Although type 1 diabetes mellitus (T1DM) is traditionally viewed as a youth-onset disorder, the number of older adults being diagnosed with this disease is growing. Improvements in the average life expectancy of people with T1DM have also contributed to the growing number of older people living with this disease. We summarize the evidence regarding the epidemiology (incidence, prevalence and excess mortality) of T1DM in older adults (ages \u226560 years) as well as the genetics, immunology and diagnostic challenges. Several studies report an incidence peak of T1DM in older adults of a similar size to or exceeding that in children, and population prevalence generally increases with increasing age. Glutamic acid decarboxylase antibody positivity is frequently observed in adult-onset T1DM. Guidelines for differentiating T1DM from type 2 diabetes mellitus in older adults recommend measuring levels of C-peptide and autoantibodies, including glutamic acid decarboxylase antibodies. However, there is no gold standard for differentiating T1DM from type 2 diabetes mellitus in people aged 60 years and over. As such, the global variation observed in T1DM epidemiology might be in part explained by misclassification, which increases with increasing age of diabetes mellitus onset. With a growing global population of older adults with T1DM, improved genetic and immunological evidence is needed to differentiate diabetes mellitus type at older ages so that a clear epidemiological picture can emerge.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Aged",
- "Middle Aged",
- "Incidence",
- "Prevalence",
- "Autoantibodies",
- "Aged, 80 and over"
- ]
- },
- {
- "PMID": "39447596",
- "Title": "Psychotherapie, Psychosomatik, medizinische Psychologie",
- "ArticleTitle": "[Patients with Diabetes Mellitus and Comorbid Mental Disorders - Is there a Psychotherapeutic Undertreatment? - Results of the DiMPS Study].",
- "Abstract": "Equating the frequency of mental disorders with the need for psychotherapeutic and/or psychopharmacological treatment without considering the specific treatment needs and preferences of patients may lead to an overestimation of the need for care.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Mental Disorders",
- "Psychotherapy",
- "Germany",
- "Adult",
- "Aged",
- "Cross-Sectional Studies",
- "Comorbidity",
- "Diabetes Mellitus, Type 2",
- "Longitudinal Studies",
- "Diabetes Mellitus, Type 1",
- "Undertreatment"
- ]
- },
- {
- "PMID": "39446990",
- "Title": "Diabetes technology & therapeutics",
- "ArticleTitle": "Possible Glycemic Effects of Vagus Nerve Stimulation Evaluated by Continuous Glucose Monitoring in People with Diabetes and Autonomic Neuropathy: A Randomized, Sham-Controlled Trial.",
- "Abstract": {
- "b": [
- {
- "i": "Objective:"
- },
- {
- "i": "Methods:"
- },
- {
- "i": "Results:"
- },
- {
- "i": "Conclusions:"
- }
- ],
- "i": "P"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Diabetic Neuropathies",
- "Vagus Nerve Stimulation",
- "Middle Aged",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus, Type 2",
- "Blood Glucose Self-Monitoring",
- "Blood Glucose",
- "Adult",
- "Glycated Hemoglobin",
- "Aged",
- "Glycemic Control",
- "Treatment Outcome",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39446857",
- "Title": "PloS one",
- "ArticleTitle": "Association of variants in AGTR1, ACE, MTHFR genes with microalbuminuria and risk factors for the onset of diabetic nephropathy in adolescents with type 1 diabetes in the population of Serbia.",
- "Abstract": "Our data suggest that common variants in the AGTR1, ACE, and MTHFR genes are not strongly associated with diabetic nephropathy in our patients with type 1 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Methylenetetrahydrofolate Reductase (NADPH2)",
- "Diabetes Mellitus, Type 1",
- "Albuminuria",
- "Female",
- "Male",
- "Adolescent",
- "Diabetic Nephropathies",
- "Receptor, Angiotensin, Type 1",
- "Risk Factors",
- "Serbia",
- "Peptidyl-Dipeptidase A",
- "Genetic Predisposition to Disease",
- "Child",
- "Polymorphism, Single Nucleotide",
- "Genotype",
- "Blood Pressure"
- ]
- },
- {
- "PMID": "39446565",
- "Title": "Diabetes",
- "ArticleTitle": "Emerging Concepts and Success Stories in Type 1 Diabetes Research: A Road Map for a Bright Future.",
- "Abstract": "Type 1 diabetes treatment stands at a crucial and exciting crossroad since the 2022 U.S. Food and Drug Administration approval of teplizumab to delay disease development. In this article, we discuss four major conceptual and practical issues that emerged as key to further advancement in type 1 diabetes research and therapies. First, collaborative networks leveraging the synergy between the type 1 diabetes research and care community members are key to fostering innovation, know-how, and translation into the clinical arena worldwide. Second, recent clinical trials in presymptomatic stage 2 and recent-onset stage 3 disease have shown the promise, and potential pitfalls, of using immunomodulatory and/or \u03b2-cell protective agents to achieve sustained remission or prevention. Third, the increasingly appreciated heterogeneity of clinical, immunological, and metabolic phenotypes and disease trajectories is of critical importance to advance the decision-making process for tailored type 1 diabetes care and therapy. Fourth, the clinical benefits of early diagnosis of \u03b2-cell autoimmunity warrant consideration of general population screening for islet autoantibodies, which requires further efforts to address the technical, organizational, and ethical challenges inherent to a sustainable program. Efforts are underway to integrate these four concepts into the future directions of type 1 diabetes research and therapy.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Biomedical Research",
- "Diabetes Mellitus, Type 1",
- "Insulin-Secreting Cells"
- ]
- },
- {
- "PMID": "39444012",
- "Title": "BMC health services research",
- "ArticleTitle": "Bridging the gap: a qualitative process evaluation from the perspectives of healthcare professionals of an audit-and-feedback-based intervention to improve transition to adult care for young people living with type 1 diabetes.",
- "Abstract": "BTG resulted in a CoP among practitioners delivering transition care to youth with T1D, which could be scaled up to promote a learning health system in pediatric diabetes care. Qualitative process evaluation is a useful tool for understanding how contextual factors affect the implementation and outcomes of complex QI interventions.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Transition to Adult Care",
- "Qualitative Research",
- "Quality Improvement",
- "Adolescent",
- "Young Adult",
- "Health Personnel",
- "Male",
- "Female",
- "Adult",
- "COVID-19",
- "Interviews as Topic",
- "SARS-CoV-2"
- ]
- },
- {
- "PMID": "39443628",
- "Title": "Scientific reports",
- "ArticleTitle": "The effect of war and siege on children with diabetes admitted to ayder comprehensive specialized hospital in mekelle, tigray, ethiopia: a cross-sectional study.",
- "Abstract": "The armed conflict in Tigray, which spanned from November 2020 to November 2022, along with the accompanying siege, led to the near-total collapse of Tigray's healthcare system. Type 1 Diabetes Mellitus, the most common chronic condition in children, requires significant lifestyle adjustments, including daily insulin injections, regular glucose monitoring, and dietary modifications; all of which are severely impacted by war and siege. This study compared Type 1 diabetes care for children at the Ayder Comprehensive Specialized Hospital, Tigray, during the conflict and siege period with that of the pre-war period. We conducted a retrospective cross-sectional survey, analyzing data from September 2019 to August 2020 (pre-war period) and comparing it with data from September 2021 to August 2022 (war and siege period). Descriptive statistics, including frequencies and percentages, were employed, and Pearson's or Spearman's correlation analyses were used to evaluate correlations where appropriate. We identified 143 pediatric patients admitted (56 during the pre-war period and 87 during the war and siege period), with a mean age of 109 months in both periods. During the war and siege, a higher proportion of diabetes admissions were due to diabetic ketoacidosis (DKA) (90%) compared to the pre-war period (75%). In the pre-war period, the most common trigger for DKA was infections (35%), while in the war and siege period, it shifted to malnutrition (47%), infections (46%), lack of access to healthcare facilities (31%), and running out of medicines (24%). Complications such as death, renal failure, cerebral edema, and shock were more prevalent during the war and siege periods. The case fatality rate was significantly higher during the war and siege (9%) compared to the pre-war period (0%), correlating strongly with the severity of DKA, the degree of hypokalemia, the presence of complications, and admission during the war and siege. Our study showed the negative impact of war and siege on diabetes care in children demonstrating a high rate of DKA admissions with increased severity, complications, malnutrition, and case fatality rates. People with diabetes especially type 1 deserve great attention during such a crisis as the lack of insulin could lead to severe complications including death.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Ethiopia",
- "Child",
- "Cross-Sectional Studies",
- "Male",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Retrospective Studies",
- "Child, Preschool",
- "Armed Conflicts",
- "Adolescent",
- "Hospitals, Special",
- "Hospitalization",
- "Infant"
- ]
- },
- {
- "PMID": "39442806",
- "Title": "Diabetes research and clinical practice",
- "ArticleTitle": "Time in range and mean glucose cut-off points for reduction of fetal outcomes in pregnant women with type 1 diabetes using automated insulin delivery systems.",
- "Abstract": "TIRp\u00a0>\u00a059.1\u00a0% and mean glucose\u00a0<\u00a0133\u00a0mg/dl in the second trimester, is associated with lower fetal outcomes of large for gestational age. One of the strategies that would improve TIRp is the early use of AHCL systems. Further studies are needed before a strong recommendation can be made.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Pregnancy",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Adult",
- "Blood Glucose",
- "Insulin Infusion Systems",
- "Prospective Studies",
- "Insulin",
- "Pregnancy in Diabetics",
- "Pregnancy Outcome",
- "Hypoglycemic Agents",
- "Fetal Macrosomia",
- "Blood Glucose Self-Monitoring"
- ]
- },
- {
- "PMID": "39441297",
- "Title": "Georgian medical news",
- "ArticleTitle": "EVALUATION OF DENTAL AND PERIODONTAL STATUS IN CHILDREN WITH TYPE 1 DIABETES MELLITUS.",
- "Abstract": "Children with T1DM exhibit poor oral health conditions related to the level of metabolic control. Maintenance of toothbrushing habits and regular dental check-ups recommended to manage and prevent these complications. Additionally, proper management of metabolic control can also help mitigate the adverse effects on oral health.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Child",
- "Adolescent",
- "Male",
- "Female",
- "Dental Caries",
- "Oral Health",
- "Periodontal Index",
- "Glycated Hemoglobin",
- "Dental Plaque Index",
- "DMF Index",
- "Periodontal Diseases"
- ]
- },
- {
- "PMID": "39438880",
- "Title": "Cardiovascular diabetology",
- "ArticleTitle": "Evaluation of the Steno Type 1 Risk Engine in predicting cardiovascular events in an ethnic mixed population of type 1 diabetes mellitus and its association with chronic microangiopathy complications.",
- "Abstract": "ST1RE performed well in predicting CV events at 5 and 10 years of follow-up. Moreover, higher ST1RE scores were associated with the progression of microangiopathy complications in this genetically heterogeneous T1D population.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Female",
- "Risk Assessment",
- "Retrospective Studies",
- "Adult",
- "Predictive Value of Tests",
- "Time Factors",
- "Heart Disease Risk Factors",
- "Cardiovascular Diseases",
- "Young Adult",
- "Prognosis",
- "Diabetic Angiopathies",
- "Decision Support Techniques",
- "Disease Progression",
- "Ethnic and Racial Minorities",
- "Risk Factors",
- "Middle Aged"
- ]
- },
- {
- "PMID": "39438440",
- "Title": "Nature communications",
- "ArticleTitle": "Uncovering genetic loci and biological pathways associated with age-related cataracts through GWAS meta-analysis.",
- "Abstract": "Age-related cataracts is a highly prevalent eye disorder that results in the clouding of the crystalline lens and is one of the leading causes of visual impairment and blindness. The disease is influenced by multiple factors including genetics, prolonged exposure to ultraviolet radiation, and a history of diabetes. However, the extent to which each of these factors contributes to the development of cataracts remains unclear. Our study identified 101 independent genome-wide significant loci, 57 of which are novel. We identified multiple genes and biological pathways associated with the cataracts, including four drug-gene interactions. Our results suggest a causal association between type 1 diabetes and cataracts. Also, we highlighted a surrogate measure of UV light exposure as a marker of cataract risk in adults.",
- "Predictions": [],
- "MeshTerms": [
- "Cataract",
- "Humans",
- "Genome-Wide Association Study",
- "Genetic Loci",
- "Genetic Predisposition to Disease",
- "Ultraviolet Rays",
- "Polymorphism, Single Nucleotide",
- "Diabetes Mellitus, Type 1",
- "Aging"
- ]
- },
- {
- "PMID": "39437874",
- "Title": "Brain research",
- "ArticleTitle": "Quantification of white matter hyperintensities in type 1 diabetes and its relation to neuropathy and clinical characteristics.",
- "Abstract": "Our findings indicate increased burden of periventricular WMHs in diabetes which were associated to DPN severity and measurements reflecting neurodegeneration. Deep WMHs, often considered as chronic ischemic, were not significantly different. Mechanisms reflecting neurodegeneration and accelerated brain aging could be an overlooked aspect of peripheral and central neuropathy.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Diabetic Neuropathies",
- "Diabetes Mellitus, Type 1",
- "White Matter",
- "Magnetic Resonance Imaging",
- "Adult",
- "Middle Aged",
- "Brain"
- ]
- },
- {
- "PMID": "39437698",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "Subcutaneous rapid-acting insulin analogues in mild to moderate diabetic ketoacidosis: A meta-analysis of randomized controlled trials.",
- "Abstract": "In this meta-analysis of eight RCTs we found that SC RAIAs and regular IV insulin are comparable in resolving mild to moderate DKA in children and adults. PROSPERO registration: CRD42023485032.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetic Ketoacidosis",
- "Randomized Controlled Trials as Topic",
- "Injections, Subcutaneous",
- "Hypoglycemic Agents",
- "Insulin, Short-Acting",
- "Diabetes Mellitus, Type 1",
- "Treatment Outcome",
- "Insulin",
- "Severity of Illness Index"
- ]
- },
- {
- "PMID": "39436890",
- "Title": "PloS one",
- "ArticleTitle": "Type 1 diabetes and parasite infection: An exploratory study in NOD mice.",
- "Abstract": "Microorganisms have long been suspected to influence the outcome of immune-related syndromes, particularly autoimmune diseases. Type 1 diabetes (T1D) results from the autoimmune destruction of the insulin-producing beta cells of pancreatic islets, causing high glycemia levels. Genetics is part of its aetiology, but environmental factors, particularly infectious microorganisms, also play a role. Bacteria, viruses, and parasites influence the outcome of T1D in mice and humans. We used nonobese diabetic (NOD) mice, which spontaneously develop T1D, to investigate the influence of a parasitic infection, leishmaniasis. Leishmania amazonensis is an intracellular eukaryotic parasite that replicates predominantly in macrophages and is responsible for cutaneous leishmaniasis. The implication of Th1 immune responses in T1D and leishmaniasis led us to study this parasite in the NOD mouse model. We previously constructed osteopontin knockout mice with a NOD genetic background and demonstrated that this protein plays a role in the T1D phenotype. In addition, osteopontin (OPN) has been found to play a role in the immune response to various infectious microorganisms and to be implicated in other autoimmune conditions, such as multiple sclerosis in humans and experimental autoimmune encephalomyelitis (EAE) in mice. We present herein data demonstrating the role of OPN in the response to Leishmania in NOD mice and the influence of this parasitic infection on T1D. This exploratory study aimed to investigate the environmental infectious component of the autoimmune response, including Th1 immunity, which is common to both T1D and leishmaniasis.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Diabetes Mellitus, Type 1",
- "Mice, Inbred NOD",
- "Mice",
- "Osteopontin",
- "Female",
- "Leishmaniasis",
- "Th1 Cells",
- "Mice, Knockout",
- "Leishmania",
- "Leishmaniasis, Cutaneous"
- ]
- },
- {
- "PMID": "39436695",
- "Title": "The Journal of clinical investigation",
- "ArticleTitle": "Attenuated kidney oxidative metabolism in young adults with type 1 diabetes.",
- "Abstract": "BACKGROUNDIn type 1 diabetes (T1D), impaired insulin sensitivity may contribute to the development of diabetic kidney disease (DKD) through alterations in kidney oxidative metabolism.METHODSYoung adults with T1D (n = 30) and healthy controls (HCs) (n = 20) underwent hyperinsulinemic-euglycemic clamp studies, MRI, 11C-acetate PET, kidney biopsies, single-cell RNA-Seq, and spatial metabolomics to assess this relationship.RESULTSParticipants with T1D had significantly higher glomerular basement membrane (GBM) thickness compared with HCs. T1D participants exhibited lower insulin sensitivity and cortical oxidative metabolism, correlating with higher insulin sensitivity. Proximal tubular transcripts of TCA cycle and oxidative phosphorylation enzymes were lower in T1D. Spatial metabolomics showed reductions in tubular TCA cycle intermediates, indicating mitochondrial dysfunction. The Slingshot algorithm identified a lineage of proximal tubular cells progressing from stable to adaptive/maladaptive subtypes, using pseudotime trajectory analysis, which computationally orders cells along a continuum of states. This analysis revealed distinct distribution patterns between T1D and HCs, with attenuated oxidative metabolism in T1D attributed to a greater proportion of adaptive/maladaptive subtypes with low expression of TCA cycle and oxidative phosphorylation transcripts. Pseudotime progression associated with higher HbA1c, BMI, and GBM, and lower insulin sensitivity and cortical oxidative metabolism.CONCLUSIONThese early structural and metabolic changes in T1D kidneys may precede clinical DKD.TRIAL REGISTRATIONClinicalTrials.gov NCT04074668.FUNDINGUniversity of Michigan O'Brien Kidney Translational Core Center grant (P30 DK081943); CROCODILE studies by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (P30 DK116073), Juvenile Diabetes Research Foundation (JDRF) (2-SRA-2019-845-S-B), Boettcher Foundation, Intramural Research Program at NIDDK and Centers for Disease Control and Prevention (CKD Initiative) under Inter-Agency Agreement #21FED2100157DPG.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Female",
- "Adult",
- "Diabetic Nephropathies",
- "Kidney",
- "Insulin Resistance",
- "Young Adult",
- "Citric Acid Cycle",
- "Oxidation-Reduction"
- ]
- },
- {
- "PMID": "39434552",
- "Title": "Annals of medicine",
- "ArticleTitle": "Increased purchases of prescription medicines in offspring of women with type 1 diabetes: a Finnish register-based cohort study between 1995 and 2018.",
- "Abstract": "Our findings suggest that exposed offspring purchase more reimbursable prescription medicines than reference offspring from age seven to thirty years. More research is needed to examine the effects of intrauterine exposure to hyperglycemia on long-term health in offspring.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Finland",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Child",
- "Adult",
- "Pregnancy",
- "Adolescent",
- "Registries",
- "Male",
- "Prescription Drugs",
- "Prenatal Exposure Delayed Effects",
- "Longitudinal Studies",
- "Young Adult",
- "Hyperglycemia",
- "Cohort Studies"
- ]
- },
- {
- "PMID": "39434445",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "The associations between functional vitamin K status and all-cause mortality, cardiovascular disease and end-stage kidney disease in persons with type 1 diabetes.",
- "Abstract": "In persons with type 1 diabetes, lower vitamin K status was associated with higher mortality, CVD and progression to ESKD, however, not after adjustment for other risk factors. Interventional studies are needed to elucidate the role of vitamin K in persons with type 1 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Female",
- "Kidney Failure, Chronic",
- "Vitamin K Deficiency",
- "Middle Aged",
- "Cardiovascular Diseases",
- "Adult",
- "Diabetic Nephropathies",
- "Vitamin K",
- "Matrix Gla Protein",
- "Extracellular Matrix Proteins",
- "Calcium-Binding Proteins",
- "Proportional Hazards Models",
- "Disease Progression",
- "Cause of Death",
- "Cohort Studies",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39434271",
- "Title": "JPMA. The Journal of the Pakistan Medical Association",
- "ArticleTitle": "Assessment of growth status in children and adolescents with type 1 diabetes mellitus in Baghdad: a case-control study.",
- "Abstract": "Children with type 1 diabetes mellitus had significantly lower mean height, weight and body mass index Z scores compared to their counterparts in the control group. Pubertal age group, poor glycaemic control, longer disease duration, and using conventional insulin regimen were the factors affecting growth parameters.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Child",
- "Male",
- "Female",
- "Case-Control Studies",
- "Adolescent",
- "Body Mass Index",
- "Child, Preschool",
- "Body Height",
- "Iraq",
- "Body Weight",
- "Glycated Hemoglobin"
- ]
- },
- {
- "PMID": "39433215",
- "Title": "Diabetes research and clinical practice",
- "ArticleTitle": "Beyond the insulin pump: Unraveling diabetes tech dependency.",
- "Abstract": "The use of technology for Type 1 diabetes (T1D) has significantly developed in the last 20\u00a0years leading to several benefits in life-style management but also to potentially overreliance and addiction to such life changing devices. Insulin pumps (CSII) being small, discreet and sophisticated, offer features such as customizable basal rates, bolus calculators and integration with Continuous Glucose Monitoring (CGM) systems becoming a must have for diabetic patients. Indeed CGM, firstly introduced in the late 1990s and now being highly sophisticated provide trends and patterns hence allowing a better management of T1D. In this review we inquire the multifactorial aspects of dependency on diabetes technology, focusing not only on the benefits and the advancements these automations offer, but also the challenges, limits and possible risks associated with overreliance on them. Specifically, the impact that early introduction to technology had on patients, the dependency on CSII and CGM, the importance of learning and self-management skills and strategies for addressing unexpected events.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Insulin Infusion Systems",
- "Diabetes Mellitus, Type 1",
- "Blood Glucose Self-Monitoring",
- "Insulin",
- "Hypoglycemic Agents",
- "Blood Glucose",
- "Self-Management"
- ]
- },
- {
- "PMID": "39432892",
- "Title": "JMIR formative research",
- "ArticleTitle": "Feasibility and Acceptability of a Self-Guided Digital Family Skills Management Intervention for Children Newly Diagnosed With Type 1 Diabetes: Pilot Randomized Controlled Trial.",
- "Abstract": "ClinicalTrials.gov NCT03720912; https://clinicaltrials.gov/study/NCT03720912.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Female",
- "Male",
- "Pilot Projects",
- "Child",
- "Feasibility Studies",
- "Adolescent",
- "Prospective Studies",
- "Social Support",
- "Child, Preschool"
- ]
- },
- {
- "PMID": "39432714",
- "Title": "Diabetic medicine : a journal of the British Diabetic Association",
- "ArticleTitle": "The diabetes annual review in a postal box: A qualitative study exploring the views of people living with diabetes (DiaBox-Qual).",
- "Abstract": "Postal boxes for annual reviews were well-received by those living with diabetes. Designed well, they have the potential to overcome more than just the physical barriers to annual review attendance.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Qualitative Research",
- "Diabetes Mellitus, Type 2",
- "Adult",
- "Aged",
- "Diabetes Mellitus, Type 1",
- "Postal Service",
- "Self Care",
- "Focus Groups"
- ]
- },
- {
- "PMID": "39432633",
- "Title": "Medicine",
- "ArticleTitle": "Exploring the mechanism of comorbidity in patients with T1DM and COVID-19: Integrating bioinformatics and Mendelian randomization methods.",
- "Abstract": "During the coronavirus disease 2019 (COVID-19) pandemic, the incidence of type 1 diabetes mellitus (T1DM) has increased. Additionally, evidence suggests that individuals with diabetes mellitus may have increased susceptibility to severe acute respiratory syndrome coronavirus 2 infection. However, the specific causal relationships and interaction mechanisms between T1DM and COVID-19 remain unclear. This study aims to investigate the causal relationship between T1DM and COVID-19, utilizing differential gene expression and Mendelian randomization analyses. Differentially expressed gene sets from datasets GSE156035 and GSE171110 were intersected to identify shared genes, analyzed for functional enrichment. Mendelian randomization models were employed to assess causal effects, revealing no direct causal link between T1DM and COVID-19 in the European population (P\u2005>\u2005.05). Notably, DNA replication and sister chromatid cohesion 1 (DSCC1) showed negative causal associations with both diseases (T1DM: OR\u2005=\u20050.943, 95% CI: 0.898-0.991, P\u2005=\u2005.020; COVID-19: OR\u2005=\u20050.919, 95% CI: 0.882-0.958, P\u2005<\u2005.001), suggesting a protective effect against their comorbidity. This genetic evidence highlights DSCC1 as a potential target for monitoring and managing the co-occurrence of T1DM and COVID-19.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Mendelian Randomization Analysis",
- "COVID-19",
- "Computational Biology",
- "Comorbidity",
- "Diabetes Mellitus, Type 1",
- "SARS-CoV-2"
- ]
- },
- {
- "PMID": "39431295",
- "Title": "Journal of diabetes science and technology",
- "ArticleTitle": "Psychosocial Aspects of Diabetes Technologies: Commentary on the Current Status of the Evidence and Suggestions for Future Directions.",
- "Abstract": "Diabetes technologies, including continuous glucose monitors, insulin pumps, and automated insulin delivery systems offer the possibility of improving glycemic outcomes, including reduced hemoglobin A1c, increased time in range, and reduced hypoglycemia. Given the rapid expansion in the use of diabetes technology over the past few years, and touted promise of these devices for improving both clinical and psychosocial outcomes, it is critically important to understand issues in technology adoption, equity in access, maintaining long-term usage, opportunities for expanded device benefit, and limitations of the existing evidence base. We provide a brief overview of the status of the literature-with a focus on psychosocial outcomes-and provide recommendations for future work and considerations in clinical applications. Despite the wealth of the existing literature exploring psychosocial outcomes, there is substantial room to expand our current knowledge base to more comprehensively address reasons for differential effects, with increased attention to issues of health equity and data harmonization around patient-reported outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Blood Glucose",
- "Blood Glucose Self-Monitoring",
- "Diabetes Mellitus",
- "Diabetes Mellitus, Type 1",
- "Glycemic Control",
- "Hypoglycemic Agents",
- "Insulin",
- "Insulin Infusion Systems"
- ]
- },
- {
- "PMID": "39429740",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "A novel class of oral, non-immunosuppressive, beta cell-targeting, TXNIP-inhibiting T1D drugs is emerging.",
- "Abstract": "Diabetes treatment options have improved dramatically over the last 100 years, however, close to 2 million individuals in the U.S. alone live with type 1 diabetes (T1D) and are still dependent on multiple daily insulin injections and/or continuous insulin infusion with a pump to stay alive and no oral medications are available. After decades of focusing on immunosuppressive/immunomodulatory approaches for T1D, it has now become apparent that at least after disease onset, this by itself may not be sufficient, and in order to be effective, therapies need to also address beta cell health. This Perspective article discusses the emergence of such a beta cell-targeting, novel class of oral T1D drugs targeting thioredoxin-interacting protein (TXNIP) and some very recent advances in this field that start to address this unmet medical need. It thereby focuses on repurposing of the antihypertensive drug, verapamil found to non-specifically inhibit TXNIP and on TIX100, a new chemical entity specifically developed as an oral anti-diabetic drug to inhibit TXNIP. Both have shown striking anti-diabetic effects in preclinical studies. Verapamil has also proven to be beneficial in adults and children with recent onset T1D, while TIX100 has just been cleared by the U.S. Food and Drug Administration (FDA) to proceed to clinical trials. Taken together, we propose that such non-immunosuppressive, adjunctive therapies to insulin, alone or in combination with immune modulatory approaches, are critical in order to achieve effective and durable disease-modifying treatments for T1D.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Carrier Proteins",
- "Diabetes Mellitus, Type 1",
- "Insulin-Secreting Cells",
- "Hypoglycemic Agents",
- "Administration, Oral",
- "Animals",
- "Thioredoxins"
- ]
- },
- {
- "PMID": "39428561",
- "Title": "Nursing & health sciences",
- "ArticleTitle": "A Qualitative Evidence Synthesis of Continuous Subcutaneous Insulin Infusion: Acceptability, Implementation, Equity.",
- "Abstract": "This work provides a synthesis of the perceptions of people with type 1 diabetes mellitus (T1DM) and healthcare professionals about the acceptability, implementation, and equity of continuous subcutaneous insulin infusion (CSII). A qualitative evidence synthesis was carried out. Three online databases (Medline, Embase, and Web of Science) were searched. Qualitative articles which were available in Spanish or English were included. A descriptive thematic synthesis was conducted according to PRISMA and ENTREQ guidelines. Thirty-two references met the inclusion criteria of the study and were included out of an initial 345 identified references. Seven main themes were identified: (a) acceptability, (b) adaptation to the insulin pump, (c) facilitators for the adequate use of insulin pump, (d) variability of acceptability, (e) barriers for the use of insulin pump, (f) feasibility and implementation considerations, and (g) equity. CSII is well accepted by most people with T1DM, with some exceptions. CSII can relieve management burden, increase autonomy and flexibility and improve family relationships. There were multiple perceived barriers to its continued use. Future studies should continue to analyze inequalities in access and use of the CSII.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Qualitative Research",
- "Diabetes Mellitus, Type 1",
- "Insulin Infusion Systems",
- "Insulin",
- "Infusions, Subcutaneous",
- "Patient Acceptance of Health Care",
- "Hypoglycemic Agents"
- ]
- },
- {
- "PMID": "39428134",
- "Title": "Medical engineering & physics",
- "ArticleTitle": "Platform for precise, personalised glucose forecasting through continuous glucose and physical activity monitoring and deep learning.",
- "Abstract": "Emerging research has demonstrated the advantage of continuous glucose monitoring for use in artificial pancreas and diabetes management in general. Recent studies demonstrate that glucose level forecasting using deep learning can help avoid postprandial hyperglycemia (\u2265 180 mg/dL) or hypoglycemia (\u226470 mg/dL) from delayed or increased insulin dosing in artificial pancreas. In this paper, a novel hybrid deep learning framework with integration of content-based attention learning is presented, to effectively predict the glucose measurements with prediction horizons (PH) = 15, 30 and, 60 minutes for T1D and T2D patients based on past data. We also present a complete cloud-based system and mobile app used for collecting CGM sensor, physical activity data, CHO values and insulin measurements to perform glucose forecasts using the proposed model running on Cloud. This model was validated using clinical data of individual with Type 1 diabetes (OhioT1DM) and individual with Type 2 diabetes. The mean absolute relative difference (MARD) was 12.33\u00b13.15, 7.14\u00b11.76% for PH=60 and, 30 min respectively on OhioT1DM clinical Dataset. The root mean squared error (RMSE) was 29.41\u00b15.92 mg/dL and 17.19\u00b13.22 mg/dL and the mean absolute error (MAE) was 21.96\u00b14.67 mg/dL and 12.58\u00b12.34 mg/dL for PH=60 and, 30 min respectively on the same clinical dataset. It was observed that inclusion of physical activity leads to improved glucose forecasting accuracy. Furthermore, all these results were obtained by training the model on only 8 days of clinical data of a single patient, followed by testing on clinical data on the following days. The results indicate that training on a single patient data may lead to better personalisation and better glucose forecasting results compared to existing works.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Deep Learning",
- "Blood Glucose",
- "Exercise",
- "Blood Glucose Self-Monitoring",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Precision Medicine",
- "Forecasting",
- "Cloud Computing",
- "Monitoring, Physiologic"
- ]
- },
- {
- "PMID": "39427575",
- "Title": "Psychiatry research",
- "ArticleTitle": "Impact of mental disorders on the all-cause mortality and cardiovascular disease outcomes in adults with new-onset type 1 diabetes: A nationwide cohort study.",
- "Abstract": "Mental disorders are associated with an elevated risk of all-cause mortality and CVD in adults with newly diagnosed type 1 diabetes. Early detection and greater attention to premature death and CVD development are required in patients with new-onset type 1 diabetes and mental disorders.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Cardiovascular Diseases",
- "Diabetes Mellitus, Type 1",
- "Adult",
- "Mental Disorders",
- "Middle Aged",
- "Republic of Korea",
- "Cohort Studies",
- "Young Adult",
- "Proportional Hazards Models",
- "Cause of Death",
- "Comorbidity"
- ]
- },
- {
- "PMID": "39427562",
- "Title": "Placenta",
- "ArticleTitle": "Gene expression profiles in placenta and their association with anesthesia, delivery mode and maternal diabetes.",
- "Abstract": "The findings reveal suppression of immune pathways and upregulation of ribosome activity in the placenta by maternal diabetes highlighting the importance of confounding factors when examining cell and tissue expression profiles. Further studies should determine whether the observed gene expression differences are related to underlying causes for cesarean section deliveries.",
- "Predictions": [],
- "MeshTerms": [
- "Pregnancy",
- "Female",
- "Humans",
- "Placenta",
- "Adult",
- "Diabetes, Gestational",
- "Transcriptome",
- "Cesarean Section",
- "Delivery, Obstetric",
- "Diabetes Mellitus, Type 1",
- "Gene Expression Profiling",
- "Pregnancy in Diabetics",
- "Anesthesia, Obstetrical"
- ]
- },
- {
- "PMID": "39426005",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "All-cause mortality and factors associated with it in Finnish patients with type 1 diabetes.",
- "Abstract": "There's substantial excess mortality due to DM1 in Finland. Interventions should focus on addressing both renal and cardiovascular risk factors but also pay more attention to mental health.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Finland",
- "Male",
- "Female",
- "Middle Aged",
- "Adult",
- "Risk Factors",
- "Registries",
- "Young Adult",
- "Cause of Death",
- "Diabetic Nephropathies",
- "Aged",
- "Comorbidity",
- "Adolescent",
- "Renal Insufficiency, Chronic",
- "Glomerular Filtration Rate",
- "Glycated Hemoglobin",
- "Mortality",
- "Cohort Studies",
- "Albuminuria"
- ]
- },
- {
- "PMID": "39425874",
- "Title": "Molecular biology reports",
- "ArticleTitle": "Association of polymorphism of NLRP3, ICAM-1, PTPN22, INS genes in childhood onset type 1 diabetes in a Pakistani population.",
- "Abstract": "The present study provides evidence that SNPs in the PTPN22, INS, NLRP3, and ICAM-1 genes are associated with the development of T1D. Further research is needed to explore their potential use in genetic screening and personalized medication.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Protein Tyrosine Phosphatase, Non-Receptor Type 22",
- "Intercellular Adhesion Molecule-1",
- "NLR Family, Pyrin Domain-Containing 3 Protein",
- "Diabetes Mellitus, Type 1",
- "Child",
- "Polymorphism, Single Nucleotide",
- "Male",
- "Female",
- "Genetic Predisposition to Disease",
- "Adolescent",
- "Pakistan",
- "Case-Control Studies",
- "Child, Preschool",
- "Gene Frequency",
- "Insulin",
- "Linkage Disequilibrium",
- "Genotype",
- "Haplotypes",
- "Genetic Association Studies"
- ]
- },
- {
- "PMID": "39423463",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "Characterizing the relationship between social determinants of health and risk of albuminuria among children with type 1 diabetes.",
- "Abstract": "In a cohort of 2303 children with type 1 diabetes (T1D), we found that non-English speaking status (HR 2.82, 95% CI 1.54-5.18) and public insurance (HR 1.48, 95% CI 1.07-2.05) were associated with an increased risk of incident albuminuria, after adjusting for T1D-related variables (age, hemoglobin A1c, diabetic ketoacidosis episodes with acute kidney injury).",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Albuminuria",
- "Female",
- "Male",
- "Child",
- "Social Determinants of Health",
- "Diabetic Nephropathies",
- "Adolescent",
- "Risk Factors",
- "Cohort Studies",
- "Child, Preschool",
- "Incidence"
- ]
- },
- {
- "PMID": "39423118",
- "Title": "Diabetes care",
- "ArticleTitle": "Efficacy and Safety of a Tubeless AID System Compared With Pump Therapy With CGM in the Treatment of Type 1 Diabetes in Adults With Suboptimal Glycemia: A Randomized, Parallel-Group Clinical Trial.",
- "Abstract": "Use of the tubeless AID system led to improved glycemic outcomes compared with pump therapy with CGM among adults with type 1 diabetes, underscoring the clinical benefit of AID and bolstering recommendations to establish AID systems as preferred therapy for this population.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Adult",
- "Insulin Infusion Systems",
- "Middle Aged",
- "Male",
- "Female",
- "Blood Glucose",
- "Insulin",
- "Adolescent",
- "Aged",
- "Young Adult",
- "Hypoglycemic Agents",
- "Glycated Hemoglobin",
- "Blood Glucose Self-Monitoring"
- ]
- },
- {
- "PMID": "39422057",
- "Title": "The Journal of international medical research",
- "ArticleTitle": "Factors associated with severe diabetic ketoacidosis in patients diagnosed with type 1 diabetes: a decade-long cross-sectional analysis.",
- "Abstract": "The present findings highlight the need for improving awareness about diabetes symptoms among physicians and the public to reduce the occurrence and severity of DKA at the onset of T1DM.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetic Ketoacidosis",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Female",
- "Adult",
- "Cross-Sectional Studies",
- "Retrospective Studies",
- "Severity of Illness Index",
- "Middle Aged",
- "Risk Factors",
- "Young Adult",
- "Body Mass Index",
- "Hospitalization",
- "Adolescent"
- ]
- },
- {
- "PMID": "39420935",
- "Title": "Archives of endocrinology and metabolism",
- "ArticleTitle": "Decoding the relationship between cow's milk proteins and development of type 1 diabetes mellitus.",
- "Abstract": "The findings of this study provide further evidence for a potential role of cow's milk proteins in triggering T1DM. The in silico analysis suggests that molecular mimicry mechanisms between cow's milk proteins and human beta-cell antigens may contribute to the autoimmune response leading to T1DM.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 1",
- "Humans",
- "Animals",
- "Cattle",
- "Milk Proteins",
- "Insulin-Secreting Cells",
- "Lactoglobulins",
- "Molecular Mimicry",
- "Insulin",
- "Autoantigens",
- "Zinc Transporter 8",
- "Glutamate Decarboxylase",
- "Computer Simulation",
- "Amino Acid Sequence",
- "Serum Albumin, Bovine",
- "Computational Biology"
- ]
- },
- {
- "PMID": "39420902",
- "Title": "Archives of endocrinology and metabolism",
- "ArticleTitle": "Clinical screening for GCK-MODY in 2,989 patients from the Brazilian Monogenic Diabetes Study Group (BRASMOD) and the Brazilian Type 1 Diabetes Study Group (BrazDiab1SG).",
- "Abstract": "This study identified a highly accurate (98%) composite model for differentiating GCK-MODY and T1D. This model may help clinicians select patients for genetic evaluation of monogenic diabetes, enabling them to implement correct treatment without overusing limited resources.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Diabetes Mellitus, Type 2",
- "Brazil",
- "Diabetes Mellitus, Type 1",
- "Adult",
- "Glycated Hemoglobin",
- "Adolescent",
- "ROC Curve",
- "Young Adult",
- "Mass Screening",
- "Child",
- "Blood Glucose",
- "Middle Aged",
- "Glucokinase",
- "Cohort Studies"
- ]
- },
- {
- "PMID": "39420900",
- "Title": "Archives of endocrinology and metabolism",
- "ArticleTitle": "Whom should we target? A brief report on a prospective study to identify predictors of mental health and self-care worsening in patients with diabetes mellitus during the COVID-19 pandemic.",
- "Abstract": "Some clinical and socioeconomic characteristics may be suitable for identifying patients at higher risk of mental health and self-care worsening, signaling who needs to be monitored more closely during crisis situations.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "COVID-19",
- "Female",
- "Male",
- "Middle Aged",
- "Prospective Studies",
- "Self Care",
- "Brazil",
- "Adult",
- "Aged",
- "Mental Health",
- "Diabetes Mellitus, Type 2",
- "Mental Disorders",
- "SARS-CoV-2",
- "Diabetes Mellitus, Type 1",
- "Pandemics"
- ]
- },
- {
- "PMID": "39420899",
- "Title": "Archives of endocrinology and metabolism",
- "ArticleTitle": "Clinical features most frequently present in patients with concomitant diabetic kidney disease and diabetic retinopathy.",
- "Abstract": "Among patients with DKD and type 2 diabetes, insulin use, longer diabetes duration, and higher systolic blood pressure level were associated with the presence of DR.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Diabetic Retinopathy",
- "Middle Aged",
- "Male",
- "Cross-Sectional Studies",
- "Diabetic Nephropathies",
- "Aged",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Brazil",
- "Adult",
- "Risk Factors",
- "Glomerular Filtration Rate"
- ]
- },
- {
- "PMID": "39420895",
- "Title": "Archives of endocrinology and metabolism",
- "ArticleTitle": "Euglycemic diabetic ketoacidosis in a patient with new-onset type 1 diabetes following a ketogenic diet: a potential risk of a dangerous dietary trend.",
- "Abstract": "Euglycemic diabetic ketoacidosis (DKA) is a rare complication of diabetes mellitus (DM) characterized by metabolic acidosis, ketosis, and blood glucose levels < 250 mg/dL. The prevalence of euglycemic DKA is increasing with the popularity of ketogenic (low-carbohydrate) diets. We present herein the case of a patient with newly diagnosed type 1 DM who developed euglycemic DKA following a ketogenic diet. A 22-year-old woman presented to the emergency department with malaise, fatigue, nausea, and vomiting. She had no family history of DM. She had consulted her primary care physician 2 weeks before due to hair loss, numbness, and tingling sensation in her fingertips. Her fasting blood glucose was 205 mg/dL at that time. Reluctant to use medication to control her blood glucose levels, she started a ketogenic diet. On admission, she was conscious, oriented, cooperative, and tachycardic. Her body mass index was 17.6 kg/m",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diet, Ketogenic",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Diabetic Ketoacidosis",
- "Young Adult",
- "Blood Glucose"
- ]
- },
- {
- "PMID": "39420876",
- "Title": "Archives of endocrinology and metabolism",
- "ArticleTitle": "Underreporting of diabetes mellitus as the cause of death in Bauru, State of S\u00e3o Paulo, Brazil over 40 years: a documental study.",
- "Abstract": "The underreporting of DM as the cause of death was very frequently found, and was associated with male gender, decade of death, shorter DM duration and DM2. If our data could be applied to the whole country, DM would possibly emerge as a more prominent cause of death in Brazil. Future studies in other cities and geographic regions are warranted to confirm our findings.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Brazil",
- "Male",
- "Female",
- "Cause of Death",
- "Middle Aged",
- "Adult",
- "Diabetes Mellitus, Type 2",
- "Aged",
- "Diabetes Mellitus, Type 1",
- "Young Adult",
- "Sex Factors",
- "Aged, 80 and over",
- "Adolescent"
- ]
- },
- {
- "PMID": "39420751",
- "Title": "Gut microbes",
- "ArticleTitle": "Gut microbial metabolic signatures in diabetes mellitus and potential preventive and therapeutic applications.",
- "Abstract": "Diabetes mellitus can be subdivided into several categories based on origin and clinical characteristics. The most common forms of diabetes are type 1 (T1D), type 2 diabetes (T2D) and gestational diabetes mellitus (GDM). T1D and T2D are chronic diseases affecting around 537 million adults worldwide and it is projected that these numbers will increase by 12% over the next two decades, while GDM affects up to 30% of women during pregnancy, depending on diagnosis methods. These forms of diabetes have varied origins: T1D is an autoimmune disease, while T2D is commonly associated with, but not limited to, certain lifestyle patterns and GDM can result of a combination of genetic predisposition and pregnancy factors. Despite some pathogenic differences among these forms of diabetes, there are some common markers associated with their development. For instance, gut barrier impairment and inflammation associated with an unbalanced gut microbiota and their metabolites may be common factors in diabetes development and progression. Here, we summarize the microbial signatures that have been linked to diabetes, how they are connected to diet and, ultimately, the impact on metabolite profiles resulting from host-gut microbiota-diet interactions. Additionally, we summarize recent advances relating to promising preventive and therapeutic interventions focusing on the targeted modulation of the gut microbiota to alleviate T1D, T2D and GDM.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Gastrointestinal Microbiome",
- "Diabetes Mellitus, Type 2",
- "Pregnancy",
- "Diabetes, Gestational",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Animals",
- "Diet",
- "Bacteria"
- ]
- },
- {
- "PMID": "39420387",
- "Title": "Journal of medical case reports",
- "ArticleTitle": "Treatment switch from multiple daily insulin injections to sulphonylureas in an African young adult diagnosed with HNF1A MODY: a case report.",
- "Abstract": "This case reveals that HNF1A maturity onset diabetes of the young (and probably other causes of monogenic diabetes) can present in sub-Saharan Africa. A diagnosis of maturity onset diabetes of the young can have significant life-changing therapeutic implications.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Diabetes Mellitus, Type 2",
- "Young Adult",
- "Hepatocyte Nuclear Factor 1-alpha",
- "Hypoglycemic Agents",
- "Insulin",
- "Sulfonylurea Compounds",
- "Diabetes Mellitus, Type 1",
- "Treatment Outcome"
- ]
- },
- {
- "PMID": "39420367",
- "Title": "Cardiovascular diabetology",
- "ArticleTitle": "Unseen threat: how subclinical atherosclerosis increases mortality risk in patients with type 1 diabetes.",
- "Abstract": "Subclinical atherosclerosis is independently associated with increased overall mortality and MACE in patients with type 1 diabetes. Identifying clinical predictors can improve risk stratification and personalised therapeutic strategies to prevent MACEs in this high-risk population.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Female",
- "Asymptomatic Diseases",
- "Middle Aged",
- "Risk Assessment",
- "Adult",
- "Time Factors",
- "Prevalence",
- "Prognosis",
- "Aged",
- "Risk Factors",
- "Spain",
- "Cause of Death",
- "Heart Disease Risk Factors",
- "Atherosclerosis",
- "Carotid Artery Diseases",
- "Biomarkers"
- ]
- },
- {
- "PMID": "39420138",
- "Title": "Journal of molecular medicine (Berlin, Germany)",
- "ArticleTitle": "Therapy concepts in type 1 diabetes mellitus treatment: disease modifying versus curative approaches.",
- "Abstract": "For many autoimmune diseases, including type 1 diabetes mellitus (T1DM), efforts have been made to modify the disease process through pharmacotherapy. The ultimate goal must be to develop therapies with curative potential by achieving an organ without signs of parenchymal cell destruction and without signs of immune cell infiltration. In the case of the pancreas, this means regenerated and well-preserved beta cells in the islets without activated infiltrating immune cells. Recent research has opened up the prospect of successful antibody combination therapy for autoimmune diabetes with curative potential. This goal cannot be achieved with monotherapies. The requirements for the implementation of such a therapy with curative potential for the benefit of patients with T1DM and LADA (latent autoimmune diabetes in adults) are considered.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Animals",
- "Insulin-Secreting Cells",
- "Immunotherapy"
- ]
- },
- {
- "PMID": "39419943",
- "Title": "Journal of molecular histology",
- "ArticleTitle": "Type I Diabetes Mellitus impairs cytotoxic immunity through CEACAM5 upregulation in colorectal cancer : Exploring the intersection of autoimmune dysfunction and cancer progression: the role of NF-\u03baB p65 in colorectal cancer.",
- "Abstract": "Type 1 diabetes (T1D) is characterized by an autoimmune-mediated destruction of pancreatic beta cells and a chronic inflammatory state, which may influence the progression of colorectal cancer (CRC) through immune system dysregulation and enhanced tumor immune evasion. This study aims to elucidate the role of p65 in modulating the tumor microenvironment in CRC within the context of T1D and to determine how this modulation affects tumor growth, immune cell infiltration, and the expression of immune evasion molecules such as CEACAM5. NOD mice, which model T1D, were inoculated with MC38 colon carcinoma cells engineered to knock down p65. Tumor growth was monitored, and the tumor microenvironment was analyzed using flow cytometry to assess the infiltration of immune cells. The expression of Ki-67 and CEACAM5 in tumor cells was also evaluated. Additionally, in vitro assays were conducted to study the proliferation and activation of T cells co-cultured with tumor cells. Knockdown of p65 in tumor cells significantly inhibited tumor growth in NOD mice. This was accompanied by an increased infiltration of cytotoxic CD8+ T cells and no significant change in CD4+\u2009or Foxp3\u2009+ T regulatory cells within the tumor microenvironment. There was a notable reduction in the expression of Ki-67 and CEACAM5, indicating decreased proliferation and potential immune evasion capabilities of the tumor cells. Our findings demonstrate that the NF-\u03baB p65 subunit plays a crucial role in promoting tumor growth and modulating the immune microenvironment in CRC, particularly in the context of T1D. Knocking down p65 not only reduces tumor progression but also enhances the anti-tumor immune response by decreasing immune evasion mechanisms. These results suggest that targeting the NF-\u03baB pathway may be a viable strategy to improve the efficacy of cancer immunotherapy, especially in patients with autoimmune diseases like T1D. Physical activity enhances the effect of immune checkpoint blockade by inhibiting the intratumoral HIF1-\u03b1/CEACAM5 axis.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Colorectal Neoplasms",
- "Diabetes Mellitus, Type 1",
- "Transcription Factor RelA",
- "Mice",
- "Tumor Microenvironment",
- "Disease Progression",
- "Mice, Inbred NOD",
- "Cell Line, Tumor",
- "Up-Regulation",
- "Humans",
- "Carcinoembryonic Antigen",
- "Female",
- "Cell Proliferation",
- "Gene Expression Regulation, Neoplastic",
- "GPI-Linked Proteins"
- ]
- },
- {
- "PMID": "39419452",
- "Title": "Antiviral research",
- "ArticleTitle": "Vemurafenib inhibits the replication of diabetogenic enteroviruses in intestinal epithelial and pancreatic beta cells.",
- "Abstract": "Enteroviruses, which infect via the gut, have been implicated in type 1 diabetes (T1D) development. Prolonged faecal shedding of enterovirus has been associated with islet autoimmunity. Additionally, enteroviral proteins and viral RNA have been detected in the pancreatic islets of individuals with recent-onset T1D, implicating their possible role in beta cell destruction. Despite this, no approved antiviral drugs currently exist that specifically target enterovirus infections for utilisation in disease interventions. Drug repurposing allows for the discovery of new clinical uses for existing drugs and can expedite drug discovery. Previously, the cancer drug Vemurafenib demonstrated unprecedented antiviral activity against several enteroviruses. In the present study, we assessed the efficacy of Vemurafenib and an analogue thereof in preventing infection or reducing the replication of enteroviruses associated with T1D. We tested Vemurafenib in intestinal epithelial cells (IECs) and insulin-producing beta cells. Additionally, we established a protocol for infecting human stem cell-derived islets (SC-islets) and used Vemurafenib and its analogue in this model. Our studies revealed that Vemurafenib exhibited strong antiviral properties in IECs and a beta cell line. The antiviral effect was also seen with the Vemurafenib analogue. SC-islets expressed the viral receptors CAR and DAF, with their highest expression in insulin- and glucagon-positive cells, respectively. SC-islets were successfully infected by CVBs and the antiviral activity of Vemurafenib and its analogue was confirmed in most SC-islet batches. In summary, our observations suggest that Vemurafenib and its analogue warrant further exploration as potential antiviral agents for the treatment of enterovirus-induced diseases, including T1D.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Virus Replication",
- "Insulin-Secreting Cells",
- "Vemurafenib",
- "Enterovirus",
- "Antiviral Agents",
- "Diabetes Mellitus, Type 1",
- "Cell Line",
- "Enterovirus Infections",
- "Epithelial Cells",
- "Intestinal Mucosa"
- ]
- },
- {
- "PMID": "39419044",
- "Title": "The lancet. Diabetes & endocrinology",
- "ArticleTitle": "Continuous glucose sensor accuracy: beyond the headline metric.",
- "Abstract": "The promotion of continuous glucose monitoring (CGM) to standard of care for type 1 diabetes and insulin-treated type 2 diabetes reflects a robust and wide evidence base for the technology's effectiveness supported by real-world efficacy data. Multiple CGM devices are available worldwide and are marketed, in part, based on accuracy data. In this Viewpoint, we argue that accuracy metrics are no longer a point of difference between CGM devices as almost all exceed an acceptable threshold. We also argue that domains of standardisation, clinical outcomes, and sustainability should now be given primacy as CGM devices seek to be implemented for new indications. These domains are key for the success of the next generation of CGM devices. Additionally, we discuss the need to address inequalities in accessing clinically impactful technologies.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Blood Glucose",
- "Blood Glucose Self-Monitoring",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39418532",
- "Title": "Diabetes care",
- "ArticleTitle": "Eighteen-Month Hybrid Closed-Loop Use in Very Young Children With Type 1 Diabetes: A Single-Arm Multicenter Trial.",
- "Abstract": "Use of the Cambridge hybrid CL system led to sustained improvements in glycemic control lasting more than 18 months in very young children with T1D.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Child, Preschool",
- "Male",
- "Female",
- "Insulin Infusion Systems",
- "Infant",
- "Child",
- "Cross-Over Studies",
- "Blood Glucose",
- "Hypoglycemic Agents",
- "Insulin"
- ]
- },
- {
- "PMID": "39414864",
- "Title": "Scientific reports",
- "ArticleTitle": "Clinical importance of cytokine (IL-6, IL-8, and IL-10) and vitamin D levels among patients with Type-1 diabetes.",
- "Abstract": "Type-1 diabetes (T1D) is an autoimmune disorder characterized by impaired insulin release by islet \u03b2 cells. It has been shown that proinflammatory cytokines released during the disease can exacerbate the condition, while anti-inflammatory cytokines offer protection. This study analyzed the clinical role of interleukin (IL)-6, -8, -10, and vitamin D levels in T1D patients compared to healthy controls. The levels of IL-6, IL-8, IL-10, and vitamin D in the participants' serum samples were analyzed using ELISA. The findings showed that T1D patients had significantly increased levels (p\u2009<\u20090.0001) of fasting blood glucose, HbA1c, systolic blood pressure, low-density lipoprotein, triglycerides, cholesterol, and very low-density lipoprotein and decreased levels of high-density lipoprotein and vitamin D (p\u2009<\u20090.0001) compared to healthy controls. Moreover, the levels of IL-6, IL-8, and IL-10 were also significantly greater (p\u2009<\u20090.0001) in T1D patients. The study also determined the significance of these cytokines among T1D patients and healthy controls using ROC curves. Furthermore, we found that smokers had significantly higher levels of IL-6 (p\u2009=\u20090.01) and IL-8 (p\u2009=\u20090.003) than non-smokers. These results showed that elevated levels of IL-6, IL-8, and IL-10, decreased vitamin D levels, and smoking among T1D participants could contribute to the worsening of T1D disease and could serve as predictive indicators.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Vitamin D",
- "Male",
- "Female",
- "Adult",
- "Interleukin-6",
- "Interleukin-10",
- "Interleukin-8",
- "Middle Aged",
- "Case-Control Studies",
- "Cytokines",
- "Blood Glucose",
- "Young Adult",
- "Clinical Relevance"
- ]
- },
- {
- "PMID": "39412084",
- "Title": "Acta paediatrica (Oslo, Norway : 1992)",
- "ArticleTitle": "Low-carbohydrate diet proved effective and safe for youths with type 1 diabetes: A randomised trial.",
- "Abstract": "Both diets improved glycaemic outcomes in adolescents and youths with type 1 diabetes, without increasing hypoglycaemia or cardiovascular risk factors, indicating comparable safety and efficacy.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Adolescent",
- "Diet, Carbohydrate-Restricted",
- "Blood Glucose",
- "Child",
- "Young Adult",
- "Diet, Mediterranean",
- "Glycated Hemoglobin"
- ]
- },
- {
- "PMID": "39411880",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Use of continuous glucose monitoring and hybrid closed-loop therapy in pregnancy.",
- "Abstract": "Continuous glucose monitoring (CGM) has led to a paradigm shift in the management of pregnant women with type 1 diabetes (T1D), with improved glycaemic control, less hypoglycaemia and fewer pregnancy complications. Data on CGM use in pregnant women with type 2 diabetes (T2D) are limited. A large randomized controlled trial (RCT) on CGM use in people with T2D in pregnancy is ongoing. Small studies on CGM use in women with gestational diabetes (GDM) have suggested improved glycaemic control and better qualification when insulin is needed. However, none of these studies was powered to evaluate pregnancy outcomes. Several large RCTs are ongoing in women with GDM. In addition to CGM, other technologies, such as advanced hybrid closed-loop (AHCL) systems have further improved glycaemic management in people with T1D. AHCL therapy adapts insulin delivery via a predictive algorithm integrated with CGM and an insulin pump. A large RCT with the AHCL CamAPS\u00ae FX demonstrated a 10% increase in time in range compared to standard insulin therapy in a pregnant population with T1D. Recently, an RCT of an AHCL system not approved for use in pregnancy (780G MiniMed) has also demonstrated additional benefits of AHCL therapy compared to standard insulin therapy, with improved time in range overnight, less hypoglycaemia and improved treatment satisfaction. More evidence is needed on the impact of AHCL therapy on maternal and neonatal outcomes and on which glycaemic targets with CGM should be used in pregnant women with T2D and GDM. We review the current evidence on the use of CGM and AHCL therapy in pregnancy.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Pregnancy",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Blood Glucose Self-Monitoring",
- "Pregnancy in Diabetics",
- "Diabetes, Gestational",
- "Insulin Infusion Systems",
- "Diabetes Mellitus, Type 2",
- "Insulin",
- "Hypoglycemic Agents",
- "Blood Glucose",
- "Glycemic Control",
- "Randomized Controlled Trials as Topic",
- "Hypoglycemia",
- "Pregnancy Outcome",
- "Algorithms",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39411715",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "TNF-\u03b1 inhibitors for type 1 diabetes: exploring the path to a pivotal clinical trial.",
- "Abstract": "Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing \u03b2-cells in the pancreas. This destruction leads to chronic hyperglycemia, necessitating lifelong insulin therapy to manage blood glucose levels. Typically diagnosed in children and young adults, T1D can, however, occur at any age. Ongoing research aims to uncover the precise mechanisms underlying T1D and to develop potential interventions. These include efforts to modulate the immune system, regenerate \u03b2-cells, and create advanced insulin delivery systems. Emerging therapies, such as closed-loop insulin pumps, stem cell-derived \u03b2-cell replacement and disease-modifying therapies (DMTs), offer hope for improving the quality of life for individuals with T1D and potentially moving towards a cure. Currently, there are no disease-modifying therapies approved for stage 3 T1D. Preserving \u03b2-cell function in stage 3 T1D is associated with better clinical outcomes, including lower HbA1c and decreased risk of hypoglycemia, neuropathy, and retinopathy. Tumor Necrosis Factor alpha (TNF-\u03b1) inhibitors have demonstrated efficacy at preserving \u03b2-cell function by measurement of C-peptide in two clinical trials in people with stage 3 T1D. However, TNF-\u03b1 inhibitors have yet to be evaluated in a pivotal trial for T1D. To address the promising clinical findings of TNF-\u03b1 inhibitors in T1D, Breakthrough T1D convened a panel of key opinion leaders (KOLs) in the field. The workshop aimed to outline an optimal clinical path for moving TNF-\u03b1 inhibitors to a pivotal clinical trial in T1D. Here, we summarize the evidence for the beneficial use of TNF-\u03b1 inhibitors in T1D and considerations for strategies collectively identified to advance TNF-\u03b1 inhibitors beyond phase 2 clinical studies for stage 3 T1D.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Tumor Necrosis Factor-alpha",
- "Clinical Trials as Topic",
- "Insulin-Secreting Cells",
- "Hypoglycemic Agents",
- "Animals"
- ]
- },
- {
- "PMID": "39411309",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Clinical perspective on innovative insulin delivery technologies in diabetes management.",
- "Abstract": "The present study highlights that physicians are generally supportive of utilizing new technology. The questionnaires and the open discussion revealed the expectation that the Smart MDI technology provides better control, primarily by identifying missed boluses, while expressing concerns on the use of the technology by teenagers and children, who might forget the device and be reluctant to use in public, and by the older population, who might be challenged by the technology.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Insulin",
- "Insulin Infusion Systems",
- "Surveys and Questionnaires",
- "Hypoglycemic Agents",
- "Diabetes Mellitus",
- "Blood Glucose Self-Monitoring",
- "Diabetes Mellitus, Type 1",
- "Disease Management",
- "Blood Glucose"
- ]
- },
- {
- "PMID": "39410774",
- "Title": "Journal of pediatric gastroenterology and nutrition",
- "ArticleTitle": "Is HLA-DQ typing useful in screening for celiac disease among Arabs with type 1 diabetes? A case-control study.",
- "Abstract": "Only 4% of Saudi patients with T1D carry DQ-genotypes at no risk to develop CD, which supports the European guidelines that recommend celiac serology test as the most cost-effective screening method. We identified the risk gradient associated with DQ-genotypes to develop CD in our population which could help in counseling patients for the risk to develop CD and planning follow-up serology tests.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Celiac Disease",
- "Diabetes Mellitus, Type 1",
- "Adolescent",
- "Case-Control Studies",
- "Female",
- "Male",
- "HLA-DQ Antigens",
- "Child",
- "Young Adult",
- "Arabs",
- "Genotype",
- "Genetic Predisposition to Disease",
- "Adult",
- "Mass Screening"
- ]
- },
- {
- "PMID": "39408940",
- "Title": "International journal of molecular sciences",
- "ArticleTitle": "Unravelling the Role of Gut and Oral Microbiota in the Pediatric Population with Type 1 Diabetes Mellitus.",
- "Abstract": "Type 1 Diabetes Mellitus (T1DM) is a chronic autoimmune disease that results in the destruction of pancreatic \u03b2 cells, leading to hyperglycaemia and the need for lifelong insulin therapy. Although genetic predisposition and environmental factors are considered key contributors to T1DM, the exact causes of the disease remain partially unclear. Recent evidence has focused on the relationship between the gut, the oral cavity, immune regulation, and systemic inflammation. In individuals with T1DM, changes in the gut and oral microbial composition are commonly observed, indicating that dysbiosis may contribute to immune dysregulation. Gut dysbiosis can influence the immune system through increased intestinal permeability, altered production of short chain fatty acids (SCFAs), and interactions with the mucosal immune system, potentially triggering the autoimmune response. Similarly, oral dysbiosis may contribute to the development of systemic inflammation and thus influence the progression of T1DM. A comprehensive understanding of these relationships is essential for the identification of biomarkers for early diagnosis and monitoring, as well as for the development of therapies aimed at restoring microbial balance. This review presents a synthesis of current research on the connection between T1DM and microbiome dysbiosis, with a focus on the gut and oral microbiomes in pediatric populations. It explores potential mechanisms by which microbial dysbiosis contributes to the pathogenesis of T1DM and examines the potential of microbiome-based therapies, including probiotics, prebiotics, synbiotics, and faecal microbiota transplantation (FMT). This complex relationship highlights the need for longitudinal studies to monitor microbiome changes over time, investigate causal relationships between specific microbial species and T1DM, and develop personalised medicine approaches.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Gastrointestinal Microbiome",
- "Dysbiosis",
- "Child",
- "Mouth",
- "Probiotics",
- "Fecal Microbiota Transplantation",
- "Prebiotics",
- "Microbiota"
- ]
- },
- {
- "PMID": "39408305",
- "Title": "Nutrients",
- "ArticleTitle": "Nutrition and Glycemic Control in Children and Adolescents with Type 1 Diabetes Mellitus Attending Diabetes Camps.",
- "Abstract": {
- "b": "Conclusions:"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Adolescent",
- "Child",
- "Glycemic Control",
- "Patient Education as Topic",
- "Camping",
- "Blood Glucose",
- "Female",
- "Nutritional Status",
- "Male",
- "Insulin",
- "Blood Glucose Self-Monitoring"
- ]
- },
- {
- "PMID": "39407190",
- "Title": "BMC oral health",
- "ArticleTitle": "Genetic and therapeutic for oral lichen planus and diabetes mellitus: a comprehensive study.",
- "Abstract": "The study highlighted a complex interplay between diabetes and OLP, underscoring the efficacy of integrated therapeutic strategies that target both conditions. The findings suggest that both pharmaceutical and herbal treatments can effectively manage the clinical manifestations of OLP and associated metabolic challenges. This holistic approach to treatment could significantly enhance patient outcomes by addressing the interconnected aspects of these chronic conditions.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Lichen Planus, Oral",
- "Glycated Hemoglobin",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Mendelian Randomization Analysis",
- "Blood Glucose",
- "Drugs, Chinese Herbal",
- "Hypoglycemic Agents"
- ]
- },
- {
- "PMID": "39406740",
- "Title": "Nature communications",
- "ArticleTitle": "TGF-\u03b2-mediated crosstalk between TIGIT",
- "Abstract": "Type 1 diabetes (T1D) is a chronic autoimmune condition characterized by hyperglycemia resulting from the destruction of insulin-producing \u03b2-cells that is traditionally deemed irreversible, but partial remission (PR) with temporary reversal of hyperglycemia is sometimes observed. Here we use single-cell RNA sequencing to delineate the immune cell landscape across patients in different T1D stages. Together with cohort validation and functional assays, we observe dynamic changes in TIGIT",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 1",
- "Animals",
- "T-Lymphocytes, Regulatory",
- "CD8-Positive T-Lymphocytes",
- "Antigens, Differentiation, T-Lymphocyte",
- "Mice",
- "Humans",
- "Transforming Growth Factor beta",
- "Receptors, Immunologic",
- "Male",
- "Disease Progression",
- "Female",
- "Diabetes Mellitus, Experimental",
- "Adult",
- "Mice, Inbred NOD",
- "Receptors, CCR7",
- "Insulin-Secreting Cells",
- "Adolescent",
- "Young Adult",
- "Cell Communication",
- "T Lineage-Specific Activation Antigen 1"
- ]
- },
- {
- "PMID": "39405732",
- "Title": "Computers in biology and medicine",
- "ArticleTitle": "Riemannian manifold-based geometric clustering of continuous glucose monitoring to improve personalized diabetes management.",
- "Abstract": "This study demonstrates the utility of UMAP in enhancing the analysis of CGM data for diabetes management. We revealed distinct clustering of glycemic profiles between healthy individuals and diabetics on daily insulin indicating that in most instances insulin does not restore a normal glycemic phenotype. In addition, the SS quantifies day by day the degree of this continued dysglycemia and therefore potentially offers a novel approach for personalized diabetes care.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Blood Glucose Self-Monitoring",
- "Blood Glucose",
- "Precision Medicine",
- "Male",
- "Female",
- "Cluster Analysis",
- "Insulin",
- "Adult",
- "Glycated Hemoglobin",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39404844",
- "Title": "Diabetologia",
- "ArticleTitle": "Quantitative analysis of islet prohormone convertase 1/3 expression in human pancreas donors with diabetes.",
- "Abstract": "Our high-resolution histomorphological analysis of human pancreatic islets from donors with and without diabetes has uncovered details of the cellular origin of islet prohormone peptide processing defects. Reduced beta cell PC1/3 and increased alpha cell PC1/3 in islets from donors with type 1 diabetes pinpointed the functional deterioration of beta cells and the concomitant potential increase in PC1/3 usage for prohormone processing in alpha cells during the pathogenesis of type 1 diabetes. Our finding of PC1/3 loss in beta cells may inform the discovery of new prohormone biomarkers as indicators of beta cell dysfunction, and the finding of elevated PC1/3 expression in alpha cells may encourage the design of therapeutic targets via leveraging alpha cell adaptation in diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Proprotein Convertase 1",
- "Diabetes Mellitus, Type 1",
- "Islets of Langerhans",
- "Male",
- "Female",
- "Adult",
- "Glucagon-Secreting Cells",
- "Tissue Donors",
- "Middle Aged",
- "Diabetes Mellitus, Type 2",
- "Insulin-Secreting Cells",
- "Cross-Sectional Studies",
- "Young Adult",
- "Pancreas"
- ]
- },
- {
- "PMID": "39402605",
- "Title": "Italian journal of pediatrics",
- "ArticleTitle": "Promising predictors of diabetic peripheral neuropathy in children and adolescents with type 1 diabetes mellitus.",
- "Abstract": "Despite limited research in pediatrics, MNSI and serum NSE are promising predictive tools for DPN in children and adolescents with T1DM, even when they are asymptomatic. Poor glycemic control and lipid profile changes may play a critical role in the development of DPN in these patients, despite conflicting results in various studies.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 1",
- "Diabetic Neuropathies",
- "Male",
- "Female",
- "Adolescent",
- "Child",
- "Case-Control Studies",
- "Biomarkers",
- "Neural Conduction",
- "Phosphopyruvate Hydratase",
- "Predictive Value of Tests",
- "HSP27 Heat-Shock Proteins",
- "Neurologic Examination",
- "Prevalence",
- "Heat-Shock Proteins",
- "Molecular Chaperones"
- ]
- },
- {
- "PMID": "39401129",
- "Title": "Cell transplantation",
- "ArticleTitle": "Xenogenic Engraftment of Human-Induced Pluripotent Stem Cell-Derived Pancreatic Islet Cells in an Immunosuppressive Diabetic G\u00f6ttingen Mini-Pig Model.",
- "Abstract": "In the development of cell therapy products, immunocompromised animal models closer in size to humans are valuable for enhancing the translatability of ",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Swine",
- "Humans",
- "Swine, Miniature",
- "Induced Pluripotent Stem Cells",
- "Islets of Langerhans",
- "Islets of Langerhans Transplantation",
- "Diabetes Mellitus, Experimental",
- "Transplantation, Heterologous",
- "Diabetes Mellitus, Type 1",
- "Disease Models, Animal",
- "Immunosuppressive Agents"
- ]
- },
- {
- "PMID": "39399499",
- "Title": "Frontiers in immunology",
- "ArticleTitle": "Enhancing human islet xenotransplant survival and function in diabetic immunocompetent mice through LRH-1/NR5A2 pharmacological activation.",
- "Abstract": "The intricate etiology of type 1 diabetes mellitus (T1D), characterized by harmful interactions between the immune system and insulin-producing beta cells, has hindered the development of effective therapies including human islet transplantation, which requires strong immunosuppressants that impair beta cell survival and function. As such alternative immunomodulating therapies are required for successful transplantation. The discovery that pharmacological activation of the nuclear receptor LRH-1/NR5A2 can reverse hyperglycemia in mouse models of T1D by altering, and not suppressing the autoimmune attack, prompted us to investigate whether LRH-1/NR5A2 activation could improve human islet function/survival after xenotransplantation in immunocompetent mice. Human islets were transplanted under the kidney capsule of streptozotocin (STZ)-induced diabetic mice, and treatment with BL001 (LRH-1/NR5A2 agonist) or vehicle was administered one week post-transplant. Our study, encompassing 3 independent experiments with 3 different islet donors, revealed that mice treated for 8 weeks with BL001 exhibited lower blood glucose levels correlating with improved mouse survival rates as compared to vehicle-treated controls. Human C-peptide was detectable in BL001-treated mice at both 4 and 8 weeks indicating functional islet beta cells. Accordingly, in mice treated with BL001 for 8 weeks, the beta cell mass was preserved, while a significant decrease in alpha cells was observed compared to mice treated with BL001 for only 4 weeks. In contrast, vehicle-treated mice exhibited a reduction in insulin-expressing cells at 8 weeks compared to those at 4 weeks. These results suggest that BL001 significantly enhances the survival, engraftment, and functionality of human islets in a STZ-induced diabetic mouse model.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Humans",
- "Islets of Langerhans Transplantation",
- "Diabetes Mellitus, Experimental",
- "Mice",
- "Graft Survival",
- "Transplantation, Heterologous",
- "Receptors, Cytoplasmic and Nuclear",
- "Diabetes Mellitus, Type 1",
- "Male",
- "Blood Glucose",
- "Islets of Langerhans",
- "Insulin-Secreting Cells"
- ]
- },
- {
- "PMID": "39398332",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Exploring the influencing factors of non-insulin drug prescriptions in discharged patients with type 1 diabetes.",
- "Abstract": "We identified notable factors that influence discharge prescriptions in patients with T1D. In order to enhance the treatment outcome for the patient, clinicians ought to have a special focus on these indicators or factors.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Diabetes Mellitus, Type 1",
- "Adult",
- "Hypoglycemic Agents",
- "Middle Aged",
- "Patient Discharge",
- "Insulin",
- "Drug Prescriptions",
- "Blood Glucose",
- "Young Adult",
- "Body Mass Index",
- "Adolescent"
- ]
- },
- {
- "PMID": "39397502",
- "Title": "The Israel Medical Association journal : IMAJ",
- "ArticleTitle": "Hospitalization Outcomes of Patients with Type 2 Diabetes Mellitus Complicated with Diabetic Ketoacidosis.",
- "Abstract": "Our findings underscore the importance of recognizing DKA as a substantial complication in diabetic patients, particularly those with T2DM. Vigilance in management, adherence to DKA guidelines, and awareness of triggers such as SGLT2 inhibitors are crucial for improving outcomes in this population.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetic Ketoacidosis",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Retrospective Studies",
- "Middle Aged",
- "Hospitalization",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Hospital Mortality",
- "Aged",
- "Israel",
- "Diabetes Mellitus, Type 1",
- "Adult",
- "Length of Stay",
- "Patient Readmission"
- ]
- },
- {
- "PMID": "39397476",
- "Title": "Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences",
- "ArticleTitle": "[Fulminant type 1 diabetes mellitus with acute pancreatitis: A case report and literature review].",
- "Abstract": "The objective was to report a relatively rare case of fulminant type 1 diabetes (FT1DM) complicated with acute pancreatitis (AP), to summarize the characteristics as well as experience of diagnosis and treatment, and to explore its pathogenesis. Clinical data of a case of FT1DM complicated with AP in the Department of Endocrinology of our hospital were analyzed retrospectively. A 66-year-old male presented with acute fever and abdominal pain, accompanying with the significantly elevated pancreatic enzymes, and his abdominal CT scan showed exudation around the pancreas. The clinical manifestations mentioned above were consistent with the diagnosis of AP. Five days after onset, the patient developed clinical symptoms, such as obvious thirst, polyuria, polyasthenia and fatigue. Meanwhile, his plasma glucose increased significantly and the diabetic ketoacidosis (DKA) occurred. The patient's fasting and postprandial 2 hours C peptide decreased significantly (all 0.02 \u03bcg/L), glycated hemoglobin level was not high (6%), and his islet-related autoantibodies were undetectable. Thus, the patient could be diagnosed with FT1DM. After the treatment of fasting, fluid replacement, anti-infection, somatostatin, anticoagulation and intravenous insulin sequential subcutaneous insulin pump, the patient gained the alleviation of pancreatitis, restoration of oral intake, and relatively stable blood glucose levels. Summarizing the characte-ristics of this case and reviewing the literature, FT1DM complicated with AP was relatively rare in FT1DM. Its common characteristics were described below: (1) Most cases started with AP and the blood glucose elevated within 1 week, or some cases had the simultaneously onset of AP and FT1DM. (2) The clinical course of AP was short and relieved no more than 1 week; Pancreatic imaging could completely return to normal within 1 to 4 weeks after onset. (3) The etiology of AP most was idiopathic; The elevation of pancreatic enzyme level was slight and the recovery was rapidly compared with AP of other etiologies. FT1DM could be complicated with AP, which was different from the physiological manifestations of pancreatic disease in general FT1DM patients. Virus infection mignt be the common cause of AP and FT1DM, and AP might be the early clinical manifestation of some FT1DM. The FT1DM patients developed with abdominal pain was easy to be missed, misdiagnosed and delayed, which should receive more attention in clinic.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Diabetes Mellitus, Type 1",
- "Aged",
- "Pancreatitis",
- "Acute Disease",
- "Diabetic Ketoacidosis"
- ]
- },
- {
- "PMID": "39396694",
- "Title": "Experimental eye research",
- "ArticleTitle": "Hyperglycemia-depleted glutamine contributes to the pathogenesis of diabetic corneal endothelial dysfunction.",
- "Abstract": "Diabetic mellitus (DM) causes various complications, including the corneal endothelial dysfunction that leads to corneal edema and vision loss, especially in the DM patients with intraocular surgeries. However, the pathogenic mechanism of hyperglycemia-caused corneal endothelial dysfunction remains incomplete understood. Here we firstly screened and identified the glutamine contents of aqueous humor (AH) were significantly reduced in the type 2 diabetic patients and type 1 and type 2 diabetic mice. To explore the potential therapeutic effects of glutamine (Gln) supplement on the protection of diabetic corneal endothelial dysfunction, we performed the anterior chamber perfusion with the addition of L-alanyl-L-glutamine (Ala-Gln), and confirmed that Ala-Gln supplement not only accelerated the resolution of corneal edema and recovery of corneal thickness, but also preserved the regular arrangement and barrier-pump function of cornea. Mechanistically, we revealed that the supplements of Ala-Gln protect corneal endothelial cells (CECs) from the deleterious effects of high glucose-induced oxidative stress, mitochondrial dysfunction, and cell apoptosis. Overall, these results indicate the Gln depletion plays an important role in the diabetic corneal endothelial dysfunction, while the Ala-Gln supplement during intraocular surgery provide an effective prevention strategy through regulating the redox homeostasis and mitochondrial function of corneal endothelium.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Endothelium, Corneal",
- "Glutamine",
- "Mice",
- "Diabetes Mellitus, Experimental",
- "Hyperglycemia",
- "Humans",
- "Male",
- "Oxidative Stress",
- "Mice, Inbred C57BL",
- "Aqueous Humor",
- "Diabetes Mellitus, Type 2",
- "Apoptosis",
- "Female",
- "Middle Aged",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39396521",
- "Title": "Immunity",
- "ArticleTitle": "Autoimmune CD4",
- "Abstract": "Self-reactive T\u00a0cells experience chronic antigen exposure but do not exhibit signs of exhaustion. Here, we investigated the mechanisms for sustained, functioning autoimmune CD4",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "CD4-Positive T-Lymphocytes",
- "Hepatocyte Nuclear Factor 1-alpha",
- "Mice",
- "Diabetes Mellitus, Type 1",
- "Lymphocyte Activation",
- "Mice, Inbred NOD",
- "Cell Differentiation",
- "Epigenesis, Genetic",
- "Autoimmunity",
- "T Cell Transcription Factor 1",
- "DNA Methylation"
- ]
- },
- {
- "PMID": "39395647",
- "Title": "Brain research",
- "ArticleTitle": "Ferroptosis-associated alterations in diabetes following ischemic stroke: Insights from RNA sequencing.",
- "Abstract": "Our bulk RNA sequencing and bioinformatics analyses show that altered ferroptosis signaling pathway was associated with the exacerbation of experimental stroke injury under diabetic condition. Especially, additional investigation into the mechanisms of SLC25A28 and SCP2 in diabetes-exacerbated stroke will be explored in the future study.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Ferroptosis",
- "Male",
- "Mice",
- "Diabetes Mellitus, Experimental",
- "Ischemic Stroke",
- "Sequence Analysis, RNA",
- "Mice, Inbred C57BL",
- "Infarction, Middle Cerebral Artery",
- "Brain Ischemia",
- "Diabetes Mellitus, Type 1",
- "Stroke",
- "Disease Models, Animal"
- ]
- },
- {
- "PMID": "39395533",
- "Title": "Contemporary clinical trials",
- "ArticleTitle": "DiaBetter Together: Clinical trial protocol for a strengths-based Peer Mentor intervention for young adults with type 1 diabetes transitioning to adult care.",
- "Abstract": "The goal of this research is to evaluate a developmentally appropriate, supportive intervention that can improve T1D self-management and successful transfer of care during the difficult young adult years and promote optimal T1D health outcomes.",
- "Predictions": [],
- "MeshTerms": [
- "Adolescent",
- "Adult",
- "Female",
- "Humans",
- "Male",
- "Young Adult",
- "Diabetes Mellitus, Type 1",
- "Mentors",
- "Peer Group",
- "Quality of Life",
- "Self Care",
- "Transition to Adult Care"
- ]
- },
- {
- "PMID": "39476370",
- "Title": "Journal of medical Internet research",
- "ArticleTitle": "Characterization of Telecare Conversations on Lifestyle Management and Their Relation to Health Care Utilization for Patients with Heart Failure: Mixed Methods Study.",
- "Abstract": "Our approach and findings offer novel perspectives on the content, structure, and clinical associations of telehealth conversations on lifestyle management for patients with HF. Hence, our study could inform ways to enhance telehealth programs for self-care management in chronic conditions.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Heart Failure",
- "Telemedicine",
- "Female",
- "Male",
- "Life Style",
- "Aged",
- "Middle Aged",
- "Patient Acceptance of Health Care",
- "Diabetes Mellitus, Type 2",
- "Communication"
- ]
- },
- {
- "PMID": "39476235",
- "Title": "JAMA network open",
- "ArticleTitle": "Cardiovascular Risks With SGLT2 Inhibitors in Clinical Practice Among Patients With Type 2 Diabetes.",
- "Abstract": "In this cohort study of patients with T2D, the use of SGLT2is vs DPP4is was associated with reduced total cardiovascular burden, suggesting that long-term use of this therapy may optimize treatment benefit among patients with chronic CVD. The SGLT2i-associated benefit among patients with high risk of CVD encourages the prioritization of SGLT2i use for these vulnerable individuals.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Male",
- "Female",
- "Middle Aged",
- "Retrospective Studies",
- "Cardiovascular Diseases",
- "Dipeptidyl-Peptidase IV Inhibitors",
- "Aged",
- "Taiwan",
- "Heart Disease Risk Factors",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39476038",
- "Title": "Arquivos brasileiros de cardiologia",
- "ArticleTitle": "Causal Relationship between Television Viewing Time, Cardiovascular Diseases, and Potential Mechanisms.",
- "Abstract": "An overview of the effect of television viewing time on cardiovascular diseases and biomarkers of cardiometabolic risk.",
- "Predictions": [],
- "MeshTerms": [
- "Television",
- "Screen Time",
- "Cardiovascular Diseases",
- "Polymorphism, Single Nucleotide",
- "Sedentary Behavior",
- "Diabetes Mellitus, Type 2",
- "Biomarkers",
- "UK Biobank",
- "Leisure Activities"
- ]
- },
- {
- "PMID": "39475846",
- "Title": "Journal of molecular endocrinology",
- "ArticleTitle": "The role of mu-opioid receptors in pancreatic islet \u03b1-cells.",
- "Abstract": "Diabetes is a complex disease that impacts more than 500 million people across the world. Many of these individuals will develop diabetic neuropathy as a comorbidity, which is historically treated with exogenous opioids, such as morphine, oxycodone, or tramadol. Although these opioids are effective analgesics, growing evidence indicates that they may directly impact the endocrine pancreas function in patients. One common feature of these exogenous opioid ligands is their preference for the mu-opioid receptor (MOPR), so we aimed to determine whether endogenous MOPRs directly regulate pancreatic islet metabolism and hormone secretion. We show that pharmacological antagonism of MOPRs enhances glucagon secretion, but not insulin secretion, from human islets under high-glucose conditions. This increased secretion is accompanied by increased cAMP signaling. mRNA expression of MOPRs is robust in nondiabetic human islets but downregulated in islets from T2D donors, suggesting a link between metabolism and MOPR expression. Conditional genetic knockout of MOPRs in murine \u03b1-cells increases glucagon secretion under high-glucose conditions without increasing glucagon content. Consistent with downregulation of MOPRs during metabolic disease, conditional MOPR knockout mice treated with a high-fat diet show impaired glucose tolerance, increased glucagon secretion, increased insulin content, and increased islet size. Together, these results demonstrate a direct mechanism of action for endogenous opioid regulation of endocrine pancreas.",
- "Predictions": [],
- "MeshTerms": [
- "Receptors, Opioid, mu",
- "Animals",
- "Humans",
- "Glucagon-Secreting Cells",
- "Mice, Knockout",
- "Glucagon",
- "Mice",
- "Male",
- "Glucose",
- "Insulin",
- "Islets of Langerhans",
- "Cyclic AMP",
- "Diabetes Mellitus, Type 2",
- "Diet, High-Fat",
- "Female"
- ]
- },
- {
- "PMID": "39475132",
- "Title": "Endokrynologia Polska",
- "ArticleTitle": "Identification of fibrosis-associated lncRNAs in diabetic cardiomyopathy patients.",
- "Abstract": "Our study disclosed a subset of lncRNAs and mRNAs that are implicated in diabetic cardiomyopathy and myocardial fibrosis, thereby presenting themselves as promising biomarkers and therapeutic targets for the management of both diabetic cardiomyopathy and myocardial fibrosis.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetic Cardiomyopathies",
- "RNA, Long Noncoding",
- "Rats",
- "Animals",
- "Humans",
- "Fibrosis",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Middle Aged",
- "RNA, Messenger"
- ]
- },
- {
- "PMID": "39475130",
- "Title": "Endokrynologia Polska",
- "ArticleTitle": "The correlation between S-nitrosylation and type 2 diabetes mellitus: a review.",
- "Abstract": "Type 2 diabetes mellitus (T2DM) represents a chronic metabolic disorder, constituting over 90% of all diabetes cases. Its primary characteristics include insulin deficiency and insulin resistance. The aetiology of T2DM is complex, which is attributed to a convergence of genetic and environmental factors. Moreover, it can engender various complications such as diabetes retinopathy, diabetes nephropathy, and diabetes neuropathy. T2DM cannot be cured fundamentally, it can only delay the development of the disease by controlling the blood sugar level. If the blood sugar is at a high level for a long time, it will aggravate the disease progress, and even lead to death in serious cases. Therefore, understanding the pathogenesis of diabetes, early detection, and intervention are the main means of treatment. S-nitrosylation (SNO), a post-translational modification of proteins based on redox, possesses the capacity to regulate a variety of physiological and pathological processes, and it is also involved in the occurrence and development of T2DM. However, the relationship between the dysregulation of SNO homeostasis and the occurrence of diabetes is not fully understood. This article reviews the correlation between SNO and T2DM, elucidating the mechanism by which SNO contributes to T2DM, encompassing diminishing insulin secretion, inducing insulin resistance, and affecting glucokinase activity. Understanding the correlation between SNO and T2DM provides a new research direction for the pathogenesis and treatment targets of diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 2",
- "Humans",
- "Insulin Resistance",
- "Protein Processing, Post-Translational",
- "Insulin"
- ]
- },
- {
- "PMID": "39475035",
- "Title": "British journal of hospital medicine (London, England : 2005)",
- "ArticleTitle": "Advances in Research on the Anticancer Properties and Mechanisms of Metformin in Lung Cancer.",
- "Abstract": "Lung cancer is a leading cause of death globally with high mortality and morbidity. Patients are often diagnosed at an advanced stage. Metformin has become a primary medication used in the clinical management of type 2 diabetes mellitus (T2DM) due to its relative safety, low cost, and effectiveness, mainly exerting its hypoglycemic effect by inhibiting hepatic gluconeogenesis and insulin resistance. Research data indicate that metformin extends the distant metastasis-free survival (DMFS) and progression-free survival (PFS) of diabetic patients with lung cancer, improving overall survival rates. Metformin lowers the risk of tumour development through various mechanisms, including the adenosine 5'-monophosphate-activated protein kinase/liver kinase B1/mechanistic target of rapamycin (AMPK/LKB1/mTOR) pathway, insulin-like growth factor-1 receptor pathway, apoptosis, and autophagy. However, research findings are not entirely consistent. This article reviews the research progress of metformin in terms of lung cancer treatment within the past few years, aiming to provide a more comprehensive understanding of how metformin exerts its anti-cancer impact and how it can be clinically applied, as well as provide new insights for lung cancer treatment.",
- "Predictions": [],
- "MeshTerms": [
- "Metformin",
- "Humans",
- "Lung Neoplasms",
- "Hypoglycemic Agents",
- "Antineoplastic Agents",
- "Diabetes Mellitus, Type 2",
- "Autophagy",
- "Signal Transduction",
- "TOR Serine-Threonine Kinases"
- ]
- },
- {
- "PMID": "39475024",
- "Title": "British journal of hospital medicine (London, England : 2005)",
- "ArticleTitle": "Impact of Co-Management Mode on Diagnosis and Treatment Compliance in Community-Level Diabetic Patients with Retinopathy.",
- "Abstract": {
- "b": "Conclusion",
- "i": "p"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetic Retinopathy",
- "Male",
- "Female",
- "Middle Aged",
- "Retrospective Studies",
- "Aged",
- "Self-Management",
- "Glycated Hemoglobin",
- "Blood Glucose",
- "Patient Compliance",
- "Blood Pressure",
- "Diabetes Mellitus, Type 2",
- "China",
- "Self Care"
- ]
- },
- {
- "PMID": "39475012",
- "Title": "The British journal of nutrition",
- "ArticleTitle": "Perspective on the health effects of unsaturated fatty acids and commonly consumed plant oils high in unsaturated fat.",
- "Abstract": "Epidemiological and clinical trial evidence indicates that ",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Plant Oils",
- "Fatty Acids, Unsaturated",
- "Cardiovascular Diseases",
- "Diabetes Mellitus, Type 2",
- "Dietary Fats, Unsaturated",
- "Fatty Acids, Omega-6",
- "Diet"
- ]
- },
- {
- "PMID": "39474832",
- "Title": "Medical decision making : an international journal of the Society for Medical Decision Making",
- "ArticleTitle": "Using QALYs as an Outcome for Assessing Global Prediction Accuracy in Diabetes Simulation Models.",
- "Abstract": "Diabetes simulation models are currently validated by examining their ability to predict the incidence of individual events (e.g., myocardial infarction, stroke, amputation) or composite events (e.g., first major adverse cardiovascular event).We introduce Q",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Quality-Adjusted Life Years",
- "Computer Simulation",
- "Hypoglycemic Agents",
- "Diabetes Mellitus, Type 2",
- "Cost-Benefit Analysis",
- "United Kingdom",
- "Technology Assessment, Biomedical",
- "Diabetes Mellitus",
- "Female",
- "Male"
- ]
- },
- {
- "PMID": "39474830",
- "Title": "Nederlands tijdschrift voor geneeskunde",
- "ArticleTitle": "[Acute blindness in a patient with metformin-associated lactic acidosis].",
- "Abstract": "Lactic acidosis is a rare metabolic complication that can occur in patients with diabetes mellitus type 2 who use metformin. We discuss a 79-year old woman with metformin-associated lactic acidosis (MALA) and acute kidney injury based on gastroenteritis. Patient reported acute blindness which in literature is described as a rare presentation of a metabolic acidosis (regardless of its underlying cause). Immediate treatment with hemodialysis led to improvement of the acidosis and complete recovery of the vision. It is important that patients who use metformin are instructed to consult their health care provider and/or discontinue metformin in case of intercurrent diseases.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Metformin",
- "Acidosis, Lactic",
- "Aged",
- "Female",
- "Diabetes Mellitus, Type 2",
- "Blindness",
- "Hypoglycemic Agents",
- "Renal Dialysis",
- "Acute Kidney Injury",
- "Acute Disease",
- "Gastroenteritis",
- "Treatment Outcome"
- ]
- },
- {
- "PMID": "39474653",
- "Title": "AIDS (London, England)",
- "ArticleTitle": "Hepatic steatosis-insulin resistance and type 2 diabetes in people with HIV at diagnosis: effect of initial antiretroviral therapy.",
- "Abstract": "We evaluated the impact of hepatic steatosis-insulin resistance (HS-IR) and liver fibrosis (LF) on type 2 diabetes mellitus (DM2) using triglyceride-glucose (TyG) and Fibrosis-4 (FIB-4). The incidence of DM2 was 12.9 [95% confidence interval (CI), 16.9-9.7] and 9.8 (95% CI, 6.9-13.6) per 1000 person-years in HS-IR and LF. The prevalence of HS-IR was significantly lower at 12 and 24\u200amonths with TDF + (3TC or FTC) + RPV [hazard ratio (HR) 0.5 [95% CI, 0.3-0.8], P\u200a<\u200a0.01 at 12\u200amonths; 0.6 [0.4-0.9], P\u200a=\u200a0.01 at 24\u200amonths].",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Insulin Resistance",
- "Male",
- "HIV Infections",
- "Female",
- "Middle Aged",
- "Adult",
- "Fatty Liver",
- "Incidence",
- "Anti-Retroviral Agents",
- "Prevalence",
- "Liver Cirrhosis"
- ]
- },
- {
- "PMID": "39474644",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Cost-utility analysis of once-weekly insulin icodec and once-daily insulin glargine in patients with type 2 diabetes receiving basal-bolus insulin therapy in China.",
- "Abstract": "The conclusion drawn from this study is that, with insulin glargine as the cost reference, the economic cost of insulin icodec for Chinese type 2 diabetes patients is expected to range from $784.90 to $1145.96, providing a reference basis for clinical decision-making and healthcare policy formulation.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Insulin Glargine",
- "Cost-Benefit Analysis",
- "China",
- "Hypoglycemic Agents",
- "Quality-Adjusted Life Years",
- "Drug Administration Schedule",
- "Male",
- "Female",
- "Middle Aged",
- "Insulin"
- ]
- },
- {
- "PMID": "39474248",
- "Title": "Journal of diabetes research",
- "ArticleTitle": "Impact of Vitamin E Supplementation on High-Density Lipoprotein in Patients With Haptoglobin Genotype-Stratified Diabetes: A Systematic Review of Randomized Controlled Trials.",
- "Abstract": {
- "b": "Conclusions:"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Antioxidants",
- "Diabetes Mellitus, Type 2",
- "Dietary Supplements",
- "Genotype",
- "Haptoglobins",
- "Lipoproteins, HDL",
- "Randomized Controlled Trials as Topic",
- "Vitamin E"
- ]
- },
- {
- "PMID": "39474247",
- "Title": "Journal of diabetes research",
- "ArticleTitle": "Adipocytokines and Inflammation in Patients and a Gerbil Model: Implications for Obesity-Related and Nonobese Diabetes.",
- "Abstract": {
- "b": "Conclusions:",
- "i": "age",
- "sup": "2"
- },
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Obesity",
- "Gerbillinae",
- "Adipokines",
- "Middle Aged",
- "Male",
- "Humans",
- "Inflammation",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Adipose Tissue",
- "Adult",
- "Disease Models, Animal",
- "Blood Glucose",
- "Insulin Resistance",
- "Leptin",
- "Adiponectin"
- ]
- },
- {
- "PMID": "39473074",
- "Title": "Diabetic medicine : a journal of the British Diabetic Association",
- "ArticleTitle": "The effect of high-fibre diets on glycaemic control in women with diabetes in pregnancy: A systematic review and meta-analysis.",
- "Abstract": "High-quality dietary intervention studies in pregnancy are lacking. Our results suggest that high-fibre diets improve fasting and postprandial glycaemia and reduce the likelihood of requiring insulin in women with diabetes in pregnancy.",
- "Predictions": [],
- "MeshTerms": [
- "Female",
- "Humans",
- "Pregnancy",
- "Blood Glucose",
- "Diabetes Mellitus, Type 2",
- "Dietary Fiber",
- "Glycemic Control",
- "Insulin",
- "Pregnancy in Diabetics"
- ]
- },
- {
- "PMID": "39473051",
- "Title": "Gut microbes",
- "ArticleTitle": "Exercise-changed gut mycobiome as a potential contributor to metabolic benefits in diabetes prevention: an integrative multi-omics study.",
- "Abstract": "Our findings suggest that intense exercise training significantly remodels the human fungal microbiome composition. Changes in gut fungal composition are associated with the metabolic benefits of exercise, indicating gut mycobiome is a possible molecular transducer of exercise. Moreover, baseline gut fungal signatures predict exercise responsiveness for diabetes prevention, highlighting that targeting the gut mycobiome emerges as a prospective strategy in tailoring personalized training for diabetes prevention.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Gastrointestinal Microbiome",
- "Male",
- "Exercise",
- "Middle Aged",
- "Mycobiome",
- "Fungi",
- "Feces",
- "Proteomics",
- "Prediabetic State",
- "Metabolomics",
- "Bacteria",
- "Adult",
- "Diabetes Mellitus, Type 2",
- "Metagenomics",
- "Multiomics"
- ]
- },
- {
- "PMID": "39472884",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Association between the soluble receptor for advanced glycation end products and diabetes mellitus: systematic review and meta-analysis.",
- "Abstract": "CRD42024521252.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Biomarkers",
- "Diabetes Mellitus, Type 1",
- "Diabetes Mellitus, Type 2",
- "Receptor for Advanced Glycation End Products"
- ]
- },
- {
- "PMID": "39472855",
- "Title": "BMC psychiatry",
- "ArticleTitle": "Association of antipsychotic drugs on type 2 diabetes mellitus risk in patients with schizophrenia: a population-based cohort and in vitro glucose homeostasis-related gene expression study.",
- "Abstract": "This study demonstrates the impact of schizophrenia and APs and the risk of developing T2DM in Asian populations. Unmeasured confounding risk factors for T2DM may not have been included in the study. These findings may help psychiatric practitioners identify patients at risk of developing T2DM.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Schizophrenia",
- "Antipsychotic Agents",
- "Male",
- "Female",
- "Taiwan",
- "Adult",
- "Middle Aged",
- "Retrospective Studies",
- "Homeostasis",
- "Gene Expression",
- "Glucose",
- "Incidence",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39472574",
- "Title": "Nature communications",
- "ArticleTitle": "Identification of gut microbiome features associated with host metabolic health in a large population-based cohort.",
- "Abstract": "The complex relationship between the gut microbiome and host metabolic health has been an emerging research area. Several recent studies have highlighted the potential effects of the microbiome's diversity, composition and metabolic production capabilities on Body Mass Index (BMI), liver health, glucose homeostasis and Type-2 Diabetes (T2D). The majority of these studies were constrained by relatively small cohorts, mostly focusing on individuals with metabolic disorders, limiting a comprehensive understanding of the microbiome's role in metabolic health. Leveraging a large-scale, comprehensive cohort of nearly 9000 individuals, measured using Continuous Glucose Monitoring (CGM), Dual-energy X-ray absorptiometry (DXA) scan and liver Ultrasound (US) we examined the functional profile of the gut microbiome, and its relation to 38 metabolic health measures. We identified 145 unique bacterial pathways significantly correlated with metabolic health measures, with 86.9% of these showing significant associations with more than one metabolic health measure. Furthermore, 87,678 unique bacterial gene families were found to be significantly associated with at least one metabolic health measure. Notably, \"key\" bacterial pathways such as purine ribonucleosides degradation and anaerobic energy metabolism demonstrated multiple robust associations across various metabolic health measures, highlighting their potential roles in regulating metabolic processes. Our results remained largely unchanged after adjustments for nutritional habits and for BMI they were replicated in a geographically independent cohort. These insights pave the way for future research and potentially the development of microbiome-targeted interventions to enhance metabolic health.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Gastrointestinal Microbiome",
- "Male",
- "Female",
- "Cohort Studies",
- "Middle Aged",
- "Diabetes Mellitus, Type 2",
- "Body Mass Index",
- "Adult",
- "Liver",
- "Bacteria",
- "Absorptiometry, Photon",
- "Aged",
- "Blood Glucose"
- ]
- },
- {
- "PMID": "39472434",
- "Title": "Nature communications",
- "ArticleTitle": "Heterogeneous enhancer states orchestrate \u03b2 cell responses to metabolic stress.",
- "Abstract": "Obesity-induced \u03b2 cell dysfunction contributes to the onset of type 2 diabetes. Nevertheless, elucidating epigenetic mechanisms underlying islet dysfunction at single cell level remains challenging. Here we profile single-nuclei RNA along with enhancer marks H3K4me1 or H3K27ac in islets from lean or obese mice. Our study identifies distinct gene signatures and enhancer states correlating with \u03b2 cell dysfunction trajectory. Intriguingly, while many metabolic stress-induced genes exhibit concordant changes in both H3K4me1 and H3K27ac at their enhancers, expression changes of specific subsets are solely attributable to either H3K4me1 or H3K27ac dynamics. Remarkably, a subset of H3K4me1",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Insulin-Secreting Cells",
- "Mice",
- "Enhancer Elements, Genetic",
- "Stress, Physiological",
- "Hepatocyte Nuclear Factor 3-beta",
- "Obesity",
- "Histones",
- "Endoplasmic Reticulum Stress",
- "Mice, Inbred C57BL",
- "Nerve Growth Factor",
- "Male",
- "Single-Cell Analysis",
- "Diabetes Mellitus, Type 2",
- "Paracrine Communication",
- "Cell Communication",
- "Mice, Obese",
- "Epigenesis, Genetic"
- ]
- },
- {
- "PMID": "39471893",
- "Title": "Clinica chimica acta; international journal of clinical chemistry",
- "ArticleTitle": "HPLC-MS/MS method for simultaneous analysis of plasma 2-hydroxybutyrate and 2-hydroxyisobutyrate: Development and clinical significance.",
- "Abstract": "Recent studies have identified relationships between diabetes mellitus and short-chain fatty acids, including 2-hydroxybutyrate (2-HB) and 2-hydroxyisobutyrate (2-HiB); 2-HB has been associated to the early stages of insulin resistance, while 2-HiB with the risk and progression of complications of Type 1 diabetes. Their metabolism and pathophysiological role in humans are not fully clarified. The possible association between 2-HB and 2-HiB and diabetes mellitus was investigated with a novel mass spectrometry-based assay, capable of discriminating plasma 2-HiB and 2-HB from their HB isomers. Accuracy and precision (RSD%) were always in the range 99-102% and 0.7-3.5%, respectively. The study involved samples from subjects with normal glucose tolerance (NGT) and Type 2 diabetes (T2D), originally included in a multicenter study investigating mechanisms involved in atherothrombosis. NGT subjects exhibited concentrations of 2-HB and 2-HiB of 61 (36) and 3.1 (1.9) \u00b5mol/L, median (interquartile range), respectively, that were significantly lower than those of the T2D patients, whose values were 74 (4.0) and 3.8 (2.9) \u00b5mol/L, respectively. The pattern of association of these molecules with clinical and metabolic variables is partially different: both compounds were directly related to male sex, BMI, HbA",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Tandem Mass Spectrometry",
- "Diabetes Mellitus, Type 2",
- "Chromatography, High Pressure Liquid",
- "Hydroxybutyrates",
- "Middle Aged",
- "Adult",
- "Clinical Relevance",
- "Liquid Chromatography-Mass Spectrometry"
- ]
- },
- {
- "PMID": "39471776",
- "Title": "The journal of nutrition, health & aging",
- "ArticleTitle": "Spatiotemporal trends of Type 2 diabetes due to low physical activity from 1990 to 2019 and forecasted prevalence in 2050: A Global Burden of Disease Study 2019.",
- "Abstract": "LPA significantly impacts T2DM, particularly in low SDI regions. Promotion of physical activity is crucial to reduce this burden, particularly in regions where the disease's impact is most severe.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Global Burden of Disease",
- "Male",
- "Female",
- "Exercise",
- "Prevalence",
- "Global Health",
- "Middle Aged",
- "Disability-Adjusted Life Years",
- "Forecasting",
- "Aged",
- "Sedentary Behavior",
- "Spatio-Temporal Analysis",
- "Adult"
- ]
- },
- {
- "PMID": "39471766",
- "Title": "Geriatric nursing (New York, N.Y.)",
- "ArticleTitle": "Impact of a motor-cognitive intervention on cognitive function in middle-aged and older patients with type 2 diabetes.",
- "Abstract": "This study evaluated the impact of a motor-cognitive intervention on cognitive function in patients with type 2 diabetes mellitus (T2DM). A single-group design with repeated measures was used, with twenty-six middle-aged and older patients with T2DM (aged 68.58 \u00b1 6.15 years) tested on two occasions four weeks apart to establish a baseline before participating in the exercise programme (55-60 min per session; 3 x week) for eight weeks. Participants were then tested again immediately after the training programme. Except for phonemic fluency error scores, the baseline data remained unchanged. After the training programme, statistical tests showed a significant improvement in some variables of executive function and attention demand, (p < 0.017, Bonferroni adjustment to compensate for multiple comparisons), as well as a positive effect on information processing speed, and dual-task performance. Combining physical and cognitive stimulation can have a positive impact on the cognitive functioning of participants with T2DM.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Aged",
- "Cognition",
- "Executive Function",
- "Middle Aged",
- "Exercise Therapy",
- "Attention"
- ]
- },
- {
- "PMID": "39471690",
- "Title": "International immunopharmacology",
- "ArticleTitle": "Tirzepatide's role in targeting adipose tissue macrophages to reduce obesity-related inflammation and improve insulin resistance.",
- "Abstract": "Tirzepatide's potential as a therapeutic strategy for addressing metabolic diseases associated with obesity and T2DM by targeting ATM activity and mitigating obesity-associated inflammation.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Insulin Resistance",
- "Obesity",
- "Macrophages",
- "Adipose Tissue",
- "Male",
- "Mice",
- "Mice, Inbred C57BL",
- "Inflammation",
- "Diet, High-Fat",
- "Diabetes Mellitus, Type 2",
- "Glucagon-Like Peptide-1 Receptor",
- "Receptors, Gastrointestinal Hormone",
- "Cytokines",
- "Humans",
- "Disease Models, Animal",
- "Anti-Inflammatory Agents",
- "Glucagon-Like Peptide-1 Receptor Agonists"
- ]
- },
- {
- "PMID": "39471265",
- "Title": "Journal of managed care & specialty pharmacy",
- "ArticleTitle": "Social determinants of health and newer glucose-lowering drugs adoption among US Medicare beneficiaries with type 2 diabetes.",
- "Abstract": "We identified key contextual-level SDOH associated with real-world adoption of newer GLDs and explored their geographic variation through spatially explicit, data-driven analytical approaches. Identifying areas of strong association between SDOH and newer GLD initiation is crucial for policymakers to allocate resources and develop interventions that address structural inequities.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "United States",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Male",
- "Social Determinants of Health",
- "Aged",
- "Medicare",
- "Hypoglycemic Agents",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Middle Aged",
- "Aged, 80 and over",
- "Glucagon-Like Peptide-1 Receptor Agonists"
- ]
- },
- {
- "PMID": "39471057",
- "Title": "ACS nano",
- "ArticleTitle": "Engineering Supramolecular Nanofiber Depots from a Glucagon-Like Peptide-1 Therapeutic.",
- "Abstract": "Diabetes and obesity have emerged as major global health concerns. Glucagon-like peptide-1 (GLP-1), a natural incretin hormone, stimulates insulin production and suppresses glucagon secretion to stabilize and reduce blood glucose levels and control appetite. The therapeutic use of GLP-1 receptor agonists (e.g., semaglutide) has transformed the standard of care in recent years for treating type 2 diabetes and reversing obesity. The native GLP-1 sequence has a very short half-life, and therapeutic advances have come from molecular engineering to alter the pharmacokinetic profile of synthetic GLP-1 receptor agonists to enable once-weekly administration, reduce the frequency of injection, and improve adherence. Efforts to further extend this profile would offer additional convenience or enable entirely different treatment modalities. Here, an injectable GLP-1 receptor agonist depot is engineered through integration of a prosthetic self-assembling peptide motif to enable supramolecular nanofiber formation and hydrogelation. This supramolecular GLP-1 receptor agonistic (PA-GLP1) offers sustained release in vitro for multiple weeks, supporting long-lasting therapy. Moreover, in a rat model of type 2 diabetes, a single injection of the supramolecular PA-GLP1 formulation achieved sustained serum concentrations for at least 40 days, with an overall reduction in blood glucose levels and reduced weight gain, comparing favorably to daily injections of semaglutide. The general and modular approach is also extensible to other next-generation peptide therapies. Accordingly, the formation of supramolecular nanofiber depots offers a more convenient and long-lasting therapeutic option to manage diabetes and treat metabolic disorders.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Glucagon-Like Peptide 1",
- "Nanofibers",
- "Rats",
- "Glucagon-Like Peptide-1 Receptor",
- "Diabetes Mellitus, Type 2",
- "Humans",
- "Male",
- "Hypoglycemic Agents",
- "Rats, Sprague-Dawley",
- "Glucagon-Like Peptide-1 Receptor Agonists"
- ]
- },
- {
- "PMID": "39470862",
- "Title": "Neuromolecular medicine",
- "ArticleTitle": "Distinct Hippocampal Expression Profiles of lncRNAs in Obese Type 2 Diabetes Mice Exhibiting Cognitive Impairment.",
- "Abstract": "Cognitive dysfunction has been accepted as a possible complication of type 2 diabetes (T2D), but few studies revealed the potential roles of Long non\u2011coding RNAs (lncRNAs) in cognitive dysfunction in T2D. The current research aims to demonstrate the specific expression patterns of lncRNA-mRNA in the hippocampi of T2D db/db mice exhibiting cognitive impairment. In this study, the results from behavioral tests showed that T2D db/db mice displayed short-term and spatial working memory deficits compared to db/m mice. Furthermore, western blot analysis demonstrated that compared with db/m mice, p-GSK3\u03b2 (ser9) protein levels were markedly elevated in T2D db/db mice (P\u2009<\u20090.01). In addition, though not statistically significant, the ratio of p-Tau (Ser396) to Tau 46, \u03b1-Synuclein expression, and p-GSK3\u03b1 (ser21) expression were also relatively higher in T2D db/db mice than in db/m mice. The microarray profiling revealed that 75 lncRNAs and 26 mRNAs were dysregulated in T2D db/db mice (>\u20092.0 fold change, P\u2009<\u20090.05). GO analysis demonstrated that the differentially expressed mRNAs participated in immune response, extracellular membrane-bounded organelle, and extracellular region. KEGG analysis revealed that the differentially expressed mRNAs were mainly involved in one carbon pool by folate, glyoxylate and dicarboxylate metabolism, autophagy, glycine, serine and threonine metabolism, and B cell receptor signaling pathway. A lncRNA\u2011mRNA coexpression network containing 71 lncRNAs and 26 mRNAs was built to investigate the interaction between lncRNA and mRNA. Collectively, these results revealed the differential hippocampal expression profiles of lncRNAs in T2D mice with cognitive dysfunction, and the findings from this study provide new clues for exploring the potential roles of lncRNAs in the pathogenesis of cognitive dysfunction in T2D.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "RNA, Long Noncoding",
- "Mice",
- "Diabetes Mellitus, Type 2",
- "Hippocampus",
- "Male",
- "Cognitive Dysfunction",
- "RNA, Messenger",
- "Glycogen Synthase Kinase 3 beta",
- "Mice, Inbred C57BL",
- "tau Proteins",
- "Gene Expression Profiling",
- "Transcriptome",
- "Gene Expression Regulation",
- "Obesity",
- "Memory, Short-Term"
- ]
- },
- {
- "PMID": "39470509",
- "Title": "Medicine",
- "ArticleTitle": "Metformin: Diverse molecular mechanisms, gastrointestinal effects and overcoming intolerance in type 2 Diabetes Mellitus: A review.",
- "Abstract": "Metformin, the first line treatment for patients with type 2 diabetes mellitus, has alternative novel roles, including cancer and diabetes prevention. This narrative review aims to explore its diverse mechanisms, effects and intolerance, using sources obtained by searching Scopus, PubMed and Web of Science databases, and following Scale for the Assessment of Narrative Review Articles reporting guidelines. Metformin exerts it actions through duration influenced, and organ specific, diverse mechanisms. Its use is associated with inhibition of hepatic gluconeogenesis targeted by mitochondria and lysosomes, reduction of cholesterol levels involving brown adipose tissue, weight reduction influenced by growth differentiation factor 15 and novel commensal bacteria, in addition to counteraction of meta-inflammation alongside immuno-modulation. Interactions with the gastrointestinal tract include alteration of gut microbiota, enhancement of glucose uptake and glucagon like peptide 1 and reduction of bile acid absorption. Though beneficial, they may be linked to intolerance. Metformin related gastrointestinal adverse effects are associated with dose escalation, immediate release formulations, gut microbiota alteration, epigenetic predisposition, inhibition of organic cation transporters in addition to interactions with serotonin, histamine and the enterohepatic circulation. Potentially effective measures to overcome intolerance encompasses carefully objective targeted dose escalation, prescription of fixed dose combination, microbiome modulators and prebiotics, in addition to use of extended release formulations.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Metformin",
- "Hypoglycemic Agents",
- "Gastrointestinal Microbiome",
- "Gastrointestinal Tract"
- ]
- },
- {
- "PMID": "39470335",
- "Title": "Hepatology communications",
- "ArticleTitle": "Clinical care guidance in patients with diabetes and metabolic dysfunction-associated steatotic liver disease: A joint consensus.",
- "Abstract": "Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide, affecting >30% of the global population. Metabolic dysregulation, particularly insulin resistance and its subsequent manifestation as type 2 diabetes mellitus, serves as the fundamental pathogenesis of metabolic liver disease. Clinical evidence of the recent nomenclature evolution is accumulating. The interaction and impacts are bidirectional between MASLD and diabetes in terms of disease course, risk, and prognosis. Therefore, there is an urgent need to highlight the multifaceted links between MASLD and diabetes for both hepatologists and diabetologists. The surveillance strategy, risk stratification of management, and current therapeutic achievements of metabolic liver disease remain the major pillars in a clinical care setting. Therefore, the Taiwan Association for the Study of the Liver (TASL), Taiwanese Association of Diabetes Educators, and Diabetes Association of the Republic of China (Taiwan) collaboratively completed the first guidance in patients with diabetes and MASLD, which provides practical recommendations for patient care.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Consensus",
- "Diabetes Mellitus, Type 2",
- "Insulin Resistance",
- "Non-alcoholic Fatty Liver Disease",
- "Taiwan",
- "Review Literature as Topic"
- ]
- },
- {
- "PMID": "39470149",
- "Title": "Journal of diabetes",
- "ArticleTitle": "Association of systolic blood pressure variability with cognitive decline in type 2 diabetes: A post hoc analysis of a randomized clinical trial.",
- "Abstract": "A greater visit-to-visit systolic BPV was significantly associated with an increased risk of cognitive decline measured by DSST and an increase in white matter lesion volume in patients with type 2 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Blood Pressure",
- "Cognitive Dysfunction",
- "Middle Aged",
- "Aged",
- "Cognition",
- "Risk Factors",
- "Neuropsychological Tests",
- "Magnetic Resonance Imaging",
- "Systole"
- ]
- },
- {
- "PMID": "39470143",
- "Title": "Journal of biochemical and molecular toxicology",
- "ArticleTitle": "Sesamol Alleviated Lipotoxicity-Induced Dysfunction in MIN6 Cells via Facilitating Cellular Senescence Caused by Endoplasmic Reticulum Stress.",
- "Abstract": "Obesity is found to be a significant risk factor for type 2 diabetes mellitus (T2DM), attributed to lipotoxicity-induced \u03b2-cell dysfunction. However, the specific mechanism involved in the process remains incompletely unclarified. The current study demonstrated lipotoxicity resulted in the activation of ER stress, which increased the protein level of TXNIP, thereby inducing senescence-assiciated dysfunction in MIN6 cells under high fat environment. And we also found sesamol, a natural functional component extracted from sesame, was able to alleviate senescence-associated \u03b2-cell dysfunction induced by lipotoxicity by inhibiting ER stress and TXNIP. Our findings provided novel insights into senescence-related T2DM and propose innovative therapeutic approaches for utilizing sesamol in the treatment of T2DM in the obese elderly population.",
- "Predictions": [],
- "MeshTerms": [
- "Endoplasmic Reticulum Stress",
- "Benzodioxoles",
- "Cellular Senescence",
- "Phenols",
- "Animals",
- "Mice",
- "Cell Line",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39469571",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Tracing links between micronutrients and type 2 diabetes risk: the singular role of selenium.",
- "Abstract": "Our study presents novel evidence of a positive correlation between selenium intake and T2D risk, underscoring the importance of micronutrients in diabetes prevention and treatment strategies. Further research is necessary to confirm these findings and to clarify the specific biological mechanisms through which selenium influences diabetes risk.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Selenium",
- "Micronutrients",
- "Male",
- "Mendelian Randomization Analysis",
- "Genome-Wide Association Study",
- "Female",
- "Middle Aged",
- "Risk Factors",
- "Prospective Studies"
- ]
- },
- {
- "PMID": "39468808",
- "Title": "Sheng li xue bao : [Acta physiologica Sinica]",
- "ArticleTitle": "[Resistance exercise regulates hippocampal microglia polarization through TREM2/NF-\u03baB/STAT3 signal pathway to improve cognitive dysfunction in T2DM mice].",
- "Abstract": "The study aimed to explore the effect and mechanism of resistance exercise (RE) on cognitive dysfunction in type 2 diabetes mellitus (T2DM) mice. Six 8-week-old male m/m mice were used as control (Con) group, and db/db mice of the matched age were randomly divided into model control (db/db) group and db+RE group, with 6 mice in each group. The db+RE group was given 8 weeks of resistance climbing ladder exercise intervention. The fasting blood glucose and body weight of the mice were measured weekly. After the intervention, the spatial learning and memory of the mice were detected by Morris water maze, and the neuronal damage in the hippocampus of the mice was detected by Nissl staining. The protein expression levels of PSD93, PSD95, BDNF, CREB, p-CREB, IL-6, IL-1\u03b2, TNF-\u03b1, Iba-1, iNOS, CD206, Arg1, triggering receptor expressed on myeloid cells 2 (TREM2), NF-\u03baB, p-STAT3, and STAT3 were detected by Western blot. The mRNA expression levels of inflammatory factors and TREM2 in hippocampus were evaluated by qRT-PCR, and the expression and localization of Iba-1, CD206, CD86, and TREM2 were determined by immunofluorescence staining. The results showed that the spatial learning and memory of the db/db group were significantly declined, the neurons in the hippocampus were damaged, the protein levels of PSD93, PSD95, BDNF, CD206, Arg1, TREM2 and the ratio of p-CREB/CREB were significantly down-regulated, the mRNA and protein expression levels of IL-6, IL-1\u03b2 and TNF-\u03b1 were significantly up-regulated, and the protein levels of iNOS, Iba-1, NF-\u03baB and the ratio of p-STAT3/STAT3 were significantly increased compared with the Con group. However, the 8-week RE improved the spatial learning and memory of db/db mice, alleviated the damage of hippocampal neurons, promoted the polarization of M2 microglia, and inhibited the neuroinflammation. The above results suggest that RE can improve cognitive dysfunction in T2DM mice, and its mechanism may be related to regulating microglia polarization via TREM2/NF-\u03baB/STAT3 signaling pathway.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Mice",
- "Hippocampus",
- "Male",
- "Receptors, Immunologic",
- "Cognitive Dysfunction",
- "NF-kappa B",
- "Microglia",
- "Signal Transduction",
- "STAT3 Transcription Factor",
- "Membrane Glycoproteins",
- "Diabetes Mellitus, Type 2",
- "Physical Conditioning, Animal",
- "Diabetes Mellitus, Experimental"
- ]
- },
- {
- "PMID": "39468727",
- "Title": "Age and ageing",
- "ArticleTitle": "Assessing 1-year sodium-glucose co-transporter-2 inhibitor tolerance in older adults.",
- "Abstract": "No clinically meaningful differences in SGLT2 inhibitor intolerance were observed in patients up to 84\u00a0years. Our findings support having closer follow-up when initiating in patients 85\u00a0years and older.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Aged",
- "Female",
- "Male",
- "Retrospective Studies",
- "Aged, 80 and over",
- "Age Factors",
- "Diabetes Mellitus, Type 2",
- "Risk Factors",
- "United States",
- "Middle Aged"
- ]
- },
- {
- "PMID": "39468602",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "Lipids as the link between central obesity and diabetes: perspectives from mediation analysis.",
- "Abstract": "In central obesity-related diabetes risk, most lipids, especially lipid ratio parameters, play a significant mediating role. Given these findings, we advocate for increased efforts in multifactorial risk monitoring and joint management of diabetes. The evaluation of lipids, particularly lipid ratio parameters, may be holds substantial value in the prevention and management of diabetes risk under close monitoring of central obesity.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Obesity, Abdominal",
- "Male",
- "Female",
- "Middle Aged",
- "Lipids",
- "Mediation Analysis",
- "Adult",
- "Risk Factors",
- "Waist Circumference",
- "Longitudinal Studies",
- "Diabetes Mellitus",
- "Biomarkers",
- "Diabetes Mellitus, Type 2",
- "Follow-Up Studies",
- "Aged",
- "Prognosis",
- "Triglycerides"
- ]
- },
- {
- "PMID": "39468546",
- "Title": "Cardiovascular diabetology",
- "ArticleTitle": "The effect of empagliflozin on circulating endothelial progenitor cells in patients with diabetes and stable coronary artery disease.",
- "Abstract": "Empagliflozin treatment in patients with DM and stable CAD increases cEPC levels and function, implying a cardioprotective mechanism. These findings highlight the potential of SGLT2i in treating cardiovascular diseases, warranting further research to explore these effects and their long-term implications.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Endothelial Progenitor Cells",
- "Female",
- "Glucosides",
- "Coronary Artery Disease",
- "Benzhydryl Compounds",
- "Aged",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Prospective Studies",
- "Treatment Outcome",
- "Time Factors",
- "Cells, Cultured",
- "Diabetes Mellitus, Type 2",
- "Cell Proliferation",
- "Biomarkers",
- "Middle Aged"
- ]
- },
- {
- "PMID": "39468537",
- "Title": "BMC endocrine disorders",
- "ArticleTitle": "To analyse the correlation between UAER and eGFR and the risk factors for reducing eGFR in patients with type 2 diabetes.",
- "Abstract": "Peripheral vascular disease, systolic blood pressure, fatty liver, and beta-2-microglobulin are risk factors for decreased eGFR levels in patients with T2DM, which should be applied for control DKD. HDL and fasting CP have important effects on maintaining eGFR, and blood pressure and fasting CP can be used as new targets for subsequent diabetic kidney disease treatment.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Glomerular Filtration Rate",
- "Middle Aged",
- "Risk Factors",
- "Albuminuria",
- "Aged",
- "Follow-Up Studies",
- "Diabetic Nephropathies",
- "Prognosis",
- "Biomarkers"
- ]
- },
- {
- "PMID": "39468383",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Visit-to-visit HbA1c variability and risk of potentially avoidable hospitalisations in adults with type 2 diabetes receiving outpatient care at a tertiary hospital.",
- "Abstract": "In individuals receiving care at specialist outpatient clinics of a tertiary hospital, HbA1c variability is associated with a higher risk of PAH. Comprehensive diabetes management strategies addressing both glycaemic control and variability may offer benefits.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Middle Aged",
- "Female",
- "Glycated Hemoglobin",
- "Male",
- "Aged",
- "Tertiary Care Centers",
- "Hospitalization",
- "Singapore",
- "Adult",
- "Ambulatory Care",
- "Aged, 80 and over",
- "Cohort Studies",
- "Young Adult",
- "Risk Factors",
- "Glycemic Control",
- "Follow-Up Studies"
- ]
- },
- {
- "PMID": "39468380",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Effect of spironolactone wash-out on albuminuria after long-term treatment in individuals with type 2 diabetes and high risk of kidney disease-An observational follow-up of the PRIORITY study.",
- "Abstract": "UACR did not change after discontinuation of long-term treatment with spironolactone. However, an increase in eGFR was observed supporting a haemodynamic effect of spironolactone in the kidneys.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Spironolactone",
- "Albuminuria",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Diabetic Nephropathies",
- "Middle Aged",
- "Follow-Up Studies",
- "Glomerular Filtration Rate",
- "Mineralocorticoid Receptor Antagonists",
- "Aged",
- "Blood Pressure",
- "Creatinine",
- "Potassium"
- ]
- },
- {
- "PMID": "39468091",
- "Title": "Scientific reports",
- "ArticleTitle": "Cardiometabolic risk factor clusters in older adults using latent class analysis on the Bushehr elderly health program.",
- "Abstract": "Metabolic syndrome (MetS), comprising obesity, insulin resistance, hypertension, and dyslipidemia, increases the risk of type II diabetes mellitus and cardiovascular disease. This study aimed to identify the prevalence and determinants of specific clusters of the MetS components and tobacco consumption among older adults in Iran. The current study was conducted in the second stage of the Bushehr Elderly Health (BEH) program in southern Iran-a population-based cohort including 2424 subjects aged\u2009\u2265\u200960 years. Latent class analysis (LCA) was used to identify MetS and tobacco consumption patterns. Multinomial logistic regression was conducted to investigate factors associated with each MetS class, including sociodemographic and behavioral variables. Out of 2424 individuals, the overall percentage of people with one or more components of MetS or current tobacco use was 57.8% and 20.8%, respectively. The mean (SD) age of all participants was 69.3(6.4) years. LCA ascertained the presence of four latent classes: class 1 (\"low risk\"; with a prevalence of 35.3%), class 2 (\"MetS with medication-controlled diabetes\"; 11.1%), class 3 (\"high risk of MetS and associated medication use\"; 27.1%), and class 4 (\"central obesity and treated hypertension\"; 26.4%). Compared to participants with a body mass index (BMI)\u2009<\u200930, participants with BMI\u2009\u2265\u200930 were more likely to belong to class 3 (OR 1.91, 95% CI 1.31-2.79) and class 4 (OR 1.49, 95% CI 1.06-2.08). Polypharmacy was associated with membership in class 2 (OR 2.07, 95% CI 1.12-3.81), class 3 (OR 9.77, 95% CI 6.12-15.59), and class 4 (OR 1.76, 95% CI 1.07-2.91). The elevated triglyceride-glucose index was associated with membership in class 2 (OR 12.33, 95% CI 7.75-19.61) and class 3 (OR 12.04, 95% CI 8.31-17.45). Individuals with poor self-related health were more likely to belong to class 3 (OR 1.43; 95% CI 1.08-1.93). Four classes were identified among older adults in Iran with distinct patterns of cardiometabolic risk factors. Segmenting elderly individuals into these cardiometabolic categories has the potential to enhance the monitoring and management of cardiometabolic risk factors. This strategy may help reduce the severe outcomes of metabolic syndrome in this susceptible population.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Aged",
- "Male",
- "Female",
- "Latent Class Analysis",
- "Metabolic Syndrome",
- "Middle Aged",
- "Iran",
- "Cardiometabolic Risk Factors",
- "Prevalence",
- "Diabetes Mellitus, Type 2",
- "Risk Factors",
- "Hypertension",
- "Cardiovascular Diseases"
- ]
- },
- {
- "PMID": "39468075",
- "Title": "Nature communications",
- "ArticleTitle": "Transcriptome-wide Mendelian randomization during CD4",
- "Abstract": "Immunity has shown potentials in informing drug development for cardiometabolic diseases, such as type 2 diabetes (T2D) and coronary artery disease (CAD). Here, we performed a transcriptome-wide Mendelian randomization (MR) study to estimate the putative causal effects of 11,021 gene expression profiles during CD4",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Mendelian Randomization Analysis",
- "CD4-Positive T-Lymphocytes",
- "Diabetes Mellitus, Type 2",
- "Transcriptome",
- "Lymphocyte Activation",
- "Coronary Artery Disease",
- "Gene Expression Profiling",
- "Genetic Predisposition to Disease",
- "Polymorphism, Single Nucleotide",
- "Genome-Wide Association Study"
- ]
- },
- {
- "PMID": "39467963",
- "Title": "Heart failure reviews",
- "ArticleTitle": "Sodium-glucose cotransporter-2 inhibitors in acute myocardial infarction: a systematic review and meta-analysis of randomized controlled trials.",
- "Abstract": "We aimed to assess the efficacy and safety of sodium-glucose cotransporter-2 inhibitors (SGLT2i) versus placebo, initiated within the hospitalization period, in addition to habitual treatment, for treating adult patients with confirmed acute myocardial infarction (AMI). We also conducted subgroup analysis by diabetes mellitus (DM) status and type of AMI. We systematically searched PubMed, Embase, and Cochrane Library for randomized controlled trials (RCTs). The primary outcome was hospitalization for heart failure (HF). The secondary outcomes were all-cause death, cardiovascular death, and serious adverse events (AEs). We pooled risk ratios (RR) with a 95% confidence interval (CI) for binary outcomes. The between-study variance was assessed using tau",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Randomized Controlled Trials as Topic",
- "Myocardial Infarction",
- "Hospitalization",
- "Treatment Outcome",
- "Diabetes Mellitus, Type 2"
- ]
- },
- {
- "PMID": "39467873",
- "Title": "Diabetologia",
- "ArticleTitle": "Autoimmune diseases and the risk and prognosis of latent autoimmune diabetes in adults.",
- "Abstract": "We confirm that several common ADs confer an excess risk of LADA, especially LADA with higher GADA levels, but having such a comorbidity does not appear to affect the risk of diabetic retinopathy.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Male",
- "Autoimmune Diseases",
- "Middle Aged",
- "Latent Autoimmune Diabetes in Adults",
- "Adult",
- "Prognosis",
- "Diabetes Mellitus, Type 2",
- "Sweden",
- "Diabetic Retinopathy",
- "Aged",
- "Autoantibodies",
- "Risk Factors",
- "Comorbidity",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39467872",
- "Title": "Diabetologia",
- "ArticleTitle": "Exposure to antibiotics and risk of latent autoimmune diabetes in adults and type 2 diabetes: results from a Swedish case-control study (ESTRID) and the Norwegian HUNT study.",
- "Abstract": "We found no evidence that exposure to broad-spectrum antibiotics up to 10 years prior to diagnosis increases the risk of LADA. There was some indication of increased LADA risk with exposure to narrow-spectrum antibiotics, which warrants further investigation.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Case-Control Studies",
- "Diabetes Mellitus, Type 2",
- "Sweden",
- "Norway",
- "Anti-Bacterial Agents",
- "Female",
- "Male",
- "Adult",
- "Middle Aged",
- "Aged",
- "Risk Factors",
- "Latent Autoimmune Diabetes in Adults",
- "Diabetes Mellitus, Type 1"
- ]
- },
- {
- "PMID": "39466812",
- "Title": "PloS one",
- "ArticleTitle": "Associations of the TyG index with albuminuria and chronic kidney disease in patients with type 2 diabetes.",
- "Abstract": "The TyG index is positively associated with albuminuria and CKD in patients with T2DM and may be a marker for predicting the occurrence of early kidney injury in patients with T2DM. Clinicians should test this indicator early to detect lesions and improve patient prognosis.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Albuminuria",
- "Male",
- "Female",
- "Middle Aged",
- "Renal Insufficiency, Chronic",
- "Triglycerides",
- "Blood Glucose",
- "Adult",
- "Diabetic Nephropathies",
- "Aged",
- "Glomerular Filtration Rate",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39466719",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Subphenotypes of adult-onset diabetes: Data-driven clustering in the population-based KORA cohort.",
- "Abstract": "T2D subphenotyping based on its sample's own clinical characteristics leads to stable categorization and adequately reflects T2D heterogeneity.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Middle Aged",
- "Germany",
- "Cluster Analysis",
- "Phenotype",
- "Cohort Studies",
- "Aged",
- "Adult",
- "Age of Onset",
- "Genetic Predisposition to Disease",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39466701",
- "Title": "Diabetes, obesity & metabolism",
- "ArticleTitle": "Dietary potassium intake and its interaction with sodium intake on risk of developing cardiovascular disease in persons with type 2 diabetes: The Japan Diabetes Complication and its Prevention Prospective study (JDCP study 12).",
- "Abstract": "Low potassium intake in conjunction with high sodium intake was significantly associated with increased incident CVD in persons with T2DM. However, CVD incidence was not related to high potassium intake, regardless of sodium intake.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Middle Aged",
- "Male",
- "Female",
- "Japan",
- "Prospective Studies",
- "Cardiovascular Diseases",
- "Aged",
- "Sodium, Dietary",
- "Potassium, Dietary",
- "Adult",
- "Incidence",
- "Diabetic Angiopathies",
- "Risk Factors",
- "Follow-Up Studies"
- ]
- },
- {
- "PMID": "39466156",
- "Title": "The science of diabetes self-management and care",
- "ArticleTitle": "Characteristics and Correlates of Health Information Literacy Among Patients With Type 2 Diabetes and Metabolic Syndrome: A Cross-Sectional Study.",
- "Abstract": "Overall, the health information literacy among Chinese patients with type 2 diabetes coexisting with metabolic syndrome is suboptimal. Study findings demonstrated that personal and social contextual resources factors are significantly related to health information literacy. Health care professionals should consider strategies to enhance people's health information literacy level and promote individuals' health problem-solving, enhance chronic illness resources, and improve self-management knowledge when developing tailored interventions.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Metabolic Syndrome",
- "Female",
- "Male",
- "Health Literacy",
- "Middle Aged",
- "Cross-Sectional Studies",
- "Health Knowledge, Attitudes, Practice",
- "China",
- "Aged",
- "Adult",
- "Surveys and Questionnaires",
- "Self Efficacy",
- "Self-Management"
- ]
- },
- {
- "PMID": "39466107",
- "Title": "The science of diabetes self-management and care",
- "ArticleTitle": "Exploring Type 2 Diabetes Self-Management Practices Among African Americans in Rural Counties: A Qualitative Study.",
- "Abstract": "The decision-making involved in glycemic level management emerges as a complex developmental process influenced by disease trajectory and cultural and environmental factors. These findings may inform a conceptual framework to guide future inquiries and provide insights for primary care clinicians and diabetes care and education specialists to better understand the complexities of T2D management among African American individuals in rural settings.",
- "Predictions": [],
- "MeshTerms": [
- "Aged",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "Black or African American",
- "Diabetes Mellitus, Type 2",
- "Qualitative Research",
- "Rural Population",
- "Self Care",
- "Self-Management"
- ]
- },
- {
- "PMID": "39465848",
- "Title": "Medicine",
- "ArticleTitle": "Effect of glucagon-like peptide-1 receptor agonists on prostate cancer: A review.",
- "Abstract": "Glucagon-like peptide-1 receptor agonist (GLP-1RA) is widely used in the treatment of type 2 diabetes mellitus (T2DM) for its significant hypoglycemic effect, weight loss and small side effects. Some studies have shown that GLP-1RA has an inhibitory effect on prostate cancer, and its application will produce adverse effects associated with an increased or decreased risk of some tumors. GLP-1R is widely expressed by various types of cells and tissues in the human body, so GLP-1RA has attracted wide clinical attention to the occurrence, development and prognosis of tumors, which brings more new directions and hopes for the treatment of prostate cancer. This paper describes the expression of glucagon-like peptide-1 receptor (GLP-1R) in prostate cancer and the effects of glucagon-like peptide-1 receptor agonist (GLP-1RA) on prostate cancer.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Prostatic Neoplasms",
- "Diabetes Mellitus, Type 2",
- "Hypoglycemic Agents",
- "Glucagon-Like Peptide-1 Receptor Agonists"
- ]
- },
- {
- "PMID": "39465742",
- "Title": "Medicine",
- "ArticleTitle": "Association of metformin use with asthma development and adverse outcomes: A systematic review and meta-analysis.",
- "Abstract": "In most outcome indicators, it cannot be assumed that the use of metformin can reduce asthma-related adverse events. However, the conclusion is not so certain, and longer observation and more evidence are still required. Metformin still shows some potential in the intervention of respiratory diseases.",
- "Predictions": [],
- "MeshTerms": [
- "Metformin",
- "Humans",
- "Asthma",
- "Diabetes Mellitus, Type 2",
- "Hypoglycemic Agents",
- "Incidence"
- ]
- },
- {
- "PMID": "39465621",
- "Title": "Epidemiology and psychiatric sciences",
- "ArticleTitle": "Mediating pathways between attention deficit hyperactivity disorder and type 2 diabetes mellitus: evidence from a two-step and multivariable Mendelian randomization study.",
- "Abstract": "These findings suggest a potentially causal, positive relationship between ADHD liability and T2D, with mediation through higher BMI, more TV watching and lower EA. Intervention on these factors may thus have beneficial effects on T2D risk in individuals with ADHD.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Attention Deficit Disorder with Hyperactivity",
- "Diabetes Mellitus, Type 2",
- "Mendelian Randomization Analysis",
- "Body Mass Index",
- "Polymorphism, Single Nucleotide",
- "Male",
- "Female",
- "Sedentary Behavior",
- "Risk Factors",
- "Pediatric Obesity",
- "Blood Pressure",
- "Child",
- "Genetic Predisposition to Disease"
- ]
- },
- {
- "PMID": "39465576",
- "Title": "The British journal of nutrition",
- "ArticleTitle": "Type 2 diabetes prevention: genetic association analysis of dried fruit intake and disease risk.",
- "Abstract": "Prior research has suggested an inverse correlation between dried fruit intake and type 2 diabetes mellitus (T2DM), yet the causal link remains uncertain. This study seeks to investigate the potential causal impact of dried fruit intake on T2DM, covering cases both with and without various complications, as well as glycaemic traits, using a two-sample Mendelian randomisation (MR) approach. Using MR analysis with genome-wide association study summary statistics, the primary analysis investigated the causal relationship between dried fruit intake and T2DM, both with and without complications, as well as glycaemic traits, employing the inverse variance weighted method. Supplementary analyses were conducted using MR-Egger and the weighted median method. Heterogeneity and intercept tests were utilised to evaluate the robustness of the study outcomes. The results show a significant association between dried fruit intake and T2DM without complications, as well as fasting insulin. Sensitivity analyses confirmed the robustness of the results and the independence from multicollinearity. However, no association was found between dried fruit intake and T2DM with various complications or other glycaemic traits. The significant association between dried fruit intake and T2DM without complications and fasting insulin persisted even after adjusting for BMI. This study offers genetic evidence endorsing the protective effects of dried fruit intake against T2DM, specifically for cases without complications, and in regulating fasting insulin. These findings suggest that dried fruit intake might serve as a primary preventive strategy for T2DM.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 2",
- "Humans",
- "Fruit",
- "Mendelian Randomization Analysis",
- "Genome-Wide Association Study",
- "Diet",
- "Insulin",
- "Blood Glucose",
- "Risk Factors"
- ]
- },
- {
- "PMID": "39465442",
- "Title": "Trials",
- "ArticleTitle": "Effectiveness of specialist involvement in case discussion conferences with primary healthcare providers on the management of type 2 diabetes patients: a study protocol for a cluster randomized controlled trial.",
- "Abstract": "Chinese Clinical Trial Registry ChiCTR2300078829. Registered on December 19, 2023. https://www.chictr.org.cn/showproj.html?proj=210293.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Primary Health Care",
- "Randomized Controlled Trials as Topic",
- "China",
- "Glycated Hemoglobin",
- "Multicenter Studies as Topic",
- "Specialization",
- "Blood Glucose",
- "Interdisciplinary Communication",
- "Treatment Outcome",
- "Patient Care Team",
- "Time Factors",
- "Male"
- ]
- },
- {
- "PMID": "39465382",
- "Title": "Alzheimer's research & therapy",
- "ArticleTitle": "Molecular landscape of the overlap between Alzheimer's disease and somatic insulin-related diseases.",
- "Abstract": "Alzheimer's disease (AD) is a multifactorial disease with both genetic and environmental factors contributing to its etiology. Previous evidence has implicated disturbed insulin signaling as a key mechanism that plays a role in both neurodegenerative diseases such as AD and comorbid somatic diseases such as diabetes mellitus type 2 (DM2). In this study, we analysed available genome-wide association studies (GWASs) of AD and somatic insulin-related diseases and conditions (SID), i.e., DM2, metabolic syndrome and obesity, to identify genes associated with both AD and SID that could increase our insights into their molecular underpinnings. We then performed functional enrichment analyses of these genes. Subsequently, using (additional) GWAS data, we conducted shared genetic etiology analyses between AD and SID, on the one hand, and blood and cerebrospinal fluid (CSF) metabolite levels on the other hand. Further, integrating all these analysis results with elaborate literature searches, we built a molecular landscape of the overlap between AD and SID. From the landscape, multiple functional themes emerged, including insulin signaling, estrogen signaling, synaptic transmission, lipid metabolism and tau signaling. We also found shared genetic etiologies between AD/SID and the blood/CSF levels of multiple metabolites, pointing towards \"energy metabolism\" as a key metabolic pathway that is affected in both AD and SID. Lastly, the landscape provided leads for putative novel drug targets for AD (including MARK4, TMEM219, FKBP5, NDUFS3 and IL34) that could be further developed into new AD treatments.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Alzheimer Disease",
- "Genome-Wide Association Study",
- "Insulin",
- "Diabetes Mellitus, Type 2",
- "Obesity",
- "Metabolic Syndrome"
- ]
- },
- {
- "PMID": "39465354",
- "Title": "BMC gastroenterology",
- "ArticleTitle": "Effect of diabetes mellitus type 2 and sulfonylurea on colorectal cancer development: a case-control study.",
- "Abstract": "This study found an insignificant association between type 2 diabetes and the chance of CRC development in an adjusted state. Sulfonylurea consumption was also associated with a higher chance of CRC development among patients with T2D. These findings have implications for clinical practice and public health strategies in CRC prevention for patients with T2D.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Colorectal Neoplasms",
- "Diabetes Mellitus, Type 2",
- "Case-Control Studies",
- "Sulfonylurea Compounds",
- "Male",
- "Female",
- "Middle Aged",
- "Aged",
- "Hypoglycemic Agents",
- "Risk Factors",
- "Odds Ratio",
- "Adult"
- ]
- },
- {
- "PMID": "39465325",
- "Title": "Swiss medical weekly",
- "ArticleTitle": "Recommendations for early identification of heart failure in patients with diabetes: Consensus statement of the Swiss Society of Endocrinology and Diabetology and the Heart Failure Working Group of the Swiss Society of Cardiology.",
- "Abstract": "Diabetes is a well-recognised risk factor for the development of heart failure, with a prevalence higher than 30% in patients with diabetes aged over 60 years. Heart failure often emerges as the primary cardiovascular manifestation in patients with type 2 diabetes and appears to be even more prevalent in type 1 diabetes. In Switzerland, there are approximately 500,000 individuals with diabetes, and the number of affected people has been steadily rising in recent years. Therefore, the consequences of heart failure will affect an increasing number of patients, further straining the Swiss healthcare system. Early lifestyle modification and initiation of appropriate treatment can prevent or at least significantly delay the onset of symptomatic heart failure by several years. These facts underscore the urgent need for early detection of individuals with subclinical heart failure, which often remains undiagnosed until the first episode of acute heart failure requiring hospital admission occurs. To address this issue, the European Society of Cardiology, the American Diabetes Association (ADA) and other international professional societies have published recommendations on heart failure screening, diagnosis and management. To address this issue in Switzerland, experts from the Swiss Society of Endocrinology and Diabetology, the Swiss Society of Cardiology and the General Internal Medicine specialty met and prepared a consensus report including a simple diagnostic algorithm for use in everyday practice.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Heart Failure",
- "Switzerland",
- "Early Diagnosis",
- "Diabetes Mellitus, Type 2",
- "Diabetes Mellitus, Type 1",
- "Consensus",
- "Risk Factors",
- "Societies, Medical",
- "Cardiology",
- "Endocrinology",
- "Mass Screening"
- ]
- },
- {
- "PMID": "39465244",
- "Title": "Scientific reports",
- "ArticleTitle": "Dietary acid load adopts the effect of ApoB ins/del genetic variant (rs11279109) on obesity trait, cardiovascular markers, lipid profile, and serum leptin level among patients with diabetes: a cross-sectional study.",
- "Abstract": "ApoB insertion/deletion (ins/del) genetic variant (rs11279109) is thought to be related to cardio-metabolic markers and obesity. This association has the potential to be modified by dietary patterns. Since the majority of studies concerned the role of dietary acid load (DAL) or ApoB in type 2 diabetes mellitus\u00a0(T2DM) and its complications independently, and due to the insufficient data regarding the possible interactions between ApoB genetic variants and DAL on anthropometric and metabolic markers, we aimed to study the interaction between this genetic variant and dietary acid load (DAL) on cardio-metabolic markers, along with leptin among Iranian individuals with T2DM. 700 T2DM patients were randomly recruited. A validated semi-quantitative food frequency questionnaire was used for DAL calculation including potential renal acid load (PRAL) and net-endogenous acid production (NEAP). The polymerase chain reaction was used for genotyping the ApoB ins/del (rs11279109). The general linear model was applied to find the interactions in the crude and adjusted models. Patients with del/del genotype (rs11279109) with high PRAL intake have lower low-density lipoprotein cholesterol (LDL-C) (P",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Female",
- "Middle Aged",
- "Leptin",
- "Obesity",
- "Cross-Sectional Studies",
- "Diabetes Mellitus, Type 2",
- "Diet",
- "Biomarkers",
- "Apolipoprotein B-100",
- "Iran",
- "Lipids",
- "Acids",
- "Apolipoproteins B",
- "Aged",
- "Genotype",
- "Adult",
- "INDEL Mutation"
- ]
- },
- {
- "PMID": "39465169",
- "Title": "PeerJ",
- "ArticleTitle": "Association analysis of MTHFR (rs1801133 and rs1801131) gene polymorphism towards the development of type 2 diabetes mellitus in Dali area population from Yunnan Province, China.",
- "Abstract": "Our study suggests that the genetic variations of MTHFR C677T and A1298C are significantly associated with T2DM susceptibility in the population of the Dali area of Yunnan Province, China.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Methylenetetrahydrofolate Reductase (NADPH2)",
- "Diabetes Mellitus, Type 2",
- "China",
- "Female",
- "Male",
- "Middle Aged",
- "Case-Control Studies",
- "Genetic Predisposition to Disease",
- "Polymorphism, Single Nucleotide",
- "Genotype",
- "Aged",
- "Adult"
- ]
- },
- {
- "PMID": "39464752",
- "Title": "Romanian journal of ophthalmology",
- "ArticleTitle": "Correlations between dyslipidemia and retinal parameters measured with Angio-OCT in type II diabetics without diabetic retinopathy.",
- "Abstract": "Type II diabetes patients tend to have elevated serum lipid levels compared to normal subjects, but the impact of dyslipidemia on the onset and progression of DR is incompletely elucidated.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Dyslipidemias",
- "Middle Aged",
- "Aged",
- "Diabetic Retinopathy",
- "Case-Control Studies",
- "Tomography, Optical Coherence",
- "Retinal Vessels",
- "Fluorescein Angiography",
- "Fundus Oculi",
- "Cholesterol, LDL"
- ]
- },
- {
- "PMID": "39464252",
- "Title": "Journal of the Academy of Nutrition and Dietetics",
- "ArticleTitle": "Randomized Controlled Feasibility Trial of Late 8-Hour Time-Restricted Eating for Adolescents With Type 2 Diabetes.",
- "Abstract": "Recruitment and retention rates suggest a trial of lTRE in adolescents with T2D was feasible. lTRE was seen as acceptable by participants and adherence was high. A revised intervention, building on the successful elements of this pilot alongside adapting implementations strategies to augment adherence and engagement, should therefore be considered.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Feasibility Studies",
- "Female",
- "Adolescent",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Young Adult",
- "Blood Glucose",
- "Glycemic Control",
- "Time Factors",
- "Fasting",
- "Pediatric Obesity",
- "Body Composition",
- "Glycated Hemoglobin",
- "Meals",
- "Blood Glucose Self-Monitoring",
- "Treatment Outcome",
- "Metformin"
- ]
- },
- {
- "PMID": "39464183",
- "Title": "Frontiers in endocrinology",
- "ArticleTitle": "Risk of bone fracture by using dipeptidyl peptidase-4 inhibitors, glucagon-like peptide-1 receptor agonists, or sodium-glucose cotransporter-2 inhibitors in patients with type 2 diabetes mellitus: a network meta-analysis of population-based cohort studies.",
- "Abstract": "https://www.crd.york.ac.uk/prospero/, identifier CRD42023448720.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Fractures, Bone",
- "Dipeptidyl-Peptidase IV Inhibitors",
- "Network Meta-Analysis",
- "Hypoglycemic Agents",
- "Cohort Studies",
- "Glucagon-Like Peptide-1 Receptor Agonists"
- ]
- },
- {
- "PMID": "39463112",
- "Title": "Acta medica Indonesiana",
- "ArticleTitle": "Effectiveness and Safety of DLBS3233 in Newly Diagnosed Type 2 Diabetes Mellitus: A 12-week Clinical Trial.",
- "Abstract": "DLBS3233 showed potential for improving postprandial glucose control in newly diagnosed T2DM individuals. Although significant changes were limited, the study suggests that DLBS3233 could enhance glycemic regulation. The safety evaluation indicated no adverse effects on vital parameters. Further research with larger samples and more prolonged duration is warranted to comprehensively explore DLBS3233's potential in T2DM management.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Middle Aged",
- "Double-Blind Method",
- "Blood Glucose",
- "Adult",
- "Insulin Resistance",
- "Hypoglycemic Agents",
- "Insulin",
- "Adiponectin",
- "Treatment Outcome"
- ]
- },
- {
- "PMID": "39463020",
- "Title": "Journal of diabetes",
- "ArticleTitle": "Stratum corneum hydration levels are negatively correlated with HbA1c levels in the elderly Chinese.",
- "Abstract": "Highlights Stratum corneum hydration levels are negatively correlated with HbA1c levels and positively correlated with skin surface pH. Individuals with type 2 diabetes display lower levels of stratum corneum hydration. Because low stratum corneum hydration levels can increase circulating levels of proinflammatory cytokines, which are linked to the pathogenesis of type 2 diabetes, improvement in stratum corneum hydration can be an alternative approach in the management of type 2 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Aged",
- "Aged, 80 and over",
- "Female",
- "Humans",
- "Male",
- "Middle Aged",
- "China",
- "Diabetes Mellitus, Type 2",
- "East Asian People",
- "Epidermis",
- "Glycated Hemoglobin",
- "Hydrogen-Ion Concentration",
- "Skin"
- ]
- },
- {
- "PMID": "39462728",
- "Title": "Clinical breast cancer",
- "ArticleTitle": "Effective Strategies for the Prevention and Mitigation of Phosphatidylinositol-3-Kinase Inhibitor-Associated Hyperglycemia: Optimizing Patient Care.",
- "Abstract": "Hyperglycemia is a common adverse event (AE) associated with phosphatidylinositol-3-kinase inhibitors (PI3Kis) and considered an on-target effect. Presence of hyperglycemia is associated with poor outcomes in patients with cancer, and there is need for further refinement of hyperglycemia prevention and mitigation strategies in patients receiving PI3Kis. In this review, the authors highlight effective strategies for preventing PI3Ki-induced hyperglycemia before and during treatment as well as hyperglycemia management. Prior to initiating treatment with PI3Ki, identify baseline risk factors of patients at increased risk for developing hyperglycemia, which include older age, obesity, and glycosylated hemoglobin (HbA1c) 5.7%-6.4% (prediabetes or Type 2 diabetes). To prevent new-onset hyperglycemia, optimize blood glucose, and recommend a low-carbohydrate (60-130 g/day) diet along with regular exercise to all patients prior to initiating the PI3Ki. Prophylactic metformin may be considered in all patients starting a PI3Ki with HbA1c \u22646.4%. Although existing recommendations support monitoring fasting blood glucose (FBG) once weekly (twice-weekly for intermediate-risk, daily for high-risk patients) and HbA1c every 3 months upon initiation of PI3Ki, more frequent FBG monitoring may be considered for prompt detection of hyperglycemia. Experts also recommend considering postprandial glucose monitoring because it is an early indicator of glucose intolerance. If hyperglycemia develops, metformin (first-line) and/or sodium glucose co-transporter 2 inhibitors or thiazolidinediones (second-/third-line) are the preferred agents; consider early referral to an endocrinologist. In conclusion, hyperglycemia is a common but manageable AE associated with PI3Kis. Multidisciplinary approach to the prevention, monitoring, and management of hyperglycemia optimizes patient care and allows patients to maintain therapy on PI3Ki.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Blood Glucose",
- "Diabetes Mellitus, Type 2",
- "Glycated Hemoglobin",
- "Hyperglycemia",
- "Hypoglycemic Agents",
- "Neoplasms",
- "Phosphoinositide-3 Kinase Inhibitors"
- ]
- },
- {
- "PMID": "39462671",
- "Title": "Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi",
- "ArticleTitle": "[Functional study of amine oxidase copper-containing 1 (AOC1) in lipid metabolism].",
- "Abstract": "Amine oxidase copper-containing 1 (AOC1) is a key member of copper amine oxidase family, which is responsible for deamination oxidation of histamine and putrescine. In recent years, AOC1 has been reported to be associated with various cancers, with its expression levels significantly elevated in certain cancer cells, suggesting its potential role in cancer progression. However, its function in lipid metabolism still remains unclear. Through genetic analysis, we have discovered a potential relationship between AOC1 and lipid metabolism. To further investigate, we generated ",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Lipid Metabolism",
- "Mice",
- "Amine Oxidase (Copper-Containing)",
- "Diet, High-Fat",
- "Obesity",
- "Liver",
- "Mice, Knockout",
- "Diabetes Mellitus, Type 2",
- "Adipose Tissue, White",
- "Humans",
- "Mice, Inbred C57BL"
- ]
- },
- {
- "PMID": "39462558",
- "Title": "The journal of medical investigation : JMI",
- "ArticleTitle": "Characteristics of storage and voiding symptoms in adult patients with type 2 diabetes with lower urinary tract symptoms.",
- "Abstract": "Our analysis of diabetic patients with LUTS revealed differences in the characteristics of storage and voiding symptoms. These findings provide evidence that the features of LUTS associated with diabetes may have different pathogenic origins. J. Med. Invest. 71 : 237-245, August, 2024.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Male",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Lower Urinary Tract Symptoms",
- "Middle Aged",
- "Cross-Sectional Studies",
- "Aged",
- "Urinary Bladder, Overactive",
- "Adult"
- ]
- },
- {
- "PMID": "39462543",
- "Title": "Drug discoveries & therapeutics",
- "ArticleTitle": "Effect of switching from dulaglutide to tirzepatide on blood glucose and renal function.",
- "Abstract": "The case reports a woman in her 70s, with type 2 diabetes and chronic kidney disease in G4 stage. The patient had elevated HbA1c, and she was switched from linagliptin, a dipeptidyl peptidase 4 inhibitor, to dulaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA). Thereafter, the HbA1c level decreased; however, since the dulaglutide supply became a problem, the patient was switched to tirzepatide, a glucose-dependent insulinotropic polypeptide (GIP)/GLP-1RA. To date, no clinical studies have evaluated the efficacy and safety of switching from GLP-1RA to GIP/GLP-1RA, but we report this case because efficacy was observed in this patient. The therapeutic effects after switching to tirzepatide included decrease in HbA1c, increase in eGFR, and decrease in BUN, when compared to when dulaglutide was used. A change from dulaglutide to tirzepatide, could inhibit renal impairment progression and improve renal function.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Recombinant Fusion Proteins",
- "Glucagon-Like Peptides",
- "Immunoglobulin Fc Fragments",
- "Female",
- "Diabetes Mellitus, Type 2",
- "Aged",
- "Blood Glucose",
- "Hypoglycemic Agents",
- "Glycated Hemoglobin",
- "Renal Insufficiency, Chronic",
- "Drug Substitution",
- "Linagliptin",
- "Glomerular Filtration Rate",
- "Kidney",
- "Glucagon-Like Peptide-2 Receptor",
- "Gastric Inhibitory Polypeptide",
- "Tirzepatide",
- "Glucagon-Like Peptide-1 Receptor Agonists"
- ]
- },
- {
- "PMID": "39462334",
- "Title": "BMC cardiovascular disorders",
- "ArticleTitle": "Pattern and outcome of the first manifestation of cardiovascular disease among patients with type 2 diabetes mellitus in Cameroon: a cross-sectional study.",
- "Abstract": "Not applicable.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Male",
- "Cameroon",
- "Middle Aged",
- "Aged",
- "Cross-Sectional Studies",
- "Adult",
- "Aged, 80 and over",
- "Cardiovascular Diseases",
- "Young Adult",
- "Time Factors",
- "Adolescent",
- "Incidence",
- "Risk Factors",
- "Risk Assessment",
- "Prognosis",
- "Retrospective Studies",
- "Hospitalization",
- "Heart Failure",
- "Myocardial Infarction",
- "Stroke",
- "Hospital Mortality"
- ]
- },
- {
- "PMID": "39462138",
- "Title": "Scientific reports",
- "ArticleTitle": "DII modulates the relationship between SVD3 and NAFLD prevalence, rather than liver fibrosis severity, in hospitalized T2DM population.",
- "Abstract": "Type 2 diabetes (T2DM) patients are at high risk for non-alcoholic fatty liver disease (NAFLD). Studies show SVD3 and dietary inflammatory index (DII) are associated with NAFLD. It's unknown if they interact in T2DM patients with NAFLD. We collected data from 110 hospitalized T2DM patients, measured physiological and biochemical indicators, conducted dietary surveys, and converted data into DII and NFS, FIB-4, and BARD indices. We used logistic regression, mediation effect analysis, and moderation effect analysis to explore the relationship between DII and SVD3 with NAFLD and liver fibrosis in T2DM patients. DII was not significant in either NAFLD incidence in T2DM patients or liver fibrosis in NAFLD patients. SVD3 was positively correlated with NAFLD incidence in T2DM patients, but this correlation became insignificant as DII increased towards pro-inflammation. SVD3 is positively correlated with NAFLD incidence in T2DM patients, but this correlation becomes less significant as DII increases towards pro-inflammation.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Non-alcoholic Fatty Liver Disease",
- "Male",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Middle Aged",
- "Liver Cirrhosis",
- "Prevalence",
- "Aged",
- "Inflammation",
- "Hospitalization",
- "Diet",
- "Severity of Illness Index",
- "Risk Factors",
- "Incidence"
- ]
- },
- {
- "PMID": "39462048",
- "Title": "Scientific reports",
- "ArticleTitle": "HbA1c and leukocyte mtDNA levels as major factors associated with post-COVID-19 syndrome in type 2 diabetes patients.",
- "Abstract": "Post-COVID-19 syndrome (PCS) is an emerging health problem in people recovering from COVID-19 infection within the past 3-6 months. The current study aimed to define the predictive factors of PCS development by assessing the mitochondrial DNA (mtDNA) levels in blood leukocytes, inflammatory markers and HbA1c in type 2 diabetes patients (T2D) with regard to clinical phenotype, gender, and biological age. In this case-control study, 65 T2D patients were selected. Patients were divided into 2 groups depending on PCS presence: the PCS group (n\u2009=\u200944) and patients who did not develop PCS (n\u2009=\u200921) for up to 6 months after COVID-19 infection. HbA1c and mtDNA levels were the primary factors linked to PCS in different models. We observed significantly lower mtDNA content in T2D patients with PCS compared to those without PCS (1.26\u2009\u00b1\u20090.25 vs. 1.44\u2009\u00b1\u20090.24; p\u2009=\u20090.011). In gender-specific and age-related analyses, the mt-DNA amount did not differ significantly between the subgroups. According to the stepwise multivariate logistic regression analysis, low mtDNA content and HbA1c were independent variables associated with PCS development, regardless of oxygen, glucocorticoid therapy and COVID-19 severity. The top-performing model for PCS prediction was the gradient boosting machine (GBM). HbA1c and mtDNA had a notably greater influence than the other variables, indicating their potential as prognostic biomarkers.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "DNA, Mitochondrial",
- "Diabetes Mellitus, Type 2",
- "COVID-19",
- "Male",
- "Female",
- "Middle Aged",
- "Glycated Hemoglobin",
- "Leukocytes",
- "Case-Control Studies",
- "Aged",
- "SARS-CoV-2",
- "Post-Acute COVID-19 Syndrome",
- "Biomarkers",
- "Adult"
- ]
- },
- {
- "PMID": "39461977",
- "Title": "Scientific reports",
- "ArticleTitle": "One-year outcomes of a digital twin intervention for type 2 diabetes: a retrospective real-world study.",
- "Abstract": "This retrospective observational study, building on prior research that demonstrated the efficacy of the Digital Twin (DT) Precision Treatment Program over shorter follow-up periods\u200b\u200b, aimed to examine glycemic control and reduced anti-diabetic medication use after one-year in a DT commercial program. T2D patients enrolled had adequate hepatic and renal function and no recent cardiovascular events. DT intervention powered by artificial intelligence utilizes precision nutrition, activity, sleep, and deep breathing exercises. Outcome measures included HbA1c change, medication reduction, anthropometrics, insulin markers, and continuous glucose monitoring (CGM) metrics. Of 1985 enrollees, 132 (6.6%) were lost to follow-up, leaving 1853 participants who completed one-year. At one-year, participants exhibited significant reductions in HbA1c [mean change: -1.8% (SD 1.7%), p\u2009<\u20090.001], with 1650 (89.0%) achieving HbA1c below 7%. At baseline, participants were on mean 1.9 (SD 1.4) anti-diabetic medications, which decreased to 0.5 (SD 0.7) at one-year [change: -1.5 (SD 1.3), p\u2009<\u20090.001]. Significant reductions in weight [mean change: -4.8\u00a0kg (SD 6.0\u00a0kg), p\u2009<\u20090.001], insulin resistance [HOMA2-IR: -0.1 (SD 1.2), p\u2009<\u20090.001], and improvements in \u03b2-cell function [HOMA2-B: +21.6 (SD 47.7), p\u2009<\u20090.001] were observed, along with better CGM metrics. These findings suggest that DT intervention could play a vital role in the future of T2D care.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Retrospective Studies",
- "Middle Aged",
- "Hypoglycemic Agents",
- "Glycated Hemoglobin",
- "Aged",
- "Treatment Outcome",
- "Blood Glucose",
- "Blood Glucose Self-Monitoring",
- "Adult"
- ]
- },
- {
- "PMID": "39461936",
- "Title": "Obesity surgery",
- "ArticleTitle": "Eight Year Follow-Up After Gastric Bypass and Sleeve Gastrectomy in a Brazilian Cohort: Weight Trajectory and Health Outcomes.",
- "Abstract": "Patients undergoing RYGB showed greater weight loss and less weight regain 8\u00a0years after bariatric surgery compared to those undergoing SG.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Brazil",
- "Gastric Bypass",
- "Male",
- "Adult",
- "Retrospective Studies",
- "Obesity, Morbid",
- "Gastrectomy",
- "Follow-Up Studies",
- "Weight Loss",
- "Middle Aged",
- "Diabetes Mellitus, Type 2",
- "Body-Weight Trajectory",
- "Weight Gain",
- "Treatment Outcome",
- "Dyslipidemias",
- "Hypertension"
- ]
- },
- {
- "PMID": "39461868",
- "Title": "BMJ open",
- "ArticleTitle": "Healthy Eating and Active Lifestyles for Diabetes (HEAL-D) Online: a mixed methods evaluation exploring the feasibility of implementing a virtual culturally tailored diabetes self-management programme for African and Caribbean communities.",
- "Abstract": "This evaluation demonstrates the feasibility of delivering HEAL-D using an online platform, with its ability to achieve similar goals compared with its face-to-face counterpart. Challenges were identified around the identification, recruitment and referral of eligible patients into the programme, which need to be addressed for successful implementation on a wider scale.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Feasibility Studies",
- "Female",
- "Middle Aged",
- "Self-Management",
- "Caribbean Region",
- "Diet, Healthy",
- "London",
- "Aged",
- "Adult",
- "Program Evaluation",
- "Patient Education as Topic",
- "Surveys and Questionnaires",
- "Culturally Competent Care"
- ]
- },
- {
- "PMID": "39461703",
- "Title": "Neuroscience letters",
- "ArticleTitle": "Neurometabolic substrate transport across brain barriers in diabetes mellitus: Implications for cognitive function and neurovascular health.",
- "Abstract": "Neurometabolic homeostasis in the brain depends on the coordinated transport of glucose and other essential substrates across brain barriers, primarily the blood-brain barrier and the blood-cerebrospinal fluid barrier. In type 2 diabetes mellitus (T2DM), persistent hyperglycemia disrupts these processes, leading to neurovascular dysfunction and cognitive impairment. This review examines how T2DM alters glucose and neurometabolite transport, emphasizing the role of glucose transporters and the astrocyte-neuron lactate shuttle in maintaining cerebral energy balance. Reduced expression of glucose transporters and impaired neurovascular coupling are key contributors to cognitive decline in T2DM. Additionally, the review highlights insulin's pivotal role in the hippocampus, where it enhances neuro-glial coupling and modulates astrocyte glucose uptake to support neuronal energy demands. Synthesizing current findings, we underscore the importance of therapeutic strategies aimed at correcting glucose transport dysregulation to alleviate diabetes-associated cognitive decline.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Animals",
- "Blood-Brain Barrier",
- "Diabetes Mellitus, Type 2",
- "Glucose",
- "Cognition",
- "Brain",
- "Neurovascular Coupling",
- "Glucose Transport Proteins, Facilitative",
- "Biological Transport",
- "Astrocytes",
- "Neurons",
- "Cognitive Dysfunction"
- ]
- },
- {
- "PMID": "39461360",
- "Title": "The lancet. Diabetes & endocrinology",
- "ArticleTitle": "Younger-onset compared with later-onset type 2 diabetes: an analysis of the UK Prospective Diabetes Study (UKPDS) with up to 30 years of follow-up (UKPDS 92).",
- "Abstract": "National Institute of Health and Care Research's Biomedical Research Centre.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Middle Aged",
- "Female",
- "Adult",
- "United Kingdom",
- "Follow-Up Studies",
- "Aged",
- "Age of Onset",
- "Prospective Studies",
- "Incidence"
- ]
- },
- {
- "PMID": "39461230",
- "Title": "Journal of diabetes and its complications",
- "ArticleTitle": "Effects of moderate-intensity aerobic training on cardiac structure and function in type 2 mellitus diabetic rats: Based on echocardiography and speckle tracking.",
- "Abstract": "LS-STE was a sensitive method to assess subclinical myocardial changes in T2DM rats. MIAT had the benefit of reversing cardiac systolic subclinical dysfunction in T2DM rats.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Diabetes Mellitus, Type 2",
- "Echocardiography",
- "Rats",
- "Male",
- "Physical Conditioning, Animal",
- "Diabetes Mellitus, Experimental",
- "Heart",
- "Diabetic Cardiomyopathies",
- "Rats, Sprague-Dawley",
- "Ventricular Function, Left",
- "Heart Ventricles"
- ]
- },
- {
- "PMID": "39460755",
- "Title": "Diabetologia",
- "ArticleTitle": "Intermittently scanned continuous glucose\u00a0monitoring compared with blood glucose monitoring is associated with lower HbA",
- "Abstract": "This study shows that Swedish adults with type 2 diabetes on insulin who are using isCGM have a significantly reduced HbA",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Male",
- "Glycated Hemoglobin",
- "Middle Aged",
- "Retrospective Studies",
- "Hospitalization",
- "Blood Glucose",
- "Insulin",
- "Aged",
- "Blood Glucose Self-Monitoring",
- "Hypoglycemic Agents",
- "Sweden",
- "Diabetes Complications",
- "Adult",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39460574",
- "Title": "Journal of diabetes investigation",
- "ArticleTitle": "Association between malnutrition and adverse renal outcomes in patients with type 2 diabetes.",
- "Abstract": "We observed an association between poor nutritional status, assessed by GNRI, and adverse outcomes in patients with type 2 diabetes. Nutritional status assessment has potential utility as a prognostic tool for individuals with type 2 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Malnutrition",
- "Aged",
- "Prognosis",
- "Middle Aged",
- "Nutritional Status",
- "Glomerular Filtration Rate",
- "Risk Factors",
- "Diabetic Nephropathies",
- "Cohort Studies",
- "Follow-Up Studies",
- "Nutrition Assessment",
- "Japan",
- "Geriatric Assessment"
- ]
- },
- {
- "PMID": "39460440",
- "Title": "Pharmacotherapy",
- "ArticleTitle": "ECLIPSES: Early initiation of sodium glucose cotransporter-2 inhibitors for cardiovascular protection in patients with type 2 diabetes following acute coronary syndrome and subsequent coronary artery bypass graft surgery.",
- "Abstract": "Early initiation of SGLT2i use was not associated with a reduction in MACE in patients with T2DM who experienced ACS and underwent subsequent CABG surgery. However, no apparent safety concerns were identified. Adequately powered trials are required to confirm this finding.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Sodium-Glucose Transporter 2 Inhibitors",
- "Diabetes Mellitus, Type 2",
- "Acute Coronary Syndrome",
- "Coronary Artery Bypass",
- "Male",
- "Female",
- "Retrospective Studies",
- "Middle Aged",
- "Aged",
- "Cohort Studies"
- ]
- },
- {
- "PMID": "39459434",
- "Title": "Medicina (Kaunas, Lithuania)",
- "ArticleTitle": "Age-Related Changes in Insulin Resistance and Muscle Mass: Clinical Implications in Obese Older Adults.",
- "Abstract": "The older segment of the global population is increasing at a rapid pace. Advancements in public health and modern medicine lengthened life expectancy and reduced the burden of disease in communities worldwide. Concurrent with this demographic change is the rise in overweight people and obesity, which is evident in all age groups. There is also an aging-related reduction in muscle mass and function, or sarcopenia, that is exacerbated by sedentary lifestyle and poor nutrition. The coexistence of muscle loss and elevated body mass index, termed \"sarcopenic obesity\", has particularly deleterious consequences in older individuals. Worsening insulin resistance and a proinflammatory state operate at the pathophysiologic level and lead to adverse health outcomes such as a proclivity to cardiovascular disease, type 2 diabetes, and even cognitive dysfunction. Although the concept of sarcopenic obesity as a disease construct is being increasingly recognized, a clearer understanding is warranted in order to define its components and health impact. Research is needed at the molecular-cellular level to tie together derangements in insulin action, cytokines, myokines, and endothelial dysfunction with clinical outcomes. Lifestyle modifications as well as targeted nonpharmacologic approaches, such as supplements and antioxidants, appear to have a promising role in reducing the chronic burden of this emerging disorder. Breakthroughs in drug therapies that retard or even reverse the underlying dynamics of sarcopenia and obesity in older persons are being actively explored.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Insulin Resistance",
- "Obesity",
- "Sarcopenia",
- "Aged",
- "Aging",
- "Muscle, Skeletal",
- "Body Mass Index",
- "Male",
- "Diabetes Mellitus, Type 2",
- "Female"
- ]
- },
- {
- "PMID": "39459431",
- "Title": "Medicina (Kaunas, Lithuania)",
- "ArticleTitle": "Scoring Health Behaviors of Patients with Type 2 Diabetes.",
- "Abstract": {
- "i": "Conclusions"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Middle Aged",
- "Health Behavior",
- "Surveys and Questionnaires",
- "Aged",
- "Poland",
- "Adult",
- "Exercise",
- "Healthy Lifestyle",
- "Life Style"
- ]
- },
- {
- "PMID": "39459430",
- "Title": "Medicina (Kaunas, Lithuania)",
- "ArticleTitle": "Beyond Blood Sugar: Low Awareness of Kidney Disease among Type 2 Diabetes Mellitus Patients in Dalmatia-Insights from the First Open Public Call.",
- "Abstract": {
- "i": "Conclusions",
- "sup": "2"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Male",
- "Cross-Sectional Studies",
- "Middle Aged",
- "Aged",
- "Health Knowledge, Attitudes, Practice",
- "Lithuania",
- "Diet, Mediterranean",
- "Prevalence",
- "Kidney Diseases",
- "Blood Glucose"
- ]
- },
- {
- "PMID": "39459411",
- "Title": "Medicina (Kaunas, Lithuania)",
- "ArticleTitle": "Impact of the COVID-19 Pandemic on Lifestyle Behavior and Clinical Care Pathway Management in Type 2 Diabetes: A Retrospective Cross-Sectional Study.",
- "Abstract": {
- "i": "Conclusions:"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "COVID-19",
- "Cross-Sectional Studies",
- "Retrospective Studies",
- "Male",
- "Female",
- "Middle Aged",
- "Italy",
- "Exercise",
- "Life Style",
- "Aged",
- "Surveys and Questionnaires",
- "SARS-CoV-2",
- "Adult",
- "Pandemics"
- ]
- },
- {
- "PMID": "39459404",
- "Title": "Medicina (Kaunas, Lithuania)",
- "ArticleTitle": "Cardiovascular Risk Factors as Independent Predictors of Diabetic Retinopathy in Type II Diabetes Mellitus: The Development of a Predictive Model.",
- "Abstract": {
- "i": "Conclusions"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Diabetic Retinopathy",
- "Middle Aged",
- "Cross-Sectional Studies",
- "Retrospective Studies",
- "Aged",
- "Heart Disease Risk Factors",
- "Risk Factors",
- "Logistic Models",
- "Cardiovascular Diseases",
- "Body Mass Index",
- "ROC Curve"
- ]
- },
- {
- "PMID": "39459249",
- "Title": "Molecules (Basel, Switzerland)",
- "ArticleTitle": "Identification of Novel PPAR\u03b3 Partial Agonists Based on Virtual Screening Strategy: In Silico and In Vitro Experimental Validation.",
- "Abstract": "Thiazolidinediones (TZDs) including rosiglitazone and pioglitazone function as peroxisome proliferator-activated receptor gamma (PPAR\u03b3) full agonists, which have been known as a class to be among the most effective drugs for the treatment of type 2 diabetes mellitus (T2DM). However, side effects of TZDs such as fluid retention and weight gain are associated with their full agonistic activities toward PPAR\u03b3 induced by the AF-2 helix-involved \"locked\" mechanism. Thereby, this study aimed to obtain novel PPAR\u03b3 partial agonists without direct interaction with the AF-2 helix. Through performing virtual screening of the Targetmol L6000 Natural Product Library and utilizing molecular dynamics (MD) simulation, as well as molecular mechanics Poisson-Boltzmann surface area (MM-PBSA) analysis, four compounds including tubuloside b, podophyllotoxone, endomorphin 1 and paliperidone were identified as potential PPAR\u03b3 partial agonists. An in vitro TR-FRET competitive binding assay showed podophyllotoxone displayed the optimal binding affinity toward PPAR\u03b3 among the screened compounds, exhibiting IC",
- "Predictions": [],
- "MeshTerms": [
- "PPAR gamma",
- "Molecular Dynamics Simulation",
- "Humans",
- "Molecular Docking Simulation",
- "Hypoglycemic Agents",
- "Thiazolidinediones",
- "Protein Binding",
- "Drug Evaluation, Preclinical",
- "Rosiglitazone",
- "Diabetes Mellitus, Type 2",
- "Computer Simulation"
- ]
- },
- {
- "PMID": "39458556",
- "Title": "Nutrients",
- "ArticleTitle": "Exploring the Interplay of Genetics and Nutrition in the Rising Epidemic of Obesity and Metabolic Diseases.",
- "Abstract": {
- "b": "Discussion and Conclusions",
- "i": "LEPR"
- },
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Obesity",
- "Alpha-Ketoglutarate-Dependent Dioxygenase FTO",
- "Genetic Predisposition to Disease",
- "Metabolic Diseases",
- "Nutritional Status",
- "Receptor, Melanocortin, Type 4",
- "Diabetes Mellitus, Type 2",
- "Diet",
- "Feeding Behavior",
- "Epigenesis, Genetic",
- "Receptors, Leptin",
- "Gene-Environment Interaction"
- ]
- },
- {
- "PMID": "39458552",
- "Title": "Nutrients",
- "ArticleTitle": "The Contribution of Postprandial Glucose Levels to Hyperglycemia in Type 2 Diabetes Calculated from Continuous Glucose Monitoring Data: Real World Evidence from the DIALECT-2 Cohort.",
- "Abstract": "Both PPG and FPG contribute to hyperglycemia, with PPG playing a larger role in patients with better glycemic control, especially after breakfast. Targeting PPG may be crucial for optimizing glucose management.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Blood Glucose",
- "Postprandial Period",
- "Male",
- "Female",
- "Hyperglycemia",
- "Middle Aged",
- "Blood Glucose Self-Monitoring",
- "Aged",
- "Glycated Hemoglobin",
- "Cohort Studies",
- "Fasting",
- "Dietary Carbohydrates",
- "Meals",
- "Continuous Glucose Monitoring"
- ]
- },
- {
- "PMID": "39458507",
- "Title": "Nutrients",
- "ArticleTitle": "Development of a Diabetes Dietary Quality Index: Reproducibility and Associations with Measures of Insulin Resistance, Beta Cell Function, and Hyperglycemia.",
- "Abstract": "We identified a questionnaire-derived Diabetes Dietary Quality index that was reproducible and inversely associated with a number of type 2 diabetes mellitus and metabolic risk factors, like 2 h post-meal glucose, Hba1c and LDL, and total cholesterol. Once relative validity has been established, the Diabetes Dietary Quality index could be used by health care professionals to identify individuals with diets adversely related to development of type 2 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Insulin Resistance",
- "Male",
- "Female",
- "Diabetes Mellitus, Type 2",
- "Insulin-Secreting Cells",
- "Reproducibility of Results",
- "Adult",
- "Middle Aged",
- "Hyperglycemia",
- "Risk Factors",
- "Surveys and Questionnaires",
- "Blood Glucose",
- "Diet, Healthy",
- "Diet",
- "Insulin",
- "Diet Surveys",
- "Glucose Clamp Technique"
- ]
- },
- {
- "PMID": "39458504",
- "Title": "Nutrients",
- "ArticleTitle": "Does Online Social Support Affect the Eating Behaviors of Polish Women with Insulin Resistance?",
- "Abstract": "Our study indicates a relationship between participation in online support groups and dietary behaviors and the subjective assessment of nutrition knowledge. Future research should focus on elucidating the mechanisms behind these influences and exploring how these communities can be optimized for broader public health initiatives.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Insulin Resistance",
- "Poland",
- "Middle Aged",
- "Adult",
- "Feeding Behavior",
- "Social Support",
- "Diabetes Mellitus, Type 2",
- "Surveys and Questionnaires",
- "Diet, Healthy",
- "Self-Help Groups",
- "Diet",
- "Aged",
- "Internet"
- ]
- },
- {
- "PMID": "39458486",
- "Title": "Nutrients",
- "ArticleTitle": "Microbiota Transplantation in Individuals with Type 2 Diabetes and a High Degree of Insulin Resistance.",
- "Abstract": "The objective of this study was to determine the results of fecal microbiota transplantation (FMT) from healthy lean subjects in patients with type 2 diabetes (T2D); Methods: We designed a phase II, randomized, single-blind, parallel-arm clinical trial. Twenty-one subjects (12 men [57.1%] and 9 women [42.9%]), who had previously signed an informed consent were randomized to FMT from lean donors, a probiotic (",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Female",
- "Male",
- "Insulin Resistance",
- "Middle Aged",
- "Fecal Microbiota Transplantation",
- "Probiotics",
- "Aged",
- "Blood Glucose",
- "Single-Blind Method",
- "Glucose Tolerance Test",
- "Gastrointestinal Microbiome",
- "Insulin",
- "Body Mass Index",
- "Lactobacillus delbrueckii",
- "Treatment Outcome",
- "Glycated Hemoglobin"
- ]
- },
- {
- "PMID": "39458482",
- "Title": "Nutrients",
- "ArticleTitle": "Experiences of Postpartum Follow-Up and Participation in a Lifestyle Intervention after Gestational Diabetes: A Qualitative Study.",
- "Abstract": "The study findings can help support the development of future intervention programmes for women who have experienced gestational diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Female",
- "Diabetes, Gestational",
- "Pregnancy",
- "Adult",
- "Postpartum Period",
- "Qualitative Research",
- "Norway",
- "Follow-Up Studies",
- "Life Style",
- "Healthy Lifestyle",
- "Diabetes Mellitus, Type 2",
- "Motivation"
- ]
- },
- {
- "PMID": "39458444",
- "Title": "Nutrients",
- "ArticleTitle": "Harnessing Prebiotics to Improve Type 2 Diabetes Outcomes.",
- "Abstract": "The gut microbiota, a complex ecosystem of microorganisms in the human gastrointestinal tract (GI), plays a crucial role in maintaining metabolic health and influencing disease susceptibility. Dysbiosis, or an imbalance in gut microbiota, has been linked to the development of type 2 diabetes mellitus (T2DM) through mechanisms such as reduced glucose tolerance and increased insulin resistance. A balanced gut microbiota, or eubiosis, is associated with improved glucose metabolism and insulin sensitivity, potentially reducing the risk of diabetes-related complications. Various strategies, including the use of prebiotics like inulin, fructooligosaccharides, galactooligosaccharides, resistant starch, pectic oligosaccharides, polyphenols, \u03b2-glucan, and ",
- "Predictions": [],
- "MeshTerms": [
- "Prebiotics",
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Gastrointestinal Microbiome",
- "Dysbiosis",
- "Blood Glucose"
- ]
- },
- {
- "PMID": "39458436",
- "Title": "Nutrients",
- "ArticleTitle": {
- "i": "Akkermansia muciniphila"
- },
- "Abstract": "Overall, Akk appears to be effective at reducing the onset of type 2 diabetes and diet-induced obesity. Long-term studies with larger sample sizes are needed to confirm these beneficial effects, as the current animal studies were of short duration (less than 20 weeks).",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 2",
- "Obesity",
- "Animals",
- "Akkermansia",
- "Probiotics",
- "Gastrointestinal Microbiome",
- "Verrucomicrobia",
- "Blood Glucose",
- "Insulin",
- "Disease Models, Animal",
- "Weight Gain"
- ]
- },
- {
- "PMID": "39457303",
- "Title": "International journal of environmental research and public health",
- "ArticleTitle": "Stakeholder Perspectives on the Acceptability, Design, and Integration of Produce Prescriptions for People with Type 2 Diabetes in Australia: A Formative Study.",
- "Abstract": "Produce prescription programs can benefit both individuals and health systems; however, best practices for integrating such programs into the Australian health system are yet unknown. This study explored stakeholders' perspectives on the acceptability, potential design and integration of produce prescription programs for adults with type 2 diabetes in Australia. Purposive sampling was used to recruit 22 participants for an online workshop, representing six stakeholder groups (government, healthcare service, clinician, food retailer, consumer, non-government organisation). Participant responses were gathered through workshop discussions and a virtual collaboration tool (Mural). The workshop was video-recorded and transcribed verbatim, and thematic analysis was conducted using a deductive-inductive approach. Stakeholders recognised produce prescription as an acceptable intervention; however, they identified challenges to implementation related to contextuality, accessibility, and sustainability. Stakeholders were vocal about the approach (e.g., community-led) and infrastructure (e.g., screening tools) needed to support program design and implementation but expressed diverse views about potential funding models, indicating a need for further investigation. Aligning evaluation outcomes with existing measures in local, State and Federal initiatives was recommended, and entry points for integration were identified within and outside of the Australian health sector. Our findings provide clear considerations for future produce prescription interventions for people with type 2 diabetes.",
- "Predictions": [],
- "MeshTerms": [
- "Diabetes Mellitus, Type 2",
- "Humans",
- "Australia",
- "Stakeholder Participation",
- "Male",
- "Female",
- "Adult",
- "Middle Aged",
- "Prescriptions"
- ]
- },
- {
- "PMID": "39457293",
- "Title": "International journal of environmental research and public health",
- "ArticleTitle": "Impact of Oral Hygiene Practices in Reducing Cardiometabolic Risk, Incidence, and Mortality: A Systematic Review.",
- "Abstract": "Cardiometabolic diseases share many modifiable risk factors. However, periodontitis, a chronic inflammatory condition of the gums, is a risk factor that is rarely publicized. This systematic review aims to evaluate the impact of oral hygiene practices on the risk, incidence, and/or mortality rate of cardiovascular disease (CVD), type 2 diabetes mellitus (T2DM), and chronic kidney disease (CKD). Searches were conducted using MEDLINE, Embase, Scopus, and CINHAL. Randomized controlled trials (RCTs), quasi-RCTs, and observational studies were included. Eligible studies reported on associations of toothbrushing, interdental cleaning, mouthwash, or toothpaste use, either alone or in combination with CVD, CKD, and/or T2DM outcomes in adults \u2265 18 years. Fifty-five studies were included. Cochrane's risk of bias tool and the Newcastle-Ottawa Scale were used for quality assessment. Data synthesis is narratively presented. Toothbrushing and interdental cleaning were associated with lower risk of developing T2DM or hypertension HR 0.54 [",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Oral Hygiene",
- "Cardiovascular Diseases",
- "Incidence",
- "Diabetes Mellitus, Type 2",
- "Renal Insufficiency, Chronic",
- "Mouthwashes",
- "Risk Factors",
- "Toothbrushing"
- ]
- },
- {
- "PMID": "39457249",
- "Title": "International journal of environmental research and public health",
- "ArticleTitle": "Diabetes Distress and Health-Related Quality of Life among Patients with Type 2 Diabetes-Mediating Role of Experiential Avoidance and Moderating Role of Post-Traumatic Growth.",
- "Abstract": "These findings underscore the importance of Acceptance and Commitment Therapy as it can potentially decrease the experiential avoidance behaviour of patients. Moreover, intervention should also target the facilitation of PTG due to its beneficial effects in reducing the negative effects of diabetes distress on health and recovery.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Diabetes Mellitus, Type 2",
- "Quality of Life",
- "Male",
- "Female",
- "Middle Aged",
- "Nigeria",
- "Posttraumatic Growth, Psychological",
- "Adult",
- "Aged",
- "Stress, Psychological",
- "Cross-Sectional Studies",
- "Avoidance Learning"
- ]
- },
- {
- "PMID": "39457110",
- "Title": "International journal of molecular sciences",
- "ArticleTitle": "Sexual Dimorphism in Impairment of Acetylcholine-Mediated Vasorelaxation in Zucker Diabetic Fatty (ZDF) Rat Aorta: A Monogenic Model of Obesity-Induced Type 2 Diabetes.",
- "Abstract": "Several reports, including our previous studies, indicate that hyperglycemia and diabetes mellitus exert differential effects on vascular function in males and females. This study examines sex differences in the vascular effects of type 2 diabetes (T2D) in an established monogenic model of obesity-induced T2D, Zucker Diabetic Fatty (ZDF) rats. Acetylcholine (ACh) responses were assessed in phenylephrine pre-contracted rings before and after apocynin, a NADPH oxidase (NOX) inhibitor. The mRNA expressions of aortic endothelial NOS (eNOS), and key NOX isoforms were also measured. We demonstrated the following: (1) diabetes had contrasting effects on aortic vasorelaxation in ZDF rats, impairing relaxation to ACh in females while enhancing it in male ZDF rats; (2) inhibition of NOX, a major source of superoxide in vasculature, restored aortic vasorelaxation in female ZDF rats; and (3) eNOS and NOX4 mRNA expressions were elevated in female (but not male) ZDF rat aortas compared to their respective leans. This study highlights sexual dimorphism in ACh-mediated vasorelaxation in the aorta of ZDF rats, suggesting that superoxide may play a role in the impaired vasorelaxation observed in female ZDF rats.",
- "Predictions": [],
- "MeshTerms": [
- "Animals",
- "Acetylcholine",
- "Diabetes Mellitus, Type 2",
- "Male",
- "Female",
- "Rats, Zucker",
- "Obesity",
- "Rats",
- "Vasodilation",
- "Sex Characteristics",
- "Nitric Oxide Synthase Type III",
- "Aorta",
- "NADPH Oxidase 4",
- "Disease Models, Animal",
- "NADPH Oxidases",
- "Superoxides"
- ]
- },
- {
- "PMID": "39457081",
- "Title": "International journal of molecular sciences",
- "ArticleTitle": "Glucagon-like Peptide 1 Receptor Agonists in Cardio-Oncology: Pathophysiology of Cardiometabolic Outcomes in Cancer Patients.",
- "Abstract": "Cancer patients, especially long cancer survivors, are exposed to several cardio-metabolic diseases, including diabetes, heart failure, and atherosclerosis, which increase their risk of cardiovascular mortality. Therapy with glucagon-like peptide 1 (GLP1) receptor agonists demonstrated several beneficial cardiovascular effects, including atherosclerosis and heart failure prevention. Cardiovascular outcome trials (CVOTs) suggest that GLP-1 RA could exert cardiorenal benefits and systemic anti-inflammatory effects in patients with type-2 diabetes through the activation of cAMP and PI3K/AkT pathways and the inhibition of NLRP-3 and MyD88. In this narrative review, we highlight the biochemical properties of GLP-1 RA through a deep analysis of the clinical and preclinical evidence of the primary prevention of cardiomyopathies. The overall picture of this review encourages the study of GLP-1 RA in cancer patients with type-2 diabetes, as a potential primary prevention strategy against heart failure and atherosclerosis.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Glucagon-Like Peptide-1 Receptor",
- "Neoplasms",
- "Diabetes Mellitus, Type 2",
- "Animals",
- "Cardiovascular Diseases",
- "Atherosclerosis",
- "Heart Failure",
- "Hypoglycemic Agents",
- "Cardio-Oncology",
- "Glucagon-Like Peptide-1 Receptor Agonists"
- ]
- },
- {
- "PMID": "39457018",
- "Title": "International journal of molecular sciences",
- "ArticleTitle": "Regulation of Mitochondrial and Peroxisomal Metabolism in Female Obesity and Type 2 Diabetes.",
- "Abstract": "Obesity and type 2 diabetes (T2D) are widespread metabolic disorders that significantly impact global health today, affecting approximately 17% of adults worldwide with obesity and 9.3% with T2D. Both conditions are closely linked to disruptions in lipid metabolism, where peroxisomes play a pivotal role. Mitochondria and peroxisomes are vital organelles responsible for lipid and energy regulation, including the \u03b2-oxidation and oxidation of very long-chain fatty acids (VLCFAs), cholesterol biosynthesis, and bile acid metabolism. These processes are significantly influenced by estrogens, highlighting the interplay between these organelles' function and hormonal regulation in the development and progression of metabolic diseases, such as obesity, metabolic dysfunction-associated fatty liver disease (MAFLD), and T2D. Estrogens modulate lipid metabolism through interactions with nuclear receptors, like peroxisome proliferator-activated receptors (PPARs), which are crucial for maintaining metabolic balance. Estrogen deficiency, such as in postmenopausal women, impairs PPAR regulation, leading to lipid accumulation and increased risk of metabolic disorders. The disruption of peroxisomal-mitochondrial function and estrogen regulation exacerbates lipid imbalances, contributing to insulin resistance and ROS accumulation. This review emphasizes the critical role of these organelles and estrogens in lipid metabolism and their implications for metabolic health, suggesting that therapeutic strategies, including hormone replacement therapy, may offer potential benefits in treating and preventing metabolic diseases.",
- "Predictions": [],
- "MeshTerms": [
- "Humans",
- "Peroxisomes",
- "Diabetes Mellitus, Type 2",
- "Mitochondria",
- "Obesity",
- "Female",
- "Lipid Metabolism",
- "Animals",
- "Estrogens",
- "Peroxisome Proliferator-Activated Receptors"
- ]
- }
-]
\ No newline at end of file
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deleted file mode 100644
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--- a/model/data/training_data_paresed.json
+++ /dev/null
@@ -1,1862 +0,0 @@
-[
- {
- "text": "Current opinion in anaesthesiology \n Caring for patients with diabetes in the outpatient surgical setting: current recommendations and controversies. \n Future research needs to specifically examine chronic blood glucose control, day of surgery targets, effective home medication management and the risk of perioperative hyperglycemia in ambulatory surgery. Education, protocols and resources to support the care of perioperative patients in the outpatient setting will aid providers on the day of surgery and provide optimal diabetes care leading up to surgery.",
- "labels": [
- 0
- ]
- },
- {
- "text": "PloS one \n Burden of diabetes mellitus in Weifang: Changing trends in prevalence and deaths from 2010 to 2021. \n The city is faced with a significant challenge of diabetes, which is influenced by factors such as gender, age, cultural background, and marital status. Unspecified diabetes mellitus (DM) with ketoacidosis (10.03%) and T2DM with renal complications (0.23%) are identified as the primary direct and underlying causes of death among diabetic patients, respectively. This study serves as a valuable reference for other regions in terms of diabetes prevention, control, and the management of chronic diseases.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Open biology \n The post-translational modification O-GlcNAc is a sensor and regulator of metabolism. \n Cells must rapidly adapt to changes in nutrient conditions through responsive signalling cascades to maintain homeostasis. One of these adaptive pathways results in the post-translational modification of proteins by O-GlcNAc. O-GlcNAc modifies thousands of nuclear and cytoplasmic proteins in response to nutrient availability through the hexosamine biosynthetic pathway. O-GlcNAc is highly dynamic and can be added and removed from proteins multiple times throughout their life cycle, setting it up to be an ideal regulator of cellular processes in response to metabolic changes. Here, we describe the link between cellular metabolism and O-GlcNAc, and we explore O-GlcNAc's role in regulating cellular processes in response to nutrient levels. Specifically, we discuss the mechanisms of elevated O-GlcNAc levels in contributing to diabetes and cancer, as well as the role of decreased O-GlcNAc levels in neurodegeneration. These studies form a foundational understanding of aberrant O-GlcNAc in human disease and provide an opportunity to further improve disease identification and treatment.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Medical decision making : an international journal of the Society for Medical Decision Making \n Using QALYs as an Outcome for Assessing Global Prediction Accuracy in Diabetes Simulation Models. \n Diabetes simulation models are currently validated by examining their ability to predict the incidence of individual events (e.g., myocardial infarction, stroke, amputation) or composite events (e.g., first major adverse cardiovascular event).We introduce Q",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "BMC endocrine disorders \n Association between night blindness history and risk of diabetes in the Chinese population: a multi-center, cross sectional study. \n The results suggest that NB history might be associated with increased odds of diabetes in Chinese community-dwelling adults.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMC health services research \n Geographical Access to Point-of-care diagnostic tests for diabetes, anaemia, Hepatitis B, and human immunodeficiency virus in the Bono Region, Ghana. \n The findings revealed moderate access to all the tests in districts across the region. However, geographical access to glucose, Hb, Hep B, and HIV POC testing was poor (distance\u2009\u2265\u200910\u00a0km and travel time of \u2265\u200993\u00a0min), in the Banda district. This study showed the need to prioritise the Banda district for targeted improvement for all the tests. A further study is recommended to identify potential solutions to addressing the POC testing implementation in the BR, as demonstrated by this study.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of managed care & specialty pharmacy \n Potential benefits of incorporating social determinants of health screening on comprehensive medication management effectiveness. \n Although not statistically significant, the results of this pilot evaluation suggest the potential for meaningful clinical improvements from screening and referral of SDoH needs as a part of CMM encounters. These results should be corroborated using a larger, more robust study design.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Current diabetes reports \n Implementation Science and Pediatric Diabetes: A Scoping Review of the State of the Literature and Recommendations for Future Research. \n Of 23 papers identified, 19 were published since 2017 and 21 focused on type 1 diabetes. Most involved medical evidence-based practices (EBPs; n\u2009=\u200915), whereas fewer focused on psychosocial (n\u2009=\u20097) and diabetes education (n\u2009=\u20092). The majority either identified barriers and facilitators of implementing an EBP (n\u2009=\u200911) or were implementation trials (n\u2009=\u200911). Fewer studies documented gaps in EBP implementation in standard care (n\u2009=\u20097) or development of implementation strategies (n\u2009=\u20091). Five papers employed IS theories and two aimed to improve equity. There is a paucity of IS research in pediatric diabetes care literature. Few papers employed IS theory, used consistent IS terminology, or described IS strategies or outcomes. Guidance for future research to improve IS research in pediatric diabetes is offered.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Biogerontology \n A novel (-)-(2S)-7,4'-dihydroxyflavanone compound for treating age-related diabetes mellitus through immunoinformatics-guided activation of CISD3. \n The iron-sulfur domain (CISD) proteins of CDGSH are classified into three classes: CISD1, CISD2, and CISD3. During premature ageing, mutations that affect these proteins, namely their binding sites, could result in reduced protein production and an inability to preserve cellular integrity. Consequently, this leads to the development of conditions such as diabetes. Notably, CISD3 plays a crucial role in the management of age-related disorders such as Wolfram syndrome, which is often referred to as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness). Computational analyses have predicted that CISD3 regulates the redox state, safeguards the endoplasmic reticulum and mitochondria, and maintains intracellular calcium levels. CISD3, a member of a recently discovered gene family associated with the CDGSH iron protein apoptotic compensatory response, fulfils a crucial function in mitigating the effects of accelerated ageing. The compound \"(-)-(2S)-7,4'-Dihydroxyflavanone\" has been discovered by computational drug design as a possible activator of CISD3. It shows potential therapeutic benefits in ameliorating metabolic dysfunction and enhancing glucose regulation. The ligand binds to the binding pocket of the CISD3 protein, increasing the stability of the protein and enhancing its functionality. The current research investigates the binding processes of the molecule in various structures and its anticipated effects on these tissues, therefore providing valuable insights into the mitigation of age-related diabetes and metabolic dysfunction. The projected tripling of the worldwide population of individuals aged 50 and above by 2050 necessitates the urgent development of immunoinformatics-based approaches, including pharmaceutical therapies that target CISD3, to prevent age-related pathologies. The stimulation of CISD3, namely by compounds such as \"(-)-(2S)-7,4'-Dihydroxyflavanone\", has the potential to counteract telomere shortening and improve metabolic pathways.",
- "labels": [
- 0
- ]
- },
- {
- "text": "The journals of gerontology. Series B, Psychological sciences and social sciences \n Economic Disadvantage During Childhood, Obesity, and Diabetes Across Three Birth Cohorts of Older Mexicans. \n High body weight across Mexican birth cohorts seemed to offset the potential benefits from improvements in childhood conditions on adult diabetes risk.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Stem cell research & therapy \n Human mesenchymal stem/stromal cell based-therapy in diabetes mellitus: experimental and clinical perspectives. \n Diabetes mellitus (DM), a chronic metabolic disease, poses a significant global health challenge, with current treatments often fail to prevent the long-term disease complications. Mesenchymal stem/stromal cells (MSCs) are, adult progenitors, able to repair injured tissues, exhibiting regenerative effects and immunoregulatory and anti-inflammatory responses, so they have been emerged as a promising therapeutic approach in many immune-related and inflammatory diseases. This review summarizes the therapeutic mechanisms and outcomes of MSCs, derived from different human tissue sources (hMSCs), in the context of DM type 1 and type 2. Animal model studies and clinical trials indicate that hMSCs can facilitate pleiotropic actions in the diabetic milieu for improved metabolic indices. In addition to modulating abnormally active immune system, hMSCs can ameliorate peripheral insulin resistance, halt beta-cell destruction, preserve residual beta-cell mass, promote beta-cell regeneration and insulin production, support islet grafts, and correct lipid metabolism. Moreover, hMSC-free derivatives, importantly extracellular vesicles, have shown potent experimental anti-diabetic efficacy. Moreover, the review discusses the diverse priming strategies that are introduced to enhance the preclinical anti-diabetic actions of hMSCs. Such strategies are recommended to restore the characteristics and functions of MSCs isolated from patients with DM for autologous implications. Finally, limitations and merits for the wide spread clinical applications of MSCs in DM such as the challenge of autologous versus allogeneic MSCs, the optimal MSC tissue source and administration route, the necessity of larger clinical trials for longer evaluation duration to assess safety concerns, are briefly presented.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMC endocrine disorders \n Lipids as the link between central obesity and diabetes: perspectives from mediation analysis. \n In central obesity-related diabetes risk, most lipids, especially lipid ratio parameters, play a significant mediating role. Given these findings, we advocate for increased efforts in multifactorial risk monitoring and joint management of diabetes. The evaluation of lipids, particularly lipid ratio parameters, may be holds substantial value in the prevention and management of diabetes risk under close monitoring of central obesity.",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "Applied microbiology and biotechnology \n Gut microbiota predict retinopathy in patients with diabetes: A longitudinal cohort study. \n The gut microbiota has emerged as an independent risk factor for diabetes and its complications. This research aimed to delve into the intricate relationship between the gut microbiome and diabetic retinopathy (DR) through a dual approach of cross-sectional and prospective cohort studies. In our cross-sectional study cross-sectional investigation involving ninety-nine individuals with diabetes, distinct microbial signatures associated with DR were identified. Specifically, gut microbiome profiling revealed decreased levels of Butyricicoccus and Ruminococcus torques group, alongside upregulated methanogenesis pathways among DR patients. These individuals concurrently exhibited lower concentrations of short-chain fatty acids in their plasma. Leveraging machine learning models, including random forest classifiers, we constructed a panel of microbial genera and genes that robustly differentiated DR cases. Importantly, these genera also demonstrated significant correlations with dietary patterns and the molecular profiles of peripheral blood mononuclear cells. Building upon these findings, our prospective cohort study followed 62 diabetes patients over a 2-year period to assess the predictive value of these microbial markers. The results underlined the panel's efficacy in predicting DR incidence. By stratifying patients based on the predictive genera and metabolites identified in the cross-sectional phase, we established significant associations between reduced levels of Butyricicoccus, plasma acetate, and increased susceptibility to DR. This investigation not only deepens our understanding of how gut microbiota influences DR but also underscores the potential of microbial markers as early indicators of disease risk. These insights hold promise for developing targeted interventions aimed at mitigating the impact of diabetic complications. KEY POINTS: \u2022 Microbial signatures are differed in diabetic patients with and without retinopathy \u2022 DR-related taxa are linked to dietary habits and transcriptomic profiles \u2022 Lower abundances of Butyricicoccus and acetate were prospectively associated with DR.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Current medical research and opinion \n Technological advancements in glucose monitoring and artificial pancreas systems for shaping diabetes care. \n The management of diabetes mellitus has undergone remarkable progress with the introduction of cutting-edge technologies in glucose monitoring and artificial pancreas systems. These innovations have revolutionized diabetes care, offering patients more precise, convenient, and personalized management solutions that significantly improve their quality of life. This review aims to provide a comprehensive overview of recent technological advancements in glucose monitoring devices and artificial pancreas systems, focusing on their transformative impact on diabetes care. A detailed review of the literature was conducted to examine the evolution of glucose monitoring technologies, from traditional invasive methods to more advanced systems. The review explores minimally invasive techniques such as continuous glucose monitoring (CGM) systems and flash glucose monitoring (FGM) systems, which have already been proven to enhance glycemic control and reduce the risk of hypoglycemia. In addition, emerging non-invasive glucose monitoring technologies, including optical, electrochemical, and electro-mechanical methods, were evaluated. These techniques are paving the way for more patient-friendly options that eliminate the need for frequent finger-prick tests, thereby improving adherence and ease of use. Advancements in closed-loop artificial pancreas systems, which integrate CGM with automated insulin delivery, were also examined. These systems, often referred to as \"hybrid closed-loop\" or \"automated insulin delivery\" systems, represent a significant leap forward in diabetes care by automating the process of insulin dosing. Such advancements aim to mimic the natural function of the pancreas, allowing for better glucose regulation without the constant need for manual interventions by the patient. Technological breakthroughs in glucose monitoring and artificial pancreas systems have had a profound impact on diabetes management, providing patients with more accurate, reliable, and individualized treatment options. These innovations hold the potential to significantly improve glycemic control, reduce the incidence of diabetes-related complications, and ultimately enhance the quality of life for individuals living with diabetes. Researchers are continually exploring novel methods to measure glucose more effectively and with greater convenience, further refining the future of diabetes care. Researchers are also investigating the integration of artificial intelligence and machine learning algorithms to further enhance the precision and predictive capabilities of glucose monitoring and insulin delivery systems. With ongoing advancements in sensor technology, connectivity, and data analytics, the future of diabetes care promises to deliver even more seamless, real-time management, empowering patients with greater autonomy and improved health outcomes.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Medicine \n Association of triglyceride-glucose index with diabetes or prediabetes in Chinese hypertensive patients: A retrospective cohort study. \n Insulin resistance is a key factor in diabetes development. This study aimed to investigate the association between baseline triglyceride-glucose (TyG) index, a surrogate marker of insulin resistance, and the onset of hyperglycemia in Chinese individuals with hypertension. Using the Rich Healthcare Group database, this retrospective cohort study included 28,687 hypertensive individuals without preexisting diabetes. A wide range of demographic information and baseline biochemical indicators was collected and rigorously analyzed. This study utilized the Cox proportional hazards model and smooth curve fitting to explore the link between TyG index and the risk of developing hyperglycemia. The robustness of the findings was validated by sensitivity and subgroup analyses. During longitudinal monitoring of hypertensive patients in our retrospective cohort study, we observed that 5.31% (1524/28,687) progressed to diabetes, while 21.66% (4620/21,326) developed prediabetes. After adjusting for confounding variables, a statistically significant positive association was observed between the TyG index and the risk of hyperglycemia. Subgroup and sensitivity analyses further supported these findings, demonstrating consistent outcomes and reinforcing the robustness of our conclusions. The TyG index, which is significantly linked to hyperglycemia in hypertensives, can aid early risk identification and intervention.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Medicine \n Association between serum globulins and diabetes mellitus in American latent tuberculosis infection patients: A cross-sectional study. \n Diabetes mellitus (DM) is predisposing to the development of latent tuberculosis infection (LTBI). An understanding of the underlying factors of LTBI-DM is important for tuberculosis prevention and control. This study aims to evaluate the association between LTBI and DM among the noninstitutionalized civilian population in the United States, focusing on the impact of serum globulins. We performed a cross-sectional study design using public data from 2011 to 2012 National Health and Nutrition Examination Survey, focusing on participants diagnosed with LTBI who were aged 20 and above. Weighted Wilcoxon rank-sum and weighted chi-square tests were used to compare group differences. A multivariable logistic regression model was constructed to assess the association between serum globulin and DM, with subgroup analyses and evaluations of nonlinear relationships. Receiver operating characteristic curves were used to assess the predictive power of the models. A total of 694 participants (512 DM and 182 nonDM) were included in our study and the incidence of DM was 22%. Higher serum globulin levels were significantly associated with an increased risk of DM, with a 21% increase in risk for each unit increase in serum globulin (odds ratio\u2005=\u20051.21, 95% confidence interval [1.03, 1.43], P\u2005<\u2005.001). The relationship between serum globulin and DM was linear, and higher serum globulin levels were associated with a higher risk of DM, particularly in males (P\u2005=\u2005.043) and obese individuals (P\u2005=\u2005.019). The area under the curve for serum globulin predicting DM was 0.795, with an optimal cutoff value of 2.9. Elevated serum globulin levels are significantly associated with an increased risk of DM among individuals with LTBI, highlighting the potential role of serum globulin as a predictive biomarker for DM in this population. However, the specific mechanism between globulin and LTBI-DM needs to be further investigated.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions \n Drug-coated balloons in high-risk patients and diabetes mellitus: A meta-analysis of 10 studies. \n We confirmed a significant advantage of DCB versus DES in the treatment of de novo lesions in high-risk patients and mainly in DM, reducing overall mortality, MACE and target lesion revascularization.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Archives of Iranian medicine \n Prevalence of Chronic Kidney Disease and Associated Factors among the Diabetic and Prediabetic Population in the Bandare-Kong Cohort Study; A Population-Based Study. \n The study emphasizes the importance of early detection and management of CKD risk factors, particularly among high-risk individuals, to mitigate CKD progression and associated complications. By addressing modifiable risk factors, proactive screening, and enhanced awareness, significant strides can be made in reducing CKD burden and improving patient outcomes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Frontiers in endocrinology \n A mobile health application use among diabetes mellitus patients: a systematic review and meta-analysis. \n https://www.crd.york.ac.uk/prospero/, identifier 42024537917.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Ethnicity & disease \n Racial Disparities in Foot Examination among People with Diabetes in Brazil: A Nationwide Survey, 2019. \n Black Brazilians with diabetes had higher negligence of foot examination by health care professionals. Strengthening primary care would help mitigate systemic racism in Brazil.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Scientific reports \n Cystic fibrosis-related diabetes is associated with reduced islet protein expression of GLP-1 receptor and perturbation of cell-specific transcriptional programs. \n Insulin secretion is impaired in individuals with cystic fibrosis (CF), contributing to high rates of CF-related diabetes (CFRD) and substantially increasing disease burden. To develop improved therapies for CFRD, better knowledge of pancreatic pathology in CF is needed. Glucagon like peptide-1 (GLP-1) from islet \u03b1 cells potentiates insulin secretion by binding GLP-1 receptors (GLP-1Rs) on \u03b2 cells. We determined whether expression of GLP-1 and/or its signaling components are reduced in CFRD, thereby contributing to impaired insulin secretion. Immunohistochemistry of pancreas from humans with CFRD versus no-CF/no-diabetes revealed no difference in GLP-1 immunoreactivity per islet area, whereas GLP-1R immunoreactivity per islet area or per insulin-positive islet area was reduced in CFRD. Using spatial transcriptomics, we observed several differentially expressed \u03b1- and/or \u03b2-cell genes between CFRD and control pancreas. In CFRD, we found upregulation of \u03b1-cell PCSK1 which encodes the enzyme (PC1/3) that generates GLP-1, and downregulation of \u03b1-cell PCSK1N which inhibits PC1/3. Gene set enrichment analysis also revealed \u03b1 and \u03b2 cell-specific pathway dysregulation in CFRD. Together, our data suggest intra-islet GLP-1 is not limiting in CFRD, but its action may be restricted due to reduced GLP-1R protein levels. Thus, restoring \u03b2-cell GLP-1R protein expression may improve \u03b2-cell function in CFRD.",
- "labels": [
- 0
- ]
- },
- {
- "text": "International journal of circumpolar health \n Substance use and lifestyle risk factors for somatic disorders among psychiatric patients in Greenland. \n Patients with psychotic disorders exhibit elevated mortality and morbidity rates compared to the general population primarily due to comorbid somatic diseases. This study aims to describe the prevalence of selected risk factors and somatic disorders among psychiatric patients with a diagnosis of psychotic disorder. Material and methods: Data were retrieved from Greenland's nationwide electronic medical record. The study population consists of 104 patients diagnosed with a psychotic disorder, encompassing schizophrenia or schizotypal and delusional disorders, residing in Nuuk. The study population comprised 104 patients (68 males and 36 females) with a mean age of 40\u2009years. More than 80% were daily smokers, and 68% had harmful use of cannabis. More than half had dyslipidemia (any imbalance in lipids), while over a quarter were classified as obese with body mass index of 30\u2009kg/m2 or higher. Eighteen percent had hypertension, and six percent suffered from diabetes. This study revealed a notable prevalence of risk factors for somatic diseases, particularly smoking and cannabis use among patients with schizophrenia in Nuuk, indicating that a high prevalence of somatic diseases might be expected as the population gets older and the risk of developing somatic diseases becomes greater. Increased focus on monitoring and preventing those as part of the health care is recommended.",
- "labels": [
- 0
- ]
- },
- {
- "text": "International immunopharmacology \n Natural polysaccharides: The potential biomacromolecules for treating diabetes and its complications via AGEs-RAGE-oxidative stress axis. \n Diabetes mellitus, a chronic metabolic disorder, poses a significantly public health challenge. Extensive research highlights that contemporary dietary patterns, characterized by excessive intake of sugar, fat, and protein, are major contributors to the onset and progression of diabetes. The central element to this process is the aberrant activation of the advanced glycation end products (AGEs) - receptor for AGEs (RAGE) - oxidative stress axis, which plays a pivotal role in disrupting normal carbohydrate metabolism. This pathway presents a critical target for developing interventions aimed at mitigating diabetes and its complications. In recent years, natural polysaccharides have emerged as promising agents in the prevention and treatment of diabetes, due to their ability to inhibit AGE formation, regulate RAGE expression, and modulate the AGEs-RAGE-oxidative stress axis. In this paper, we explore the pathogenic mechanism of this axis and review the therapeutic potential of natural polysaccharides in managing diabetes and its complications. Our goal is to provide new insights for the effective management of diabetes and its associated health challenges.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n Prevalence and clinical implications of diabetes mellitus in autoimmune nodopathies: A systematic review. \n DM patients fall under the typical clinical phenotype of autoimmune nodopathy, displaying predominantly paranodal antibodies. Early suspicion is crucial, as unlike DPN, diagnosis of autoimmune nodopathy unfolds therapeutic perspectives.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Investigational new drugs \n A phase II study of ME2136 (Asenapine Maleate) plus standard antiemetic therapy for patients, including diabetic patients, receiving cisplatin-based chemotherapy. \n Olanzapine combined with the neurokinin-1 receptor antagonist, palonosetron and dexamethasone is the standard treatment for chemotherapy-induced nausea and vomiting (CINV) due to highly emetogenic chemotherapy (HEC). However, the use of olanzapine poses challenges in patients with diabetes mellitus (DM) due to the potential risk of hyperglycemia. ME2136, antipsychotic similar to olanzapine, is associated with a lower risk of hyperglycemia. This study investigated the antiemetic efficacy and safety of ME2136 for HEC. This single-arm phase 2 study examined the safety and efficacy of ME2136 5\u00a0mg for 4\u00a0days in combination with triplet-combination antiemetic therapy. Two cohorts were established for the safety assessment: DM and non-DM. Eligible patients had malignant tumors and were receiving cisplatin-based chemotherapy for the first time. The primary endpoint was the complete response (CR) rate, defined as the percentage of patients without vomiting and not requiring rescue medications in the delayed phase (24-120\u00a0h). Between December 2020 and January 2022, 40 patients were enrolled, with 20 in each cohort. All patients were included in the safety analysis and 35 in the efficacy analysis. The CR rate in the delayed phase was 71.4% [60% CI 63.1-78.6%] for all patients, 66.7% in the DM cohort, and 76.5% in the non-DM cohort. No treatment-related adverse events\u2009\u2265\u2009grade 3, including hyperglycemia, were reported. ME2136, when combined with standard triplet-combination antiemetic therapy, is expected to exert similar antiemetic effects to the standard treatment for CINV due to HEC. Currently, ME2136-02 trial is underway to examine the safety and efficacy of triplet-combination antiemetic therapy and a 5-day treatment with ME2136. This study was registered with the Japan Registry of Clinical Trials (jRCT2041200071) on 10 December 2020. Clinical trial registration: This study was registered with the Japan Registry of Clinical Trials (jRCT2041200071) on 10 December 2020.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Molecular biology reports \n Molecular remodeling in comorbidities associated with heart failure: a current update. \n Recent advances in genomics and proteomics have helped in understanding the molecular mechanisms and pathways of comorbidities and heart failure. In this narrative review, we reviewed molecular alterations in common comorbidities associated with heart failure such as obesity, diabetes mellitus, systemic hypertension, pulmonary hypertension, coronary artery disease, hypercholesteremia and lipoprotein abnormalities, chronic kidney disease, and atrial fibrillation. We searched the electronic databases, PubMed, Ovid, EMBASE, Google Scholar, CINAHL, and PhysioNet for articles without time restriction. Although the association between comorbidities and heart failure is already well established, recent studies have explored the molecular pathways in much detail. These molecular pathways demonstrate how novels drugs for heart failure works with respect to the pathways associated with comorbidities. Understanding the altered molecular milieu in heart failure and associated comorbidities could help to develop newer medications and targeted therapies that incorporate these molecular alterations as well as key molecular variations across individuals to improve therapeutic outcomes. The molecular alterations described in this study could be targeted for novel and personalized therapeutic approaches in the future. This knowledge is also critical for developing precision medicine strategies to improve the outcomes for patients living with these conditions.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery \n The Effects of Metformin on Cisplatin-Induced Ototoxicity in Diabetic Patients. \n Contrary to expectations from preclinical data, metformin did not reduce the incidence of hearing loss in patients receiving cisplatin and may, in fact, be associated with an increased risk.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Medicina (Kaunas, Lithuania) \n Associations between Systemic and Dental Diseases in Elderly Korean Population. \n ",
- "labels": [
- 0
- ]
- },
- {
- "text": "Nutrients \n Diet Quality and Eating Frequency Were Associated with Insulin-Taking Status among Adults. \n Evidence of the low diet quality and eating frequency of insulin takers may help inform and justify nutrition education to control and manage diabetes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMC nephrology \n Efficacy of continuous glucose monitoring in people living with diabetes and end stage kidney disease on dialysis: a systematic review. \n PROSPERO registration number: CRD42023371635, https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=371635 .",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "Revista de gastroenterologia de Mexico (English) \n Gastrointestinal adverse effects of old and new antidiabetics: How do we deal with them in real life? \n Diabetes is a public health problem with an estimated worldwide prevalence of 10% and a prevalence of 12% in Mexico. The costs resulting from this chronic-degenerative disease are significant. Treatment for diabetes involves different medication groups, some of which can cause significant gastrointestinal adverse effects, such as dyspepsia, nausea, vomiting, bloating, diarrhea, and constipation. The medications most frequently associated with said adverse effects are metformin, acarbose, and GLP-1 agonists. Gastrointestinal adverse effects negatively impact the quality of life and management of patients with diabetes. The factors of visceral neuropathy, acute dysglycemia, dysbiosis, and intestinal bacterial overgrowth contribute to the gastrointestinal symptoms in patients with diabetes, making it necessary to consider multiple etiologic factors in the presence of gastrointestinal symptoms, and not exclusively attribute them to the use of antidiabetics. Personalized treatment, considering gastrointestinal comorbidity and the type of drug utilized, is essential for mitigating the adverse effects and improving the quality of life in patients with diabetes. The aim of the present narrative review was to describe the gastrointestinal adverse effects of the antidiabetic drugs, their pathophysiologic mechanisms, and the corresponding therapeutic measures.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of the American Board of Family Medicine : JABFM \n Impact of Point of Care Hemoglobin A1c Testing on Time to Therapeutic Intervention. \n Without compromising accuracy, point of care testing (POCT) provides immediate results at the time of in person patient consultation. The purpose of this study was to evaluate time until therapeutic intervention with POCT HbA1c versus venipuncture, where venipuncture was considered standard of care.The primary outcome was time (hours) to implementation of a therapeutic intervention based on POCT HbA1c result, as compared with most recent venipuncture HbA1c before the study and its associated therapeutic intervention. A total of 94 POCT HbA1c tests were included in the primary analysis.For the POCT HbA1c, the mean time to therapeutic intervention was 1.6\u2009\u00b1\u20093.14\u2009hours. For the previous venipuncture HbA1c, the mean time to therapeutic intervention was 1376.66\u2009\u00b1\u20093356.6\u2009hours (",
- "labels": [
- 0
- ]
- },
- {
- "text": "Molecular metabolism \n PET imaging of sodium-glucose cotransporters (SGLTs): Unveiling metabolic dynamics in diabetes and oncology. \n SGLT-targeted PET imaging offers promising improvements in diagnostic accuracy and therapeutic planning. The findings underscore the physiological and pathological significance of SGLTs, indicating that this imaging approach could shape future diagnostic and therapeutic strategies in metabolic and oncologic fields.",
- "labels": [
- 0
- ]
- },
- {
- "text": "The American journal of cardiology \n Impact of Diabetes Mellitus on Bifurcation Percutaneous Coronary Intervention: Insights from the Prospective Global Registry for the Study of Bifurcation Lesion Interventions Registry. \n The impact of diabetes mellitus (DM) on the outcomes of bifurcation percutaneous coronary intervention (PCI) has received limited study. We compared the procedural characteristics and outcomes of patients with and without DM in 1,302 bifurcation PCIs (1,147 patients) performed at 5 centers between 2013 and 2024. The prevalence of DM was 33.8% (n = 388). Patients with diabetes were younger and had more cardiovascular risk factors and greater angiographic complexity, including more main vessel calcification and more frequent stenoses in the left main, proximal left anterior descending, and right coronary artery. There was no difference in technical (95.5% vs 94.9%, p = 0.613) or procedural success (90.2% vs 91.3%, p = 0.540); provisional stenting was used less frequently in patients with diabetes (64.5% vs 71.1%, p = 0.015). Patients with diabetes had higher rates of repeat in-hospital PCI and acute kidney injury. Other in-hospital outcomes were similar after adjusting for confounders. During a median follow-up of 1,095 days, diabetes was independently associated with greater incidence of major adverse cardiovascular events (hazard ratio [HR] 2.04, 95% confidence intervals [CI] 1.52 to 2.72, p <0.001), myocardial infarction (HR 1.94, 95% CI 1.05 to 3.25, p = 0.033), death (HR 2.26, 95% CI 1.46 to 3.51, p <0.001), and target (HR 1.6, 95% CI 1.01 to 2.66, p = 0.045) and nontarget (HR 2.00, CI 1.06 to 3.78, p = 0.032) vessel revascularization. Patients with DM who underwent bifurcation PCI had greater risk of in-hospital repeat-PCI and major adverse cardiac events during follow-up than did those without diabetes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes care \n Relationship of Plasma Apolipoprotein C-I Truncation With Risk of Diabetes in the Multi-Ethnic Study of Atherosclerosis and the Actos Now for the Prevention of Diabetes Study. \n Our results indicate that apoC-I truncation may contribute to changes in glucose levels, IR, and risk of diabetes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "American journal of physiology. Heart and circulatory physiology \n Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure. \n Diabetes mellitus (DM) is characterized by chronic hyperglycemia, and despite intensive glycemic control, the risk of heart failure in patients with diabetes remains high. Diabetes-induced heart failure (DHF) presents a unique metabolic challenge, driven by significant alterations in cardiac substrate metabolism, including increased reliance on fatty acid oxidation, reduced glucose utilization, and impaired mitochondrial function. These metabolic alterations lead to oxidative stress, lipotoxicity, and energy deficits, contributing to the progression of heart failure. Emerging research has identified novel mechanisms involved in the metabolic remodeling of diabetic hearts, such as autophagy dysregulation, epigenetic modifications, polyamine regulation, and branched-chain amino acid (BCAA) metabolism. These processes exacerbate mitochondrial dysfunction and metabolic inflexibility, further impairing cardiac function. Therapeutic interventions targeting these pathways-such as enhancing glucose oxidation, modulating fatty acid metabolism, and optimizing ketone body utilization-show promise in restoring metabolic homeostasis and improving cardiac outcomes. This review explores the key molecular mechanisms driving metabolic remodeling in diabetic hearts, highlights advanced methodologies, and presents the latest therapeutic strategies for mitigating the progression of DHF. Understanding these emerging pathways offers new opportunities to develop targeted therapies that address the root metabolic causes of heart failure in diabetes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes care \n Consensus Considerations and Good Practice Points for Use of Continuous Glucose Monitoring Systems in Hospital Settings. \n Continuous glucose monitoring (CGM) systems provide frequent glucose measurements in interstitial fluid and have been used widely in ambulatory settings for diabetes management. During the coronavirus disease 2019 (COVID-19) pandemic, regulators in the U.S. and Canada temporarily allowed for CGM systems to be used in hospitals with the aim of reducing health care professional COVID-19 exposure and limiting use of personal protective equipment. As such, studies on hospital CGM system use have been possible. With improved sensor accuracy, there is increased interest in CGM usage for diabetes management in hospitals. Laboratorians and health care professionals must determine how to integrate CGM usage into practice. The aim of this consensus guidance document is to provide an update on the application of CGM systems in hospital, with insights and opinions from laboratory medicine, endocrinology, and nursing.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Biosensors \n Noninvasive Monitoring of Glycemia Level in Diabetic Patients by Wearable Advanced Biosensors. \n We report on the possibility of noninvasive diabetes monitoring through continuous analysis of sweat. The prediction of the blood glucose level in diabetic patients is possible on the basis of their sweat glucose content due to the positive correlation discovered. The ratio between the blood glucose and sweat glucose concentrations for a certain diabetic subject is stable within weeks, excluding requirements for frequent blood probing. The glucose variations in sweat display allometric (non-linear) dependence on those in blood, allowing more precise blood glucose estimation. Selective (avoiding false-positive responses) and sensitive (sweat glucose is on average 30-50 times lower) detection is possible with biosensors based on the glucose oxidase enzyme coupled with a Prussian Blue transducer. Reliable glucose detection in just secreted sweat would allow noninvasive monitoring of the glycemia level in diabetic patients.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Revista medica de Chile \n [Characteristics of Depressed Individuals with Hypertension and/ or Diabetes Mellitus in Primary Health Care in Santiago de Chile]. \n These are people with depressive episode, hypertension and/or diabetes who, having a personal and family history of depression, are not receiving pharmacological treatment for depression, which probably affects their quality of life. Better adherence to clinical guidelines for the treatment of depression is required.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Revista medica de Chile \n [Decline in Renal Function with Age in Chile: Gender Differences and the Impact of Comorbidities]. \n eGFR progressively decreased with age in the Chilean population, showing an early decline starting from 18 years, more pronounced in women, and in the presence of chronic diseases. Our findings provide relevant population-based information for interpreting eGFR across different age groups and risk categories.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMC public health \n Longitudinal assessment of the impact of prevalent diabetes on hospital admissions and mortality in the general population: a prospective population-based study with 19 years of follow-up. \n Source: Pixabay.com. No permission or acknowledgement is required.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Scientific reports \n International dietary quality index and its association with diabetes in RaNCD cohort study. \n Diabetes and its complications pose a significant threat to global health. Various factors contribute to the development of diabetes, with diet being an important trigger. The Dietary Quality Index-International (DQI-I) serves as an indicator of changes in diet and its association with chronic diseases, including diabetes. The aim of this study is to examine the association between DQI-I and diabetes in adults. Data from the first phase of the Ravansar Non-Communicable Disease Cohort Study (RaNCD) were used for this cross-sectional study. The study included individuals from western Iran aged between 35 and 65 years. The DQI-I was used to assess diet quality and the essential aspects of a healthy diet. Multiple logistic regression analyses were performed to compare DQI-I total score and diabetes. A total of 7,079 individuals were included, including 608 diabetic and 6,471 healthy individuals. The mean DQI-I score was 60.51\u2009\u00b1\u20098.47 in healthy individuals and 63.12\u2009\u00b1\u20098.64 in diabetics. The odds of developing diabetes were higher in individuals with a higher DQI-I (adjusted odds ratio: 1.49, 95% CI: 1.30-1.73). The variety was 13.43\u2009\u00b1\u20094.47 in diabetics and 12.59\u2009\u00b1\u20094.79 in healthy individuals. Adequacy was 33.23\u2009\u00b1\u20093.71 in diabetics and 33.79\u2009\u00b1\u20093.37 in healthy individuals. Moderation was 13.27\u2009\u00b1\u20096.05 in diabetics and 11.79\u2009\u00b1\u20095.47 in healthy individuals. The overall balance was 2.88\u2009\u00b1\u20092.21 in the healthy group and 2.61\u2009\u00b1\u20092.13 in the diabetics. The macronutrient ratio was 2.15\u2009\u00b1\u20091.88 in the healthy group and 2.04\u2009\u00b1\u20091.84 in the diabetics. The fatty acid ratio was 0.72\u2009\u00b1\u20091.29 in the healthy group and 0.56\u2009\u00b1\u20091.17 in the diabetic group. The overall balance score was higher in the healthy subjects. The DQI-I total score was higher in diabetics, indicating a positive association between diabetes and the DQI-I. Therefore, the importance of continuous dietary management and education of diabetic patients should be emphasized.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Scientific reports \n Impaired glomerular filtration rate and associated factors among diabetic mellitus patients with hypertension in referral hospitals, Amhara Regional State, Ethiopia. \n Impaired glomerular filtration rate is common health problem in diabetic mellitus patients (DM) with hypertension (HTN). It is a major cause of morbidity, mortality, and poor quality of life. There is limited data on the prevalence and associated factors of impaired glomerular filtration among diabetic mellitus patients with hypertension in Ethiopia. Therefore, this study aimed to determine the prevalence of impaired glomerular filtration rate and associated factors among diabetic patients with hypertension in referral hospitals in Amhara Regional State, Ethiopia, 2020. An institution-based cross-sectional study was conducted in Amhara Regional referral hospitals from February 20 to April 30, 2020. Systemic sampling techniques were used to select diabetic mellitus patients with hypertension. Epi data version 3.0 was used to enter the coded data and then exported to STATA 14 for analysis. Glomerular filtration rate was estimated using the equations of collaboration with chronic kidney disease (CKD-EPI), diet modification in renal disease (MDRD-4), and creatinine clearance (CrCl). In bi-variable logistic regression, variables with a p-value of <\u20090.25 were included in multi-variable logistic regression. Using a 95% confidence interval, variables having a p-value\u2009\u2264\u20090.05 in multi-variable logistic regression were declared as statistically significant variables. In this study, a total of 326 study participants were involved, with a 100% response rate. The prevalence of an impaired glomerular filtration rate among diabetic patients with hypertension was 30.1% (95% CI 25.1%-35.1%), 36.6% (95% CI 30.1%-40.8%) and 45.4% (95% CI 39.9%-50.8%), using the equations CKD-EPI, MDRD-4, and CrCl, respectively. Being \u2265\u200955 years old (CKD-EPI AOR\u2009=\u20092.9, 95%: 1.5-5.5, MDRD-4 AOR\u2009=\u20092.1, 95% CI: 1.2-3.7, CrCl AOR\u2009=\u20095.9, 95% CI: 3.5-10.1), proteinuria (CKD-EPI AOR\u2009=\u20092.7, 95% CI: 1.4-5.3, MDRD-4 AOR\u2009=\u20091.9, 95% CI: 1.1-3.4, CrCl AOR\u2009=\u20091.7, 95% CI: 1.0-2.9), duration of the disease (\u2265\u20095 years) (CKD-EPI AOR\u2009=\u20097.9, 95% CI: 4.2-13.0, MDRD-4 AOR\u2009=\u20097.4, 95% CI: 4.2-13.0, CrCl AOR\u2009=\u20091.9, 95% CI: 1.2-3.3), a glucose level of \u2265\u2009150\u00a0mg/dl (CKD-EPI AOR\u2009=\u20092.3, 95% CI: 1.3-4.4, MDRD-4 AOR\u2009=\u20092.1, 95% CI: 1.2-3.8) were variables significantly associated with impaired glomerular filtration rate. The prevalence of impaired glomerular filtration rate among diabetic mellitus patients with hypertension was high. Independent predictors of impaired glomerular filtration rate were older age, duration of the disease, proteinuria, and higher blood glucose levels.",
- "labels": [
- 0
- ]
- },
- {
- "text": "International journal of biological macromolecules \n Natural polymer nanofiber dressings for effective management of chronic diabetic wounds: A comprehensive review. \n Diabetic wounds present a chronic challenge in effective treatment. Natural polymer nanofiber dressings have emerged as a promising solution due to their impressive biocompatibility, biodegradability, safety, high specific surface area, and resemblance to the extracellular matrix. These qualities make them ideal materials with excellent biological properties and cost-effectiveness. Additionally, they can effectively deliver therapeutic agents, enabling diverse treatment effects. This review offers a comprehensive overview of natural polymer-based nanofibers in diabetic wound dressings. It examines the characteristics and challenges associated with diabetic wounds and the role of natural polymers in facilitating wound healing. The review highlights the preparation, mechanism, and applications of various functional dressings composed of natural polymer nanofibers. Furthermore, it addresses the main challenges and future directions in utilizing natural polymer nanofibers for diabetic wound treatment, providing valuable insights into effective wound management for diabetic patients.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes research and clinical practice \n Salivary glycated albumin could be as reliable a marker of glycemic control as blood glycated albumin in people with diabetes. \n This exploratory research revealed that the salivary GA levels by this method were accurate and might be able to replace blood GA measurement. The home salivary GA measurement is expected to be developed that may reduce the burden and complications in people with diabetes mellitus and improve the quality of life.",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "PloS one \n Accuracy of ankle-brachial index in screening for peripheral arterial disease in people with diabetes. \n Although the ankle-brachial index (ABI) presents overall satisfactory accuracy, its sensitivity in the context of screening strategies does not ensure the detection of all individuals with peripheral arterial disease (PAD), especially in clinical situations where there is calcification of the arterial media layer. This study evaluated the accuracy of ABI in screening PAD among individuals with diabetes mellitus (DM) in a community setting. An observational study included only individuals with DM. ABI measurement was performed, and the lower limb duplex ultrasound (DU) was used as the reference standard for PAD diagnosis. Sensitivity, specificity, positive and negative predictive values (PPV and NPV), and positive and negative likelihood ratios (LR+ and LR-) of ABI were assessed. The analysis included 194 limbs from 99 participants, with a PAD prevalence identified by DU of 15.98%. ABI demonstrated an accuracy of 87.63%, with a sensitivity of 35.48%, specificity of 97.55%, PPV of 73.33%, NPV of 89.83%, LR+ of 14.46, and LR- of 0.66. ABI showed high specificity but limited sensitivity in detecting PAD among individuals with DM in a community setting. An LR- of 0.66 suggests that a normal ABI result reduces but does not eliminate the possibility of PAD, highlighting the importance of complementary diagnostic approaches to enhance accuracy in identifying PAD in high-risk patients, such as those with DM. Incorporating additional diagnostic methods may be necessary to improve the effectiveness of PAD screening in this group.",
- "labels": [
- 0
- ]
- },
- {
- "text": "International journal of implant dentistry \n Correlation between marginal bone loss around dental implants and various systemic diseases: a cross-sectional study. \n Within the limitations of the present investigation, patients diagnosed with hyperlipidemia and hypertension were more likely to exhibit MBL surrounding dental implants.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Cancer medicine \n The association of diabetes mellitus and routinely collected patient-reported outcomes in patients with cancer. A real-world cohort study. \n The results of this study suggest that patients with cancer and diabetes may be at greater risk for anxiety, depression, fatigue, higher pain interference, and reduced physical function. Strengthening diabetes management is imperative to address the negative impact of diabetes on PROs. In particular, this may be true for patients with skin, breast, prostate, and kidney cancer.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of diabetes investigation \n Association of impaired fasting glucose with cardiometabolic multimorbidity: The\u00a0Kailuan study. \n IFG was a risk factor for CMM. The effect of IFG on diabetes mellitus was stronger than that on other cardiometabolic diseases. The effects of IFG for CMM differed by sex.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Middle East African journal of ophthalmology \n Status of Health-care Systems for Diabetes Mellitus and Diabetic Retinopathy in Jordan: Stakeholders and Health-care Providers Survey. \n Advanced DM and DR care is not accessible to most people. Programmatic efforts from the government and NGOs must formulate a national action plan to reduce the human and financial impact of the disease in Jordan.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Graded association of muscle strength with all-cause and cause-specific mortality in older adults with diabetes: Prospective cohort study across 28 countries. \n Muscle strength is gradually and inversely associated with all-cause and cause-specific mortality risk in older adults with diabetes. As muscle strength is highly adaptable to resistance training at all ages, the present findings highlight the importance of improving muscle strength in older adults with diabetes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Cardiovascular diabetology \n Impact of diabetes mellitus on right ventricular dysfunction and ventricular interdependence in hypertensive patients with heart failure with reduced ejection fraction assessed via 3.0 T cardiac MRI. \n In hypertensive HFrEF patients, comorbid DM may have aggravated RV dysfunction and was an independent determinant of impaired RV strain. RV dysfunction might be directly affected by DM and partially mediated by LV strain through unfavorable ventricular independence.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMC medicine \n Unhealthy plant-based diet is associated with a higher cardiovascular disease risk in patients with prediabetes and diabetes: a large-scale population-based study. \n Adherence to an unhealthy plant-based diet is associated with a higher CVD risk in people with prediabetes or diabetes, which may be partially attributed to low consumption of whole grains, high intake of SSB, and high blood cystatin C levels.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMC primary care \n Redesigning telemedicine: preliminary findings from an innovative assisted telemedicine healthcare model. \n The 'Digisahayam' model demonstrated feasibility in enhancing healthcare accessibility and quality by bridging healthcare gaps, diagnosing chronic conditions, and improving patient outcomes. The model presents a scalable and sustainable approach to revolutionising patient care and achieving digital health equity, with the potential for adaptation in similar settings worldwide.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Annals of epidemiology \n \u200eThe association between cumulative exposure to neighborhood walkability (NW) and diabetes risk, a prospective cohort study. \n Long-term residence in more walkable neighborhoods may be protective against diabetes in women, especially postmenopausal women.",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "The Journal of nutrition \n Betaine and B \n Our findings suggest that higher GSH level and higher intake of betaine, B",
- "labels": [
- 0
- ]
- },
- {
- "text": "Brain research \n In-depth investigation of the complex pathophysiological mechanisms between diabetes and ischemic stroke through gene expression and regulatory network analysis. \n This study explores the intricate relationship between diabetes and ischemic stroke (IS) through gene expression analysis and regulatory network investigation to identify potential biomarkers and therapeutic targets. Using datasets from the Gene Expression Omnibus (GEO) database, differential gene analysis was conducted on GSE43950 (diabetes) and GSE16561 (IS), revealing overlapping differentially expressed genes (DEGs). Functional enrichment analysis, Protein-Protein Interaction (PPI) network construction, and hub gene identification were performed, followed by validation in independent datasets (GSE156035 and GSE58294). The analysis identified 307 upregulated and 156 downregulated overlapping DEGs with significant enrichment in GO and KEGG pathways. Key hub genes (TLR2, TLR4, HDAC1, ITGAM) were identified through a PPI network (257 nodes, 456 interactions), with their roles in immune and inflammatory responses highlighted through GeneMANIA analysis. TRRUST-based transcription factor enrichment analysis revealed regulatory links involving RELA, SPI1, STAT3, and SP1. Differential expression analysis confirmed that RELA and SPI1 were upregulated in diabetes, while SPI1, STAT3, and SP1 were linked to IS. These transcription factors are involved in regulating immunity and inflammation, providing insights into the molecular mechanisms underlying diabetes-IS comorbidity. This bioinformatics-driven approach offers new understanding of the gene interactions and pathways involved, paving the way for potential therapeutic targets.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Farmaceuticos comunitarios \n [Validation of the JH-SEFAC Questionnaire on Knowledge on Insulin Management by Patients with Diabetes in Community Pharmacies]. \n The JH-SEFAC questionnaire was validated to evaluate the management of insulin injectables, providing community pharmacists with a valuable tool for therapeutic education.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Frontiers in endocrinology \n The emerging modulators of non-coding RNAs in diabetic wound healing. \n Diabetic wound healing is a complex physiological process often hindered by the underlying metabolic dysfunctions associated with diabetes. Despite existing treatments, there remains a critical need to explore innovative therapeutic strategies to improve patient outcomes. This article comprehensively examines the roles of non-coding RNAs (ncRNAs), specifically microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), in regulating key phases of the wound healing process: inflammation, angiogenesis, re-epithelialization, and tissue remodeling. Through a deep review of current literature, we discuss recent discoveries of ncRNAs that have been shown to either promote or impair the wound healing process in diabetic wound healing, which were not covered in earlier reviews. This review highlights the specific mechanisms by which these ncRNAs impact cellular behaviors and pathways critical to each healing stage. Our findings indicate that understanding these recently identified ncRNAs provides new insights into their potential roles in diabetic wound healing, thereby contributing valuable knowledge for future research directions in this field.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of primary care & community health \n Longer Multimorbidity Intervals Are Associated With Lower Mortality in Diabetes: A Whole-Population Nested Case-Control Study. \n Delayed multimorbidity among patients living with diabetes may be related to a lower risk of mortality. This study suggests that we should focus on mitigating and lowering the risk of multimorbidity in clinical management of diabetes to reduce further complication and mortality.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Yonsei medical journal \n Association of the COVID-19 Pandemic with HbA1c Testing and Complication Screening in Patients with Diabetes Mellitus. \n A high level of COVID-19 transmission was associated with a decrease in undergoing fundus examination and kidney disease screening. To fully realize the potential benefit of diabetes complication screenings, further effort is required to identify and address challenges to obtaining these screenings, especially in outbreak regions.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Digestive diseases and sciences \n Association Between Body Composition Measured by Artificial Intelligence and Long-Term Sequelae After Acute Pancreatitis. \n Body composition was not associated with having a recurrent AP. At follow-up, 30% and 25% of evaluated patients developed CP and DM, respectively. A higher SAT and IMAT were associated with a lower incidence of CP and higher incidence of DM, respectively.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Biomedical physics & engineering express \n Pioneering diabetes screening tool: machine learning driven optical vascular signal analysis. \n The escalating prevalence of diabetes mellitus underscores the critical need for non-invasive screening tools capable of early disease detection. Present diagnostic techniques depend on invasive procedures, which highlights the need for advancement of non-invasive alternatives for initial disease detection. Machine learning in integration with the optical sensing technology can effectively analyze the signal patterns associated with diabetes. The objective of this research is to develop and evaluate a non-invasive optical-based method combined with machine learning algorithms for the classification of individuals into normal, prediabetic, and diabetic categories. A novel device was engineered to capture real-time optical vascular signals from participants representing the three glycemic states. The signals were then subjected to quality assessment and preprocessing to ensure data reliability. Subsequently, feature extraction was performed using time-domain analysis and wavelet scattering techniques to derive meaningful characteristics from the optical signals. The extracted features were subsequently employed to train and validate a suite of machine learning algorithms. An ensemble bagged trees classifier with wavelet scattering features and random forest classifier with time-domain features demonstrated superior performance, achieving an overall accuracy of 86.6% and 80.0% in differentiating between normal, prediabetic, and diabetic individuals based on the optical vascular signals. The proposed non-invasive optical-based approach, coupled with advanced machine learning techniques, holds promise as a potential screening tool for diabetes mellitus. The classification accuracy achieved in this study warrants further investigation and validation in larger and more diverse populations.",
- "labels": [
- 0
- ]
- },
- {
- "text": "The journal of nutrition, health & aging \n Impact of diabetes on the association between serum urate levels and incident dementia: a cohort study in the UK biobank. \n Appropriately higher urate levels within the threshold of hyperuricemia can reduce the adverse health effects of excessively high urate levels and better protect the cognitive health of people with varying diabetes status.",
- "labels": [
- 0
- ]
- },
- {
- "text": "North Carolina medical journal \n \"It Takes a Village\"- A Conversation with the Interprofessional Diabetes Clinic at the ECU Health Family Medicine Center. \n Interprofessional collaboration and shared understanding positively impact both patients and providers. Current recommendations from the CDC and experts agree that collaboration between diverse professions is necessary to improve patient outcomes and empower patients to selfmanage their chronic conditions.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Medical gas research \n Nitric oxide-based treatments improve wound healing associated with diabetes mellitus. \n Non-healing wounds are long-term complications of diabetes mellitus (DM) that increase mortality risk and amputation-related disability and decrease the quality of life. Nitric oxide (NO\u00b7)-based treatments (i.e., use of both systemic and topical NO\u00b7 donors, NO\u00b7 precursors, and NO\u00b7 inducers) have received more attention as complementary approaches in treatments of DM wounds. Here, we aimed to highlight the potential benefits of NO\u00b7-based treatments on DM wounds through a literature review of experimental and clinical evidence. Various topical NO\u00b7-based treatments have been used. In rodents, topical NO\u00b7-based therapy facilitates wound healing, manifested as an increased healing rate and a decreased half-closure time. The wound healing effect of NO\u00b7-based treatments is attributed to increasing local blood flow, angiogenesis induction, collagen synthesis and deposition, re-epithelization, anti-inflammatory and anti-oxidative properties, and potent broad-spectrum antibacterial effects. The existing literature lacks human clinical evidence on the safety and efficacy of NO\u00b7-based treatments for DM wounds. Translating experimental favors of NO\u00b7-based treatments of DM wounds into human clinical practice needs conducting clinical trials with well-predefined effect sizes, i.e., wound reduction area, rate of wound healing, and hospital length of stay.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of diabetes \n Chronic glycemic control influences the relationship between acute perioperative dysglycemia and perioperative outcome. \n In surgical patients with diabetes, prior exposure to hyperglycemia attenuates the impact of perioperative hyperglycemia and glycemic variability on inpatient mortality and ICU admission. In patients without diabetes mellitus, all absolute thresholds of dysglycemia are associated with ICU admission, unlike those with diabetes, suggesting the need to use more relative measures such as the SHR.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Global health action \n Hypertension, diabetes, and cardiovascular disease nexus: investigating the role of urbanization and lifestyle in Cabo Verde. \n These findings add to the toolset of public health practitioners and policymakers in formulating policies and interventions aimed at managing cardiovascular diseases, particularly in developing nations.",
- "labels": [
- 0
- ]
- },
- {
- "text": "The Korean journal of internal medicine \n Current status of modifiable risk factors for cardiovascular disease in Korean women. \n Hypertension, diabetes mellitus, dyslipidemia, obesity, and smoking are the primary modifiable risk factors contributing to the increasing morbidity and mortality rates from cardiovascular disease (CVD) among Korean women. Significant sex-related differences exist in the prevalence, awareness, treatment, and control of these risk factors, highlighting the importance of age- and sex-specific approaches to the management and prevention of CVD. Notably, the prevalence of hypertension and diabetes mellitus increases with age, with a higher prevalence in elderly women compared to men. Dyslipidemia and obesity are also trending upward, particularly in postmenopausal women, highlighting the impact of menopause on cardiovascular risk. The present review advocates for improved diagnostic, therapeutic, and educational efforts to mitigate the risk of CVD among Korean women, with the goals of reducing the overall burden of the disease and promoting better cardiovascular health outcomes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Synergies between diabetes and hyperhomocysteinaemia: New insights to predict and prevent adverse cardiovascular effects. \n The findings highlight the synergistic impact of diabetes and HHcy on CVD. Joint assessments of diabetes and Hcy levels should be emphasized for risk stratification and primary prevention of CVD.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Trials \n Effects of an Exercise and Lifestyle Education Program in Brazilians living with prediabetes or diabetes: study protocol for a multicenter randomized controlled trial. \n ClinicalTrials.gov, NCT03914924 . Registered on April 16, 2019.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMC primary care \n Perceptions of the 2D short animated videos for literacy against chronic diseases among adults with diabetes and/or hypertension: a qualitative study in primary care clinics. \n Animated videos are acceptable for delivering health information. Pilot testing animated videos for promoting literacy against chronic diseases in adults with diabetes and hypertension is needed for optimal utility.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Scientific data \n The Journey to a FAIR CORE DATA SET for Diabetes Research in Germany. \n The German Center for Diabetes Research (DZD) established a core data set (CDS) of clinical parameters relevant for diabetes research in 2021. The CDS is central to the design of current and future DZD studies. Here, we describe the process and outcomes of FAIRifying the initial version of the CDS. We first did a baseline evaluation of the FAIRness using the FAIR Data Maturity Model. The FAIRification process and the results of this assessment led us to convert the CDS into the recommended format for spreadsheets, annotating the parameters with standardized medical codes, licensing the data set, enriching the data set with metadata, and indexing the metadata. The FAIRified version of the CDS is more suitable for data sharing in diabetes research across DZD sites and beyond. It contributes to the reusability of health research studies.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Primary care diabetes \n Understanding primary care provider's knowledge and perceptions of diabetes self-management education and support. \n Providers have limited knowledge of the appropriate time to refer to DSMES but expressed a willingness to refer. They emphasized the importance of providing their patients with appropriate self-management education and support.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes care \n Diabetes and Driving: A Statement of the American Diabetes Association. \n Many people with diabetes in the U.S. will seek or currently hold a license to drive. For many, a driver's license is essential for everyday life. Considerable discussion has focused on whether, and the extent to which, diabetes may be a relevant factor in determining driver ability and eligibility for a license. This statement addresses such issues in relation to current scientific and medical evidence. A diagnosis of diabetes on its own is not sufficient to make judgments about an individual driver's ability or safety. This statement provides an overview of existing licensing rules for people with diabetes in the U.S., addresses the factors that affect driving ability, identifies general guidelines for assessing driver fitness and determining appropriately tailored licensing restrictions, and provides practical guidance for health care professionals regarding clinical interventions and education for people with diabetes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Medicine \n Mitochondrial diabetes presenting with spontaneous abortion and ketoacidosis onset: A case report and literature review. \n MDM presents with atypical clinical manifestations, and thorough physical examinations are crucial for its diagnosis. This case underscores the significance of genetic testing and family history in diagnosing MDM and the need for increased awareness among clinicians to prevent misdiagnosis.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Medicine \n Female and diabetes are risk factors for alpha-fetoprotein and protein induced by vitamin K absence or antagonist-II negative in hepatocellular carcinoma. \n Hepatocellular carcinoma (HCC) is a common type of tumor with a high incidence. Alpha-fetoprotein (AFP) and protein induced by vitamin K absence or antagonist-II (PIVKA-II or des-gamma-carboxy prothrombin) are proven effective biomarkers for HCC. Combining them can enhance detection rates. However, when both AFP and PIVKA-II are negative, clinical diagnosis may be missed. This study aims to explore the risk factors for AFP and PIVKA-II negativity in HCC, thereby reducing missed diagnoses. A retrospective study enrolled 609 HCC patients at Shandong Public Health Clinical Center Affiliated with Shandong University from January 2010 to March 2022. Patients with negative AFP and PIVKA-II were the observed group, and others with at least 1 positive were controls. Epidemiological, clinical, laboratory, and radiological data were collected and analyzed to identify the frequency and factors influencing AFP and PIVKA-II negativity. Receiver operating characteristic (ROC) curves were used to assess the prediction model's ability to detect negative AFP and PIVKA-II in HCC. Gender (P\u2005=\u2005.045, 95% confidence interval [95%CI]\u2005=\u20051.013-3.277), diabetes mellitus (P\u2005=\u2005.018, 95%CI\u2005=\u20051.151-4.422), tumor size (P\u2005=\u2005.000, 95%CI\u2005=\u20050.677-0.841), glutamate transpeptidase (P\u2005=\u2005.003, 95%CI\u2005=\u20050.239-0.737), total bilirubin (P\u2005=\u2005.001, 95%CI\u2005=\u20050.235-0.705), and hepatitis B virus-associated infections (P\u2005=\u2005.007, 95%CI\u2005=\u20050.077-0.661) were significantly associated with AFP and PIVKA-II negativity in HCC. The prediction model had an area under curve of 0.832 (P\u2005<\u2005.001, 95%CI\u2005=\u20050.786-0.877), with a sensitivity of 81.2% and specificity of 75.5% in all HCC patients. Female diabetic patients with levels closer to normal for glutamate transpeptidase and total bilirubin are more likely to develop AFP and PIVKA-II-negative HCC. Imaging is crucial for screening liver cancer in these patients.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Epidemiologia e prevenzione \n [The study of migrant and immigrant population from the syndemic point of view]. \n The study of health of migrant and immigrant populations is of particular interest and actual in recent years, and there is a lack of research assessing aspects of aging of permanently resident immigrants, chronic non-communicable diseases, multimorbidity, and study of second generations. This contribution proposes to describe the relationship between health and immigration and their association with frailty through the anthropological concept of syndemics. Syndemics represents a set of closely interconnected and mutually enhancing health problems, significantly influencing the overall health status of a population. This occurs within the context of a perpetual pattern of harmful social conditions. Among the syndemics described in the literature, the most interesting in this area is the one concerning the increased frailty due to the interaction among diabetes, depression, immigration, and social distress, called VIDDA (Violence, Immigration, Depression, Diabetes, and Abuse), first identified in Mexican immigrant women in the United States. The main limitation of using the syndemic approach to study the health of immigrant populations is the difficulty in moving from the anthropological, primarily qualitative approach to the epidemiological-quantitative approach. Despite this, the epidemiological study of immigrant populations could benefit from the syndemic approach, because it can better describe complex causal relationships and provide evidence for modification of the clinical approach.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of diabetes science and technology \n Psychosocial Aspects of Diabetes Technologies: Commentary on the Current Status of the Evidence and Suggestions for Future Directions. \n Diabetes technologies, including continuous glucose monitors, insulin pumps, and automated insulin delivery systems offer the possibility of improving glycemic outcomes, including reduced hemoglobin A1c, increased time in range, and reduced hypoglycemia. Given the rapid expansion in the use of diabetes technology over the past few years, and touted promise of these devices for improving both clinical and psychosocial outcomes, it is critically important to understand issues in technology adoption, equity in access, maintaining long-term usage, opportunities for expanded device benefit, and limitations of the existing evidence base. We provide a brief overview of the status of the literature-with a focus on psychosocial outcomes-and provide recommendations for future work and considerations in clinical applications. Despite the wealth of the existing literature exploring psychosocial outcomes, there is substantial room to expand our current knowledge base to more comprehensively address reasons for differential effects, with increased attention to issues of health equity and data harmonization around patient-reported outcomes.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Journal of preventive medicine and hygiene \n Longitudinal trends in physical activity levels and lifetime cardiovascular disease risk: insights from the ATTICA cohort study (2002-2022). \n Promoting and maintaining regular physical activity throughout lifespan is crucial for reducing lifetime CVD risk and related risk factors. Tailored interventions addressing demographic and socioeconomic factors may help enhance cardiovascular health outcomes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "The Pan African medical journal \n Knowledge, attitudes, and practices regarding diabetic retinopathy among patients with diabetes in Dongola, Northern State, Sudan, 2022: a cross-sectional study. \n despite the good knowledge, favorable attitude and good practices, the regular eye check-up practice was significantly low. Urban residence was significantly associated with knowledge. Similarly, knowledge was found to be significantly associated with practice level. The most common barrier to regular eye check-up was the misconception that it is not important.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Cell reports \n A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes. \n In a patient with permanent neonatal syndromic diabetes clinically similar to cases with ONECUT1 biallelic mutations, we identified a disease-causing deletion located upstream of ONECUT1. Through genetic, genomic, and functional studies, we identified a crucial regulatory region acting as an enhancer of ONECUT1 specifically during pancreatic development. This enhancer region contains a low-frequency variant showing a strong association with type 2 diabetes and other glycemic traits, thus extending the contribution of this region to common forms of diabetes. Clinical relevance is provided by experimentally tailored therapy options for patients carrying ONECUT1 coding or regulatory mutations.",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "BMC oral health \n Association between total functional tooth unit score and hemoglobin A1c levels in Japanese community-dwelling individuals: the Nagasaki Islands study. \n In this community-based cross-sectional study, total FTU was significantly associated with HbA1c levels, independent of other risk factors. This suggests that reconstructed occlusal support areas, including dentures, are associated with glycemic control in the older population.",
- "labels": [
- 0
- ]
- },
- {
- "text": "The science of diabetes self-management and care \n Participants' Perspectives on Diabetes Self-Management Programming at Church: Faith-Placed Versus Faith-Based Approach. \n Church holds promise as a setting for DSMES program delivery in Hispanic communities. Church-based DSMES programs using a FB approach may further facilitate program adoption and sustainability.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Cardiovascular diabetology \n Altered RBC deformability in diabetes: clinical characteristics and RBC pathophysiology. \n NCT00071526.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of the American Heart Association \n Association of Prepregnancy Cardiometabolic Health With Hypertensive Disorders of Pregnancy Among Historically Underrepresented Groups in the United States. \n Prepregnancy diabetes and obesity are associated with HDP across all racial and ethnic groups. Diabetes and obesity have highest population attributable fractions among Native Hawaiian and Other Pacific Islander individuals and should be aggressively targeted during childhood, adolescence, and young adulthood to reduce risk of HDPs.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMJ open \n Diabetic health literacy and associated factors among patients with diabetes attending follow-up in public hospitals of Northeastern Ethiopia: a multicentre cross-sectional study. \n The study showed that less than a quarter of the patients have high DHL, with almost half having low levels of DHL. Tailoring health education programmes to diverse educational levels, incorporating multiple information sources and fostering social support networks could enhance DHL.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMJ open \n Treatments, medical expenses and complications of hospital outpatient healthcare associated with stroke in patients with diabetes in China: a retrospective analysis of the Beijing Municipal Medical Insurance Database. \n Stroke is associated with a significant increase in complications and medications for patients with diabetes and greatly adds to the economic burden of these patients. Early identification of stroke risk factors in patients with diabetes, as well as targeted poststroke diabetes management, is crucial from a socioeconomic perspective for a comprehensive management and treatment of stroke in patients with diabetes.",
- "labels": [
- 0
- ]
- },
- {
- "text": "BMJ open \n Exploring the decision-making experience of elderly diabetes patients regarding their health-seeking behaviour: a descriptive qualitative study. \n The health-seeking behavioural decision-making level of elderly diabetic patients is relatively low. Medical and healthcare professionals should formulate targeted intervention measures aimed at improving their disease cognition level, changing their coping styles and enhancing their health-seeking behavioural decision-making level to improve their health outcomes. Meanwhile, policymakers should plan and allocate medical resources in a targeted manner based on the needs and expectations of patients.",
- "labels": [
- 0
- ]
- },
- {
- "text": "JMIR formative research \n Oral Diabetes Medication Videos on Douyin: Analysis of Information Quality and User Comment Attitudes. \n Despite most videos on Douyin being posted by doctors, with generally acceptable information quality and positive user comment attitudes, some content inaccuracies and poor actionability remain. Users show more positive attitudes toward videos with high-quality information about treatment choices. This study suggests that health care providers should ensure the accuracy and actionability of video content, enhance the information quality of treatment choices of oral diabetes medications to foster positive user attitudes, help users access accurate health information, and promote medication adherence.",
- "labels": [
- 0
- ]
- },
- {
- "text": "PloS one \n Primary care physicians' perspectives on adults with diabetes and the recommended hepatitis B vaccine: A qualitative study. \n Our findings indicate that physicians are generally aware of the existence of the CDC guidelines, but not all physicians recommend the HepB vaccine to adults with diabetes. This is because of a wide variation in treatment concerning glucose monitoring or insulin injection due to varying opinions about actual risk. We also identified barriers adults with diabetes have in receiving the HepB vaccine and strategies to increase HepB vaccination.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Molecular medicine reports \n Epigenetic regulatory mechanism of macrophage polarization in diabetic wound healing (Review). \n Diabetic wounds represent a significant complication of diabetes and present a substantial challenge to global public health. Macrophages are crucial effector cells that play a pivotal role in the pathogenesis of diabetic wounds, through their polarization into distinct functional phenotypes. The field of epigenetics has emerged as a rapidly advancing research area, as this phenomenon has the potential to markedly affect gene expression, cellular differentiation, tissue development and susceptibility to disease. Understanding epigenetic mechanisms is crucial to further exploring disease pathogenesis. A growing body of scientific evidence has highlighted the pivotal role of epigenetics in the regulation of macrophage phenotypes. Various epigenetic mechanisms, such as DNA methylation, histone modification and non\u2011coding RNAs, are involved in the modulation of macrophage phenotype differentiation in response to the various environmental stimuli present in diabetic wounds. The present review provided an overview of the various changes that take place in macrophage phenotypes and functions within diabetic wounds and discussed the emerging role of epigenetic modifications in terms of regulating macrophage plasticity in diabetic wounds. It is hoped that this synthesis of information will facilitate the elucidation of diabetic wound pathogenesis and the identification of potential therapeutic targets.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Archives of endocrinology and metabolism \n Phenotypic and molecular reanalysis of a cohort of patients with monogenic diabetes reveals a case of partial lipodystrophy due to the A8344G mutation in the mitochondrial DNA. \n Familial partial lipodystrophy (FPLD) is a very rare genetic disease characterized by insulin resistance due to a loss of subcutaneous fat from the extremities together with a progressive storage of fat around the face and neck and inside the abdomen. In over 50% of cases, molecular genetic testing reveals pathogenic variants in two nuclear genes, LMNA and PPARG. The case reported here refers to a woman phenotypically diagnosed with FPLD, who presented with diabetes and multiple cervical lipomatosis and in whom no variant had been found in the nuclear genes classically associated with this syndrome that could explain her phenotype. Genetic sequencing using a target panel containing 48 nuclear genes related to monogenic diabetes plus the whole mitochondrial genome revealed the mitochondrial variant m.A8344G in 84.1% heteroplasmy. Following molecular diagnosis, her phenotype was expanded with the recognition of additional clinical characteristics: mild sensorineural hearing loss, proximal myopathy, fatigue, cognitive impairment, sensory ataxia, cardiac abnormalities and, finally, muscle biopsy findings compatible with mitochondrial disease. Therefore, careful and detailed phenotypic and genotypic reanalysis proved crucial in improving molecular diagnosis in FPLD.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes research and clinical practice \n Nasopharyngeal carriage and antibiotic susceptibility of Streptococcus pneumoniae among diabetes patients in western Kenya. \n Nasopharyngeal carriage of S. pneumoniae is higher in patients with diabetes, with significant resistance to common antibiotics, though macrolides remain effective.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n Individual and joint effects of diabetes and depression on incident cardiovascular diseases and all-cause mortality: Results from a population-based cohort study. \n Individuals with both diabetes and depression had greater risk of CVD and all-cause mortality when compared to those with diabetes or depression alone, or those without either condition.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Journal of occupational and environmental medicine \n Developing a Job-Exposure Matrix for Sedentary Behavior: A Study Based on the Inpatient Clinico-Occupational Database of Rosai Hospital Group. \n The job-exposure matrix provides valuable insights into the health impacts of sedentary behavior in the workplace, underscoring significant disease risks associated with prolonged inactivity.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Diabetes \n Functionally Separate Populations of Ventromedial Hypothalamic Neurons in Obesity and Diabetes: A Report on Research Supported by Pathway to Stop Diabetes. \n The ventromedial hypothalamic nucleus (VMN) maintains healthy metabolic function through several important roles. Collectively, homeostasis is maintained via intermingled cells within the VMN that raise blood glucose, lower blood glucose, and stimulate energy expenditure when needed. In this article I discuss the defining factors for the VMN cell types that govern distinct functions induced by the VMN, particularly in relation to energy balance and blood glucose levels. Special attention is given to distinct features of VMN cells responsible for these processes. Finally, these topics are reviewed in the context of research funded by the American Diabetes Association Pathway to Stop Diabetes initiative, with highlighting of key findings and current unresolved questions for future investigations.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Preventing chronic disease \n Prevalence of Self-Reported Diagnosed Diabetes Among Adults, by County Metropolitan Status and Region, United States, 2019-2022. \n The association of metropolitan residence with diabetes prevalence differs across US regions. These findings can help to guide efforts in areas where diabetes prevention and care resources may be better directed.",
- "labels": [
- 0
- ]
- },
- {
- "text": "International journal of epidemiology \n Long-term exposure to PM2.5 and mortality: a national health insurance cohort study. \n This study identified the hypothesis that long-term exposure to PM2.5 is associated with mortality, and the association might be different by causes of death. Our result highlights a novel vulnerable population: the middle-aged population with risk factors related to heart failure.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Frontiers in endocrinology \n Potential pathogenic roles of ferroptosis and cuproptosis in cadmium-induced or exacerbated cardiovascular complications in individuals with diabetes. \n Diabetes and its complications are major diseases that affect human health. Diabetic cardiovascular complications such as cardiovascular diseases (CVDs) are the major complications of diabetes, which are associated with the loss of cardiovascular cells. Pathogenically the role of ferroptosis, an iron-dependent cell death, and cuproptosis, a copper-dependent cell death has recently been receiving attention for the pathogenesis of diabetes and its cardiovascular complications. How exposure to environmental metals affects these two metal-dependent cell deaths in cardiovascular pathogenesis under diabetic and nondiabetic conditions remains largely unknown. As an omnipresent environmental metal, cadmium exposure can cause oxidative stress in the diabetic cardiomyocytes, leading to iron accumulation, glutathione depletion, lipid peroxidation, and finally exacerbate ferroptosis and disrupt the cardiac. Moreover, cadmium-induced hyperglycemia can enhance the circulation of advanced glycation end products (AGEs). Excessive AGEs in diabetes promote the upregulation of copper importer solute carrier family 31 member 1 through activating transcription factor 3/transcription factor PU.1, thereby increasing intracellular Cu",
- "labels": [
- 0
- ]
- },
- {
- "text": "Primary health care research & development \n Evaluating physical activities in clinical diabetes: lifestyle scores hypothesis. \n This report contributes to diabetes cardiovascular complications management. Sedentary ADL factors need integration in healthy lifestyle education especially among the elderly.",
- "labels": [
- 0
- ]
- },
- {
- "text": "Brazilian dental journal \n Atorvastatin Accelerates Alveolar Bone Loss in Type 1 Diabetic Rats Submitted to Periodontitis. \n Periodontal bone loss is potentiated by diabetes. Despite the beneficial anti-inflammatory and antiresorptive effects of Atorvastatin (ATV) on periodontitis, it has been reported to increase the risk of diabetes, which may modify the course of periodontal disease. Therefore, this study aimed to evaluate the effect of ATV on alveolar bone in rats with periodontitis and diabetes. For this, 72 Wistar rats were divided into groups: Na\u00efve (N) not submitted to any procedure; Experimental periodontitis (EP) group submitted to ligature-induced periodontitis; diabetes mellitus (DM), submitted to EP and receiving single dose of streptozotocin (60 mg/kg, i.p.) after 12 hours of fasting; and ATV DM, submitted to EP and DM and receiving orally 27 mg/kg of ATV, 30 minutes before ligature placement, and continued daily until the 11th day. Animals from EP and DM received saline solution 0.9% as placebo. Glycemic levels measured in all animals and then were euthanized. Maxillae were collected for macroscopic, micro-tomographic, and microscopic analyses. DM caused intense bone loss (60%), characterized by a reduction in trabecular thickness and bone volume. DM reduced osteoblasts, increasing osteoclast counts, and induced an inflammatory infiltrate in the periodontium. ATV was found ineffective in protecting bone in diabetic rats, exacerbating bone loss by 21%. Additionally, ATV significantly increased blood glucose levels. In summary, ATV did not prevent alveolar bone loss or modulate inflammation in DM animals undergoing EP. ATV also increased blood glucose levels in these animals. Therefore, the systemic use of ATV in uncontrolled diabetic conditions should be carefully evaluated.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Current opinion in allergy and clinical immunology \n Expanding the spectrum of IPEX: from new clinical findings to novel treatments. \n Further research is needed to fully understand the variable clinical presentations of IPEX and optimize tailored therapies, ensuring better management and outcomes for affected individuals.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Endokrynologia Polska \n Falls in RAC-OST-POL Study: the results from 10-year prospective longitudinal observation. \n In long-term follow-up in postmenopausal women, falls were frequently observed, and their occurrence increased the fracture rate. Diabetes type 1 and depression increase the fall rate, which suggests the necessity of implementation of some preventive procedures.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes investigation \n The benefits and accuracy of real-time continuous glucose monitoring in children and adolescents with type 1 diabetes attending a summer camp. \n Rt-CGM exhibited higher usability and recommendation scores in HCPs than those in campers. This may be related to relatively lower accuracy in rt-CGM. Overall usability and recommendation are clinically satisfactory, but due to relatively low accuracy, no decision should be made based on a single, non-verified SG value alone.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetic medicine : a journal of the British Diabetic Association \n An audit and feedback-based intervention to improve diabetes management in the year after transfer to adult type 1 diabetes care: A multi-center quasi-experimental study. \n We found an effect of the intervention on glycaemic management one year following transfer to adult care. Future work will focus on refining and testing the effectiveness of the intervention in an expanded number of study sites and in collaboration with adult diabetes care providers.",
- "labels": [
- 1
- ]
- },
- {
- "text": "BMC endocrine disorders \n Association between the soluble receptor for advanced glycation end products and diabetes mellitus: systematic review and meta-analysis. \n CRD42024521252.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Cardiovascular diabetology \n Excessive occupational sitting increases risk of cardiovascular events among working individuals with type 1 diabetes in the prospective Finnish Diabetic Nephropathy Study. \n Excessive occupational sitting is associated with a higher risk of cardiovascular events and all-cause mortality in individuals with type 1 diabetes. This association persists regardless of leisure-time physical activity, after adjusting for independently associated variables identified in our cross-sectional analyses. These findings underscore the need to update physical activity guidelines to better address sedentary behavior and improve outcomes for individuals with type 1 diabetes. Targeting occupational sitting should be considered a key focus for interventions aimed at reducing overall sedentary time.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Nature communications \n Physiological and pathogenic T cell autoreactivity converge in type 1 diabetes. \n Autoimmune diseases result from autoantigen-mediated activation of adaptive immunity; intriguingly, autoantigen-specific T cells are also present in healthy donors. An assessment of dynamic changes of this autoreactive repertoire in both health and disease is thus warranted. Here we investigate the physiological versus pathogenic autoreactive processes in the context of Type 1 diabetes (T1D) and one of its landmark autoantigens, glutamic acid decarboxylase 65 (GAD65). Using single cell gene expression profiling and tandem T cell receptor (TCR) sequencing, we find that GAD65-specific true na\u00efve cells are present in both health and disease, with GAD65-specific effector and memory responses showing similar ratios in healthy donors and patients. Deeper assessment of phenotype and TCR repertoire uncover differential features in GAD65-specific TCRs, including lower clonal sizes of healthy donor-derived clonotypes in patients. We thus propose a model whereby physiological autoimmunity against GAD65 is needed during early life, and that alterations of these physiological autoimmune processes in predisposed individuals trigger overt Type 1 diabetes.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n Effects of probiotics and fibers on markers of nephropathy, inflammation, intestinal barrier dysfunction and endothelial dysfunction in individuals with type 1 diabetes and albuminuria. The ProFOS Study. \n Twelve weeks treatment with synbiotic mix had no effect on UACR or on any of the secondary endpoints in subjects with type 1 diabetes and albuminuria.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of managed care & specialty pharmacy \n Comorbid depression and anxiety and their association with health care resource utilization among individuals with type 1 diabetes in the United States. \n Comorbid depression/anxiety among individuals with T1DM results in significantly higher HCRU than T1DM alone. The findings underscore the importance of effective management of comorbid depression/anxiety in the T1DM population.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Current diabetes reports \n Implementation Science and Pediatric Diabetes: A Scoping Review of the State of the Literature and Recommendations for Future Research. \n Of 23 papers identified, 19 were published since 2017 and 21 focused on type 1 diabetes. Most involved medical evidence-based practices (EBPs; n\u2009=\u200915), whereas fewer focused on psychosocial (n\u2009=\u20097) and diabetes education (n\u2009=\u20092). The majority either identified barriers and facilitators of implementing an EBP (n\u2009=\u200911) or were implementation trials (n\u2009=\u200911). Fewer studies documented gaps in EBP implementation in standard care (n\u2009=\u20097) or development of implementation strategies (n\u2009=\u20091). Five papers employed IS theories and two aimed to improve equity. There is a paucity of IS research in pediatric diabetes care literature. Few papers employed IS theory, used consistent IS terminology, or described IS strategies or outcomes. Guidance for future research to improve IS research in pediatric diabetes is offered.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Current diabetes reports \n Impact of Digitally Enabled Peer Support Interventions on Diabetes Distress and Depressive Symptoms in People Living with Type 1 Diabetes: A Systematic Review. \n We synthesized the results of nine key studies from a review of 3,623 English-language articles published between January 2012 and January 2024. Three studies demonstrated significant reductions in diabetes distress, and two studies reported reductions in depression. Data were analyzed using a narrative approach, including thematic synthesis. This process was structured around the Behavior Change Wheel framework Effective interventions shared several common features such as (1) involved participatory development approaches, (2) included diabetes education, (3) lasted over a longer time, (4) designed with a psychological framework, and (5) utilized peer mentors. Studies showed that digitally-enabled peer support has the potential to improve diabetes distress and depression among people living with T1D despite heterogeneity in intervention approaches. Moreover, designing interventions with certain features may enhance key psychosocial outcomes.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Trials \n Hypoglycaemia Prevention, Awareness of Symptoms, and Treatment (HypoPAST): protocol for a 24-week hybrid type 1 randomised controlled trial of a fully online psycho-educational programme for adults with type 1 diabetes. \n Australian and New Zealand Clinical Trials Registry (ANZCTR): ACTRN12623000894695 (21 August 2023).",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Body weight variability as a predictor of cardiovascular outcomes in type 1 diabetes: A nationwide cohort study. \n High BWV is associated with an increased risk of CVD and all-cause mortality in individuals with T1D, independently of canonical risk factors. Weight trends, sex and glycaemic control do not modify such association while older age attenuates it.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetologia \n The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository in the AIRR Data Commons: a practical guide for access, use and contributions through the Type 1 Diabetes AIRR Consortium. \n Human molecular genetics has brought incredible insights into the variants that confer risk for the development of tissue-specific autoimmune diseases, including type 1 diabetes. The hallmark cell-mediated immune destruction that is characteristic of type 1 diabetes is closely linked with risk conferred by the HLA class II gene locus, in combination with a broad array of additional candidate genes influencing islet-resident beta cells within the pancreas, as well as function, phenotype and trafficking of immune cells to tissues. In addition to the well-studied germline SNP variants, there are critical contributions conferred by T cell receptor (TCR) and B cell receptor (BCR) genes that undergo somatic recombination to yield the Adaptive Immune Receptor Repertoire (AIRR) responsible for autoimmunity in type 1 diabetes. We therefore created the T1D TCR/BCR Repository (The Type 1 Diabetes T Cell Receptor and B Cell Receptor Repository) to study these highly variable and dynamic gene rearrangements. In addition to processed TCR and BCR sequences, the T1D TCR/BCR Repository includes detailed metadata (e.g. participant demographics, disease-associated parameters and tissue type). We introduce the Type 1 Diabetes AIRR Consortium goals and outline methods to use and deposit data to this comprehensive repository. Our ultimate goal is to facilitate research community access to rich, carefully annotated immune AIRR datasets to enable new scientific inquiry and insight into the natural history and pathogenesis of type 1 diabetes.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetologia \n Autoimmune diseases and the risk and prognosis of latent autoimmune diabetes in adults. \n We confirm that several common ADs confer an excess risk of LADA, especially LADA with higher GADA levels, but having such a comorbidity does not appear to affect the risk of diabetic retinopathy.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Diabetologia \n Exposure to antibiotics and risk of latent autoimmune diabetes in adults and type 2 diabetes: results from a Swedish case-control study (ESTRID) and the Norwegian HUNT study. \n We found no evidence that exposure to broad-spectrum antibiotics up to 10 years prior to diagnosis increases the risk of LADA. There was some indication of increased LADA risk with exposure to narrow-spectrum antibiotics, which warrants further investigation.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Current medical research and opinion \n Technological advancements in glucose monitoring and artificial pancreas systems for shaping diabetes care. \n The management of diabetes mellitus has undergone remarkable progress with the introduction of cutting-edge technologies in glucose monitoring and artificial pancreas systems. These innovations have revolutionized diabetes care, offering patients more precise, convenient, and personalized management solutions that significantly improve their quality of life. This review aims to provide a comprehensive overview of recent technological advancements in glucose monitoring devices and artificial pancreas systems, focusing on their transformative impact on diabetes care. A detailed review of the literature was conducted to examine the evolution of glucose monitoring technologies, from traditional invasive methods to more advanced systems. The review explores minimally invasive techniques such as continuous glucose monitoring (CGM) systems and flash glucose monitoring (FGM) systems, which have already been proven to enhance glycemic control and reduce the risk of hypoglycemia. In addition, emerging non-invasive glucose monitoring technologies, including optical, electrochemical, and electro-mechanical methods, were evaluated. These techniques are paving the way for more patient-friendly options that eliminate the need for frequent finger-prick tests, thereby improving adherence and ease of use. Advancements in closed-loop artificial pancreas systems, which integrate CGM with automated insulin delivery, were also examined. These systems, often referred to as \"hybrid closed-loop\" or \"automated insulin delivery\" systems, represent a significant leap forward in diabetes care by automating the process of insulin dosing. Such advancements aim to mimic the natural function of the pancreas, allowing for better glucose regulation without the constant need for manual interventions by the patient. Technological breakthroughs in glucose monitoring and artificial pancreas systems have had a profound impact on diabetes management, providing patients with more accurate, reliable, and individualized treatment options. These innovations hold the potential to significantly improve glycemic control, reduce the incidence of diabetes-related complications, and ultimately enhance the quality of life for individuals living with diabetes. Researchers are continually exploring novel methods to measure glucose more effectively and with greater convenience, further refining the future of diabetes care. Researchers are also investigating the integration of artificial intelligence and machine learning algorithms to further enhance the precision and predictive capabilities of glucose monitoring and insulin delivery systems. With ongoing advancements in sensor technology, connectivity, and data analytics, the future of diabetes care promises to deliver even more seamless, real-time management, empowering patients with greater autonomy and improved health outcomes.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Medicine \n Study on serum vitamin A level in patients with type 1 diabetes: A systematic review and meta-analysis. \n Serum VA levels seem to have decreased in T1DM patients. Further research is needed to strengthen this finding and clarify possible impact mechanisms.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Swiss medical weekly \n Recommendations for early identification of heart failure in patients with diabetes: Consensus statement of the Swiss Society of Endocrinology and Diabetology and the Heart Failure Working Group of the Swiss Society of Cardiology. \n Diabetes is a well-recognised risk factor for the development of heart failure, with a prevalence higher than 30% in patients with diabetes aged over 60 years. Heart failure often emerges as the primary cardiovascular manifestation in patients with type 2 diabetes and appears to be even more prevalent in type 1 diabetes. In Switzerland, there are approximately 500,000 individuals with diabetes, and the number of affected people has been steadily rising in recent years. Therefore, the consequences of heart failure will affect an increasing number of patients, further straining the Swiss healthcare system. Early lifestyle modification and initiation of appropriate treatment can prevent or at least significantly delay the onset of symptomatic heart failure by several years. These facts underscore the urgent need for early detection of individuals with subclinical heart failure, which often remains undiagnosed until the first episode of acute heart failure requiring hospital admission occurs. To address this issue, the European Society of Cardiology, the American Diabetes Association (ADA) and other international professional societies have published recommendations on heart failure screening, diagnosis and management. To address this issue in Switzerland, experts from the Swiss Society of Endocrinology and Diabetology, the Swiss Society of Cardiology and the General Internal Medicine specialty met and prepared a consensus report including a simple diagnostic algorithm for use in everyday practice.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Frontiers in immunology \n Circulating hsa-miR-320a and its regulatory network in type 1 diabetes mellitus. \n Our study presents a novel link between hsa-miR-320a-3p and T1D, and highlights its key regulatory role in the network of mRNA markers and transcription factors involved in T1D pathogenesis.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes \n Gut microbiota, serum metabolites, and lipids related to blood glucose control and type 1 diabetes. \n We identified distinct characteristics of gut microbiota, metabolites, and lipids in T1D patients exhibiting different levels of glycemic control. Through comprehensive analysis, microbiota (Bacteroides_nordii, Bacteroides_coprocola), metabolites (D-fructose), and lipids (Monoglycerides) may serve as potential mediators that communicated the interaction between the gut, circulatory systems, and glucose fluctuations in T1D patients.",
- "labels": [
- 1
- ]
- },
- {
- "text": "The journal of medical investigation : JMI \n Difference in the accuracy of the third-generation algorithm and the first-generation algorithm of FreeStyle Libre continuous glucose monitoring device. \n No proportional bias in the measurements by Gen. 3 algorithm was observed, but in those by Gen. 1 algorithm. J. Med. Invest. 71 : 225-231, August, 2024.",
- "labels": [
- 1
- ]
- },
- {
- "text": "BMC psychology \n Changes in health, lifestyle, and wellbeing of children with type 1 diabetes and their parents during the pandemic. \n Our findings indicate that the COVID-19 lockdown has had a significant psychological and possibly physiological impact on children with Type 1 diabetes and their parents. We conclude that there is a need for mental health support services focusing on these groups. Although full lockdown restrictions will have stopped in the past year, post-pandemic stressors may be expected to continue to adversely affect this cohort.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n Prevalence and clinical implications of diabetes mellitus in autoimmune nodopathies: A systematic review. \n DM patients fall under the typical clinical phenotype of autoimmune nodopathy, displaying predominantly paranodal antibodies. Early suspicion is crucial, as unlike DPN, diagnosis of autoimmune nodopathy unfolds therapeutic perspectives.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "International journal of molecular sciences \n Relationship Between C-Peptide Levels, Clinical Features, and Serum Data in a Brazilian Type 1 Diabetes Population with Large Variations in Genomic Ancestry. \n Type 1 diabetes (T1D) is a chronic disease characterized by the immune-mediated destruction of the pancreatic beta cells responsible for insulin production. The secreted insulin and C-peptide are equimolar. Due to its longer half-life, C-peptide has become a safer means of assessing the pancreatic reserve. C-peptide levels were evaluated in a population of patients with T1D, focusing on the relationship between this variable and other factors. In addition, the influence of C-peptide on metabolic control and microvascular complications was investigated. This cross-sectional study included 95 patients who had been diagnosed with T1D at least five years earlier. These patients were evaluated using a clinical demographic survey, anthropometric data, laboratory tests, and fundoscopy. This study showed that 29.5% of patients had residual insulin secretion, which correlated directly with their age at diagnosis. No statistically significant differences in metabolic control or microvascular complications were observed between the C-peptide level groups. In addition, our results indicate that ancestry does not influence the persistence of residual C-peptide function in our highly mixed population. It is recommended that future research consider incorporating new variables, such as HLA and pancreatic autoimmunity, as factors that may influence residual \u03b2-cell function.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of nanobiotechnology \n Islet cell spheroids produced by a thermally sensitive scaffold: a new diabetes treatment. \n The primary issues in treating type 1 diabetes mellitus (T1DM) through the transplantation of healthy islets or islet \u03b2-cells are graft rejection and a lack of available donors. Currently, the majority of approaches use cell encapsulation technology and transplant replacement cells that can release insulin to address transplant rejection and donor shortages. However, existing encapsulation materials merely serve as carriers for islet cell growth. A new treatment approach for T1DM could be developed by creating a smart responsive material that encourages the formation of islet cell spheroids to replicate their 3D connections in vivo and controls the release of insulin aggregates. In this study, we used microfluidics to create thermally sensitive porous scaffolds made of poly(N-isopropyl acrylamide)/graphene oxide (PNIPAM/GO). The material was carefully shrunk under near-infrared light, enriched with mouse insulinoma pancreatic \u03b2 cells (\u03b2-TC-6 cells), encapsulated, and cultivated to form 3D cell spheroids. The controlled contraction of the thermally responsive porous scaffold regulated insulin release from the spheroids, demonstrated using the glucose-stimulated insulin release assay (GSIS), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence assay. Eventually, implantation of the spheroids into C57BL/6\u00a0N diabetic mice enhanced the therapeutic effect, potentially offering a novel approach to the management of T1DM.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Scientific reports \n Causal relationships between allergic and autoimmune diseases with chronic rhinosinusitis. \n Chronic rhinosinusitis (CRS) is a prevalent inflammatory airway disease affecting over 10% of the global population, leading to considerable socio-economic impacts, especially in developing countries. The pathogenesis of CRS is multifactorial, involving potential contributions from both genetic and environmental factors. While the influence of allergic and autoimmune diseases on CRS has been observed, the causal relationships between these diseases and CRS remain unclear. We extracted data from large-scale genome-wide association studies (GWAS) and utilized a bidirectional two-sample Mendelian randomization (MR) analysis to explore the causal relationships between CRS and ten autoimmune and allergic diseases, including asthma, allergic rhinitis (AR), atopic dermatitis (AD), psoriasis, type 1 diabetes (T1D), hypothyroidism, celiac disease (CeD), multiple sclerosis (MS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). Additionally, we conducted colocalization analysis to determine whether the allergic/autoimmune diseases showing statistical causal relationships with CRS are driven by the same genetic variants. The MR analysis identified that AR (OR\u2009=\u20091.30; 95% CI\u2009=\u20091.21-1.40; P\u2009=\u20093.26E-13), asthma (OR\u2009=\u20091.35; 95% CI\u2009=\u20091.25-1.45; P\u2009=\u20091.35E-14), and AD (OR\u2009=\u20091.17; 95% CI\u2009=\u20091.06-1.30; P\u2009=\u20090.003) were significantly associated with an increased risk of developing CRS. Interestingly, psoriasis (OR\u2009=\u20090.05; 95% CI\u2009=\u20090.01-0.37; P\u2009=\u20090.004) appeared to have a protective effect against CRS. Associations for T1D and hypothyroidism were also suggestive as potential risk factors for CRS. No significant associations in the reverse MR analysis, suggesting a one-directional relationship. Colocalization analysis indicated that asthma (PP.H4\u2009=\u20090.99) shared the same genetic variant (IL-33 rs3939286) with CRS. In conclusion, our study confirmed the causal relationships between allergic and autoimmune diseases (AR, asthma, AD, and psoriasis) and CRS. Notably, we identified a shared genetic variant, rs3939286 in the IL-33 gene, between asthma and CRS, suggesting that targeting the IL-33 pathway may provide a therapeutic strategy for both diseases.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of the American Board of Family Medicine : JABFM \n Clinician-Reported Barriers and Needs for Implementation of Continuous Glucose Monitoring. \n Primary care clinicians face several challenges to prescribing CGM, but they are interested in learning more to help them offer it to their patients. This study reinforces the ongoing need for improved clinician education on CGM technology and continued expansion of insurance coverage for people with both type 1 and type 2 diabetes.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Cells \n Immunomodulatory Functions of TNF-Related Apoptosis-Inducing Ligand in Type 1 Diabetes. \n Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF protein superfamily and was initially identified as a protein capable of inducing apoptosis in cancer cells. In addition, TRAIL can promote pro-survival and proliferation signaling in various cell types. Subsequent studies have demonstrated that TRAIL plays several important roles in immunoregulation, immunosuppression, and immune effector functions. Type 1 diabetes (T1D) is an autoimmune disease characterized by hyperglycemia due to the loss of insulin-producing \u03b2-cells, primarily driven by T-cell-mediated pancreatic islet inflammation. Various genetic, epigenetic, and environmental factors, in conjunction with the immune system, contribute to the initiation, development, and progression of T1D. Recent reports have highlighted TRAIL as an important immunomodulatory molecule with protective effects on pancreatic islets. Experimental data suggest that TRAIL protects against T1D by reducing the proliferation of diabetogenic T cells and pancreatic islet inflammation and restoring normoglycemia in animal models. In this review, we aimed to summarize the consequences of TRAIL action in T1D, focusing on and discussing its signaling mechanisms, role in the immune system, and protective effects in T1D.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Pediatric endocrinology, diabetes, and metabolism \n Guidelines of the Polish Society of Pediatric Endocrinology and Diabetology and Pediatric Section of Diabetes Poland on insulin therapy using hybrid closed-loop systems in children and adolescents with diabetes in Poland. \n Currently, hybrid closed loop (HCL) systems represent the most advantageous therapeutic option for people with diabetes requiring intensive insulin therapy. They make it possible to achieve optimal metabolic control of the disease in any age group while improving the quality of life of children and adolescents with diabetes and their families. Therefore, we present recommendations for the use of HCL systems in children and adolescents focusing on systems currently available in Poland. These systems should be the first choice in terms of method of insulin therapy in the paediatric population. They can be implemented at any stage of diabetes management. These recommendations are based on scientific evidence and experts' experience. They include principles for the initiation, optimisation, and ongoing management of HCL therapy, as well as the required HCL-related education.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of pediatric psychology \n Barriers to healthy behaviors: perspectives from teens with comorbid Type 1 diabetes and overweight/obesity, caregivers, and pediatric endocrinologists. \n Results identify perceived limitations to engaging in recommended healthy lifestyle behaviors and diabetes management concurrently. Results may assist research and clinical care in identifying supports and guidance needed to support adolescents in meeting behavioral recommendations for their health.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Nature reviews. Endocrinology \n The epidemiology of type 1 diabetes mellitus in older adults. \n Although type 1 diabetes mellitus (T1DM) is traditionally viewed as a youth-onset disorder, the number of older adults being diagnosed with this disease is growing. Improvements in the average life expectancy of people with T1DM have also contributed to the growing number of older people living with this disease. We summarize the evidence regarding the epidemiology (incidence, prevalence and excess mortality) of T1DM in older adults (ages \u226560 years) as well as the genetics, immunology and diagnostic challenges. Several studies report an incidence peak of T1DM in older adults of a similar size to or exceeding that in children, and population prevalence generally increases with increasing age. Glutamic acid decarboxylase antibody positivity is frequently observed in adult-onset T1DM. Guidelines for differentiating T1DM from type 2 diabetes mellitus in older adults recommend measuring levels of C-peptide and autoantibodies, including glutamic acid decarboxylase antibodies. However, there is no gold standard for differentiating T1DM from type 2 diabetes mellitus in people aged 60 years and over. As such, the global variation observed in T1DM epidemiology might be in part explained by misclassification, which increases with increasing age of diabetes mellitus onset. With a growing global population of older adults with T1DM, improved genetic and immunological evidence is needed to differentiate diabetes mellitus type at older ages so that a clear epidemiological picture can emerge.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Psychotherapie, Psychosomatik, medizinische Psychologie \n [Patients with Diabetes Mellitus and Comorbid Mental Disorders - Is there a Psychotherapeutic Undertreatment? - Results of the DiMPS Study]. \n Equating the frequency of mental disorders with the need for psychotherapeutic and/or psychopharmacological treatment without considering the specific treatment needs and preferences of patients may lead to an overestimation of the need for care.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Diabetes technology & therapeutics \n Possible Glycemic Effects of Vagus Nerve Stimulation Evaluated by Continuous Glucose Monitoring in People with Diabetes and Autonomic Neuropathy: A Randomized, Sham-Controlled Trial. \n ",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "PloS one \n Association of variants in AGTR1, ACE, MTHFR genes with microalbuminuria and risk factors for the onset of diabetic nephropathy in adolescents with type 1 diabetes in the population of Serbia. \n Our data suggest that common variants in the AGTR1, ACE, and MTHFR genes are not strongly associated with diabetic nephropathy in our patients with type 1 diabetes.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetes \n Emerging Concepts and Success Stories in Type 1 Diabetes Research: A Road Map for a Bright Future. \n Type 1 diabetes treatment stands at a crucial and exciting crossroad since the 2022 U.S. Food and Drug Administration approval of teplizumab to delay disease development. In this article, we discuss four major conceptual and practical issues that emerged as key to further advancement in type 1 diabetes research and therapies. First, collaborative networks leveraging the synergy between the type 1 diabetes research and care community members are key to fostering innovation, know-how, and translation into the clinical arena worldwide. Second, recent clinical trials in presymptomatic stage 2 and recent-onset stage 3 disease have shown the promise, and potential pitfalls, of using immunomodulatory and/or \u03b2-cell protective agents to achieve sustained remission or prevention. Third, the increasingly appreciated heterogeneity of clinical, immunological, and metabolic phenotypes and disease trajectories is of critical importance to advance the decision-making process for tailored type 1 diabetes care and therapy. Fourth, the clinical benefits of early diagnosis of \u03b2-cell autoimmunity warrant consideration of general population screening for islet autoantibodies, which requires further efforts to address the technical, organizational, and ethical challenges inherent to a sustainable program. Efforts are underway to integrate these four concepts into the future directions of type 1 diabetes research and therapy.",
- "labels": [
- 1
- ]
- },
- {
- "text": "BMC health services research \n Bridging the gap: a qualitative process evaluation from the perspectives of healthcare professionals of an audit-and-feedback-based intervention to improve transition to adult care for young people living with type 1 diabetes. \n BTG resulted in a CoP among practitioners delivering transition care to youth with T1D, which could be scaled up to promote a learning health system in pediatric diabetes care. Qualitative process evaluation is a useful tool for understanding how contextual factors affect the implementation and outcomes of complex QI interventions.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Scientific reports \n The effect of war and siege on children with diabetes admitted to ayder comprehensive specialized hospital in mekelle, tigray, ethiopia: a cross-sectional study. \n The armed conflict in Tigray, which spanned from November 2020 to November 2022, along with the accompanying siege, led to the near-total collapse of Tigray's healthcare system. Type 1 Diabetes Mellitus, the most common chronic condition in children, requires significant lifestyle adjustments, including daily insulin injections, regular glucose monitoring, and dietary modifications; all of which are severely impacted by war and siege. This study compared Type 1 diabetes care for children at the Ayder Comprehensive Specialized Hospital, Tigray, during the conflict and siege period with that of the pre-war period. We conducted a retrospective cross-sectional survey, analyzing data from September 2019 to August 2020 (pre-war period) and comparing it with data from September 2021 to August 2022 (war and siege period). Descriptive statistics, including frequencies and percentages, were employed, and Pearson's or Spearman's correlation analyses were used to evaluate correlations where appropriate. We identified 143 pediatric patients admitted (56 during the pre-war period and 87 during the war and siege period), with a mean age of 109 months in both periods. During the war and siege, a higher proportion of diabetes admissions were due to diabetic ketoacidosis (DKA) (90%) compared to the pre-war period (75%). In the pre-war period, the most common trigger for DKA was infections (35%), while in the war and siege period, it shifted to malnutrition (47%), infections (46%), lack of access to healthcare facilities (31%), and running out of medicines (24%). Complications such as death, renal failure, cerebral edema, and shock were more prevalent during the war and siege periods. The case fatality rate was significantly higher during the war and siege (9%) compared to the pre-war period (0%), correlating strongly with the severity of DKA, the degree of hypokalemia, the presence of complications, and admission during the war and siege. Our study showed the negative impact of war and siege on diabetes care in children demonstrating a high rate of DKA admissions with increased severity, complications, malnutrition, and case fatality rates. People with diabetes especially type 1 deserve great attention during such a crisis as the lack of insulin could lead to severe complications including death.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetes research and clinical practice \n Time in range and mean glucose cut-off points for reduction of fetal outcomes in pregnant women with type 1 diabetes using automated insulin delivery systems. \n TIRp\u00a0>\u00a059.1\u00a0% and mean glucose\u00a0<\u00a0133\u00a0mg/dl in the second trimester, is associated with lower fetal outcomes of large for gestational age. One of the strategies that would improve TIRp is the early use of AHCL systems. Further studies are needed before a strong recommendation can be made.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Georgian medical news \n EVALUATION OF DENTAL AND PERIODONTAL STATUS IN CHILDREN WITH TYPE 1 DIABETES MELLITUS. \n Children with T1DM exhibit poor oral health conditions related to the level of metabolic control. Maintenance of toothbrushing habits and regular dental check-ups recommended to manage and prevent these complications. Additionally, proper management of metabolic control can also help mitigate the adverse effects on oral health.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Cardiovascular diabetology \n Evaluation of the Steno Type 1 Risk Engine in predicting cardiovascular events in an ethnic mixed population of type 1 diabetes mellitus and its association with chronic microangiopathy complications. \n ST1RE performed well in predicting CV events at 5 and 10 years of follow-up. Moreover, higher ST1RE scores were associated with the progression of microangiopathy complications in this genetically heterogeneous T1D population.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Nature communications \n Uncovering genetic loci and biological pathways associated with age-related cataracts through GWAS meta-analysis. \n Age-related cataracts is a highly prevalent eye disorder that results in the clouding of the crystalline lens and is one of the leading causes of visual impairment and blindness. The disease is influenced by multiple factors including genetics, prolonged exposure to ultraviolet radiation, and a history of diabetes. However, the extent to which each of these factors contributes to the development of cataracts remains unclear. Our study identified 101 independent genome-wide significant loci, 57 of which are novel. We identified multiple genes and biological pathways associated with the cataracts, including four drug-gene interactions. Our results suggest a causal association between type 1 diabetes and cataracts. Also, we highlighted a surrogate measure of UV light exposure as a marker of cataract risk in adults.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Brain research \n Quantification of white matter hyperintensities in type 1 diabetes and its relation to neuropathy and clinical characteristics. \n Our findings indicate increased burden of periventricular WMHs in diabetes which were associated to DPN severity and measurements reflecting neurodegeneration. Deep WMHs, often considered as chronic ischemic, were not significantly different. Mechanisms reflecting neurodegeneration and accelerated brain aging could be an overlooked aspect of peripheral and central neuropathy.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n Subcutaneous rapid-acting insulin analogues in mild to moderate diabetic ketoacidosis: A meta-analysis of randomized controlled trials. \n In this meta-analysis of eight RCTs we found that SC RAIAs and regular IV insulin are comparable in resolving mild to moderate DKA in children and adults. PROSPERO registration: CRD42023485032.",
- "labels": [
- 1
- ]
- },
- {
- "text": "PloS one \n Type 1 diabetes and parasite infection: An exploratory study in NOD mice. \n Microorganisms have long been suspected to influence the outcome of immune-related syndromes, particularly autoimmune diseases. Type 1 diabetes (T1D) results from the autoimmune destruction of the insulin-producing beta cells of pancreatic islets, causing high glycemia levels. Genetics is part of its aetiology, but environmental factors, particularly infectious microorganisms, also play a role. Bacteria, viruses, and parasites influence the outcome of T1D in mice and humans. We used nonobese diabetic (NOD) mice, which spontaneously develop T1D, to investigate the influence of a parasitic infection, leishmaniasis. Leishmania amazonensis is an intracellular eukaryotic parasite that replicates predominantly in macrophages and is responsible for cutaneous leishmaniasis. The implication of Th1 immune responses in T1D and leishmaniasis led us to study this parasite in the NOD mouse model. We previously constructed osteopontin knockout mice with a NOD genetic background and demonstrated that this protein plays a role in the T1D phenotype. In addition, osteopontin (OPN) has been found to play a role in the immune response to various infectious microorganisms and to be implicated in other autoimmune conditions, such as multiple sclerosis in humans and experimental autoimmune encephalomyelitis (EAE) in mice. We present herein data demonstrating the role of OPN in the response to Leishmania in NOD mice and the influence of this parasitic infection on T1D. This exploratory study aimed to investigate the environmental infectious component of the autoimmune response, including Th1 immunity, which is common to both T1D and leishmaniasis.",
- "labels": [
- 1
- ]
- },
- {
- "text": "The Journal of clinical investigation \n Attenuated kidney oxidative metabolism in young adults with type 1 diabetes. \n BACKGROUNDIn type 1 diabetes (T1D), impaired insulin sensitivity may contribute to the development of diabetic kidney disease (DKD) through alterations in kidney oxidative metabolism.METHODSYoung adults with T1D (n = 30) and healthy controls (HCs) (n = 20) underwent hyperinsulinemic-euglycemic clamp studies, MRI, 11C-acetate PET, kidney biopsies, single-cell RNA-Seq, and spatial metabolomics to assess this relationship.RESULTSParticipants with T1D had significantly higher glomerular basement membrane (GBM) thickness compared with HCs. T1D participants exhibited lower insulin sensitivity and cortical oxidative metabolism, correlating with higher insulin sensitivity. Proximal tubular transcripts of TCA cycle and oxidative phosphorylation enzymes were lower in T1D. Spatial metabolomics showed reductions in tubular TCA cycle intermediates, indicating mitochondrial dysfunction. The Slingshot algorithm identified a lineage of proximal tubular cells progressing from stable to adaptive/maladaptive subtypes, using pseudotime trajectory analysis, which computationally orders cells along a continuum of states. This analysis revealed distinct distribution patterns between T1D and HCs, with attenuated oxidative metabolism in T1D attributed to a greater proportion of adaptive/maladaptive subtypes with low expression of TCA cycle and oxidative phosphorylation transcripts. Pseudotime progression associated with higher HbA1c, BMI, and GBM, and lower insulin sensitivity and cortical oxidative metabolism.CONCLUSIONThese early structural and metabolic changes in T1D kidneys may precede clinical DKD.TRIAL REGISTRATIONClinicalTrials.gov NCT04074668.FUNDINGUniversity of Michigan O'Brien Kidney Translational Core Center grant (P30 DK081943); CROCODILE studies by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (P30 DK116073), Juvenile Diabetes Research Foundation (JDRF) (2-SRA-2019-845-S-B), Boettcher Foundation, Intramural Research Program at NIDDK and Centers for Disease Control and Prevention (CKD Initiative) under Inter-Agency Agreement #21FED2100157DPG.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Annals of medicine \n Increased purchases of prescription medicines in offspring of women with type 1 diabetes: a Finnish register-based cohort study between 1995 and 2018. \n Our findings suggest that exposed offspring purchase more reimbursable prescription medicines than reference offspring from age seven to thirty years. More research is needed to examine the effects of intrauterine exposure to hyperglycemia on long-term health in offspring.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n The associations between functional vitamin K status and all-cause mortality, cardiovascular disease and end-stage kidney disease in persons with type 1 diabetes. \n In persons with type 1 diabetes, lower vitamin K status was associated with higher mortality, CVD and progression to ESKD, however, not after adjustment for other risk factors. Interventional studies are needed to elucidate the role of vitamin K in persons with type 1 diabetes.",
- "labels": [
- 1
- ]
- },
- {
- "text": "JPMA. The Journal of the Pakistan Medical Association \n Assessment of growth status in children and adolescents with type 1 diabetes mellitus in Baghdad: a case-control study. \n Children with type 1 diabetes mellitus had significantly lower mean height, weight and body mass index Z scores compared to their counterparts in the control group. Pubertal age group, poor glycaemic control, longer disease duration, and using conventional insulin regimen were the factors affecting growth parameters.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetes research and clinical practice \n Beyond the insulin pump: Unraveling diabetes tech dependency. \n The use of technology for Type 1 diabetes (T1D) has significantly developed in the last 20\u00a0years leading to several benefits in life-style management but also to potentially overreliance and addiction to such life changing devices. Insulin pumps (CSII) being small, discreet and sophisticated, offer features such as customizable basal rates, bolus calculators and integration with Continuous Glucose Monitoring (CGM) systems becoming a must have for diabetic patients. Indeed CGM, firstly introduced in the late 1990s and now being highly sophisticated provide trends and patterns hence allowing a better management of T1D. In this review we inquire the multifactorial aspects of dependency on diabetes technology, focusing not only on the benefits and the advancements these automations offer, but also the challenges, limits and possible risks associated with overreliance on them. Specifically, the impact that early introduction to technology had on patients, the dependency on CSII and CGM, the importance of learning and self-management skills and strategies for addressing unexpected events.",
- "labels": [
- 1
- ]
- },
- {
- "text": "JMIR formative research \n Feasibility and Acceptability of a Self-Guided Digital Family Skills Management Intervention for Children Newly Diagnosed With Type 1 Diabetes: Pilot Randomized Controlled Trial. \n ClinicalTrials.gov NCT03720912; https://clinicaltrials.gov/study/NCT03720912.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetic medicine : a journal of the British Diabetic Association \n The diabetes annual review in a postal box: A qualitative study exploring the views of people living with diabetes (DiaBox-Qual). \n Postal boxes for annual reviews were well-received by those living with diabetes. Designed well, they have the potential to overcome more than just the physical barriers to annual review attendance.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Medicine \n Exploring the mechanism of comorbidity in patients with T1DM and COVID-19: Integrating bioinformatics and Mendelian randomization methods. \n During the coronavirus disease 2019 (COVID-19) pandemic, the incidence of type 1 diabetes mellitus (T1DM) has increased. Additionally, evidence suggests that individuals with diabetes mellitus may have increased susceptibility to severe acute respiratory syndrome coronavirus 2 infection. However, the specific causal relationships and interaction mechanisms between T1DM and COVID-19 remain unclear. This study aims to investigate the causal relationship between T1DM and COVID-19, utilizing differential gene expression and Mendelian randomization analyses. Differentially expressed gene sets from datasets GSE156035 and GSE171110 were intersected to identify shared genes, analyzed for functional enrichment. Mendelian randomization models were employed to assess causal effects, revealing no direct causal link between T1DM and COVID-19 in the European population (P\u2005>\u2005.05). Notably, DNA replication and sister chromatid cohesion 1 (DSCC1) showed negative causal associations with both diseases (T1DM: OR\u2005=\u20050.943, 95% CI: 0.898-0.991, P\u2005=\u2005.020; COVID-19: OR\u2005=\u20050.919, 95% CI: 0.882-0.958, P\u2005<\u2005.001), suggesting a protective effect against their comorbidity. This genetic evidence highlights DSCC1 as a potential target for monitoring and managing the co-occurrence of T1DM and COVID-19.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes science and technology \n Psychosocial Aspects of Diabetes Technologies: Commentary on the Current Status of the Evidence and Suggestions for Future Directions. \n Diabetes technologies, including continuous glucose monitors, insulin pumps, and automated insulin delivery systems offer the possibility of improving glycemic outcomes, including reduced hemoglobin A1c, increased time in range, and reduced hypoglycemia. Given the rapid expansion in the use of diabetes technology over the past few years, and touted promise of these devices for improving both clinical and psychosocial outcomes, it is critically important to understand issues in technology adoption, equity in access, maintaining long-term usage, opportunities for expanded device benefit, and limitations of the existing evidence base. We provide a brief overview of the status of the literature-with a focus on psychosocial outcomes-and provide recommendations for future work and considerations in clinical applications. Despite the wealth of the existing literature exploring psychosocial outcomes, there is substantial room to expand our current knowledge base to more comprehensively address reasons for differential effects, with increased attention to issues of health equity and data harmonization around patient-reported outcomes.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Frontiers in endocrinology \n A novel class of oral, non-immunosuppressive, beta cell-targeting, TXNIP-inhibiting T1D drugs is emerging. \n Diabetes treatment options have improved dramatically over the last 100 years, however, close to 2 million individuals in the U.S. alone live with type 1 diabetes (T1D) and are still dependent on multiple daily insulin injections and/or continuous insulin infusion with a pump to stay alive and no oral medications are available. After decades of focusing on immunosuppressive/immunomodulatory approaches for T1D, it has now become apparent that at least after disease onset, this by itself may not be sufficient, and in order to be effective, therapies need to also address beta cell health. This Perspective article discusses the emergence of such a beta cell-targeting, novel class of oral T1D drugs targeting thioredoxin-interacting protein (TXNIP) and some very recent advances in this field that start to address this unmet medical need. It thereby focuses on repurposing of the antihypertensive drug, verapamil found to non-specifically inhibit TXNIP and on TIX100, a new chemical entity specifically developed as an oral anti-diabetic drug to inhibit TXNIP. Both have shown striking anti-diabetic effects in preclinical studies. Verapamil has also proven to be beneficial in adults and children with recent onset T1D, while TIX100 has just been cleared by the U.S. Food and Drug Administration (FDA) to proceed to clinical trials. Taken together, we propose that such non-immunosuppressive, adjunctive therapies to insulin, alone or in combination with immune modulatory approaches, are critical in order to achieve effective and durable disease-modifying treatments for T1D.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Nursing & health sciences \n A Qualitative Evidence Synthesis of Continuous Subcutaneous Insulin Infusion: Acceptability, Implementation, Equity. \n This work provides a synthesis of the perceptions of people with type 1 diabetes mellitus (T1DM) and healthcare professionals about the acceptability, implementation, and equity of continuous subcutaneous insulin infusion (CSII). A qualitative evidence synthesis was carried out. Three online databases (Medline, Embase, and Web of Science) were searched. Qualitative articles which were available in Spanish or English were included. A descriptive thematic synthesis was conducted according to PRISMA and ENTREQ guidelines. Thirty-two references met the inclusion criteria of the study and were included out of an initial 345 identified references. Seven main themes were identified: (a) acceptability, (b) adaptation to the insulin pump, (c) facilitators for the adequate use of insulin pump, (d) variability of acceptability, (e) barriers for the use of insulin pump, (f) feasibility and implementation considerations, and (g) equity. CSII is well accepted by most people with T1DM, with some exceptions. CSII can relieve management burden, increase autonomy and flexibility and improve family relationships. There were multiple perceived barriers to its continued use. Future studies should continue to analyze inequalities in access and use of the CSII.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Medical engineering & physics \n Platform for precise, personalised glucose forecasting through continuous glucose and physical activity monitoring and deep learning. \n Emerging research has demonstrated the advantage of continuous glucose monitoring for use in artificial pancreas and diabetes management in general. Recent studies demonstrate that glucose level forecasting using deep learning can help avoid postprandial hyperglycemia (\u2265 180 mg/dL) or hypoglycemia (\u226470 mg/dL) from delayed or increased insulin dosing in artificial pancreas. In this paper, a novel hybrid deep learning framework with integration of content-based attention learning is presented, to effectively predict the glucose measurements with prediction horizons (PH) = 15, 30 and, 60 minutes for T1D and T2D patients based on past data. We also present a complete cloud-based system and mobile app used for collecting CGM sensor, physical activity data, CHO values and insulin measurements to perform glucose forecasts using the proposed model running on Cloud. This model was validated using clinical data of individual with Type 1 diabetes (OhioT1DM) and individual with Type 2 diabetes. The mean absolute relative difference (MARD) was 12.33\u00b13.15, 7.14\u00b11.76% for PH=60 and, 30 min respectively on OhioT1DM clinical Dataset. The root mean squared error (RMSE) was 29.41\u00b15.92 mg/dL and 17.19\u00b13.22 mg/dL and the mean absolute error (MAE) was 21.96\u00b14.67 mg/dL and 12.58\u00b12.34 mg/dL for PH=60 and, 30 min respectively on the same clinical dataset. It was observed that inclusion of physical activity leads to improved glucose forecasting accuracy. Furthermore, all these results were obtained by training the model on only 8 days of clinical data of a single patient, followed by testing on clinical data on the following days. The results indicate that training on a single patient data may lead to better personalisation and better glucose forecasting results compared to existing works.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Psychiatry research \n Impact of mental disorders on the all-cause mortality and cardiovascular disease outcomes in adults with new-onset type 1 diabetes: A nationwide cohort study. \n Mental disorders are associated with an elevated risk of all-cause mortality and CVD in adults with newly diagnosed type 1 diabetes. Early detection and greater attention to premature death and CVD development are required in patients with new-onset type 1 diabetes and mental disorders.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Placenta \n Gene expression profiles in placenta and their association with anesthesia, delivery mode and maternal diabetes. \n The findings reveal suppression of immune pathways and upregulation of ribosome activity in the placenta by maternal diabetes highlighting the importance of confounding factors when examining cell and tissue expression profiles. Further studies should determine whether the observed gene expression differences are related to underlying causes for cesarean section deliveries.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n All-cause mortality and factors associated with it in Finnish patients with type 1 diabetes. \n There's substantial excess mortality due to DM1 in Finland. Interventions should focus on addressing both renal and cardiovascular risk factors but also pay more attention to mental health.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Molecular biology reports \n Association of polymorphism of NLRP3, ICAM-1, PTPN22, INS genes in childhood onset type 1 diabetes in a Pakistani population. \n The present study provides evidence that SNPs in the PTPN22, INS, NLRP3, and ICAM-1 genes are associated with the development of T1D. Further research is needed to explore their potential use in genetic screening and personalized medication.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n Characterizing the relationship between social determinants of health and risk of albuminuria among children with type 1 diabetes. \n In a cohort of 2303 children with type 1 diabetes (T1D), we found that non-English speaking status (HR 2.82, 95% CI 1.54-5.18) and public insurance (HR 1.48, 95% CI 1.07-2.05) were associated with an increased risk of incident albuminuria, after adjusting for T1D-related variables (age, hemoglobin A1c, diabetic ketoacidosis episodes with acute kidney injury).",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetes care \n Efficacy and Safety of a Tubeless AID System Compared With Pump Therapy With CGM in the Treatment of Type 1 Diabetes in Adults With Suboptimal Glycemia: A Randomized, Parallel-Group Clinical Trial. \n Use of the tubeless AID system led to improved glycemic outcomes compared with pump therapy with CGM among adults with type 1 diabetes, underscoring the clinical benefit of AID and bolstering recommendations to establish AID systems as preferred therapy for this population.",
- "labels": [
- 1
- ]
- },
- {
- "text": "The Journal of international medical research \n Factors associated with severe diabetic ketoacidosis in patients diagnosed with type 1 diabetes: a decade-long cross-sectional analysis. \n The present findings highlight the need for improving awareness about diabetes symptoms among physicians and the public to reduce the occurrence and severity of DKA at the onset of T1DM.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Archives of endocrinology and metabolism \n Decoding the relationship between cow's milk proteins and development of type 1 diabetes mellitus. \n The findings of this study provide further evidence for a potential role of cow's milk proteins in triggering T1DM. The in silico analysis suggests that molecular mimicry mechanisms between cow's milk proteins and human beta-cell antigens may contribute to the autoimmune response leading to T1DM.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Archives of endocrinology and metabolism \n Clinical screening for GCK-MODY in 2,989 patients from the Brazilian Monogenic Diabetes Study Group (BRASMOD) and the Brazilian Type 1 Diabetes Study Group (BrazDiab1SG). \n This study identified a highly accurate (98%) composite model for differentiating GCK-MODY and T1D. This model may help clinicians select patients for genetic evaluation of monogenic diabetes, enabling them to implement correct treatment without overusing limited resources.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Archives of endocrinology and metabolism \n Whom should we target? A brief report on a prospective study to identify predictors of mental health and self-care worsening in patients with diabetes mellitus during the COVID-19 pandemic. \n Some clinical and socioeconomic characteristics may be suitable for identifying patients at higher risk of mental health and self-care worsening, signaling who needs to be monitored more closely during crisis situations.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Archives of endocrinology and metabolism \n Clinical features most frequently present in patients with concomitant diabetic kidney disease and diabetic retinopathy. \n Among patients with DKD and type 2 diabetes, insulin use, longer diabetes duration, and higher systolic blood pressure level were associated with the presence of DR.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Archives of endocrinology and metabolism \n Euglycemic diabetic ketoacidosis in a patient with new-onset type 1 diabetes following a ketogenic diet: a potential risk of a dangerous dietary trend. \n Euglycemic diabetic ketoacidosis (DKA) is a rare complication of diabetes mellitus (DM) characterized by metabolic acidosis, ketosis, and blood glucose levels < 250 mg/dL. The prevalence of euglycemic DKA is increasing with the popularity of ketogenic (low-carbohydrate) diets. We present herein the case of a patient with newly diagnosed type 1 DM who developed euglycemic DKA following a ketogenic diet. A 22-year-old woman presented to the emergency department with malaise, fatigue, nausea, and vomiting. She had no family history of DM. She had consulted her primary care physician 2 weeks before due to hair loss, numbness, and tingling sensation in her fingertips. Her fasting blood glucose was 205 mg/dL at that time. Reluctant to use medication to control her blood glucose levels, she started a ketogenic diet. On admission, she was conscious, oriented, cooperative, and tachycardic. Her body mass index was 17.6 kg/m",
- "labels": [
- 1
- ]
- },
- {
- "text": "Archives of endocrinology and metabolism \n Underreporting of diabetes mellitus as the cause of death in Bauru, State of S\u00e3o Paulo, Brazil over 40 years: a documental study. \n The underreporting of DM as the cause of death was very frequently found, and was associated with male gender, decade of death, shorter DM duration and DM2. If our data could be applied to the whole country, DM would possibly emerge as a more prominent cause of death in Brazil. Future studies in other cities and geographic regions are warranted to confirm our findings.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Gut microbes \n Gut microbial metabolic signatures in diabetes mellitus and potential preventive and therapeutic applications. \n Diabetes mellitus can be subdivided into several categories based on origin and clinical characteristics. The most common forms of diabetes are type 1 (T1D), type 2 diabetes (T2D) and gestational diabetes mellitus (GDM). T1D and T2D are chronic diseases affecting around 537 million adults worldwide and it is projected that these numbers will increase by 12% over the next two decades, while GDM affects up to 30% of women during pregnancy, depending on diagnosis methods. These forms of diabetes have varied origins: T1D is an autoimmune disease, while T2D is commonly associated with, but not limited to, certain lifestyle patterns and GDM can result of a combination of genetic predisposition and pregnancy factors. Despite some pathogenic differences among these forms of diabetes, there are some common markers associated with their development. For instance, gut barrier impairment and inflammation associated with an unbalanced gut microbiota and their metabolites may be common factors in diabetes development and progression. Here, we summarize the microbial signatures that have been linked to diabetes, how they are connected to diet and, ultimately, the impact on metabolite profiles resulting from host-gut microbiota-diet interactions. Additionally, we summarize recent advances relating to promising preventive and therapeutic interventions focusing on the targeted modulation of the gut microbiota to alleviate T1D, T2D and GDM.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Journal of medical case reports \n Treatment switch from multiple daily insulin injections to sulphonylureas in an African young adult diagnosed with HNF1A MODY: a case report. \n This case reveals that HNF1A maturity onset diabetes of the young (and probably other causes of monogenic diabetes) can present in sub-Saharan Africa. A diagnosis of maturity onset diabetes of the young can have significant life-changing therapeutic implications.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Cardiovascular diabetology \n Unseen threat: how subclinical atherosclerosis increases mortality risk in patients with type 1 diabetes. \n Subclinical atherosclerosis is independently associated with increased overall mortality and MACE in patients with type 1 diabetes. Identifying clinical predictors can improve risk stratification and personalised therapeutic strategies to prevent MACEs in this high-risk population.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of molecular medicine (Berlin, Germany) \n Therapy concepts in type 1 diabetes mellitus treatment: disease modifying versus curative approaches. \n For many autoimmune diseases, including type 1 diabetes mellitus (T1DM), efforts have been made to modify the disease process through pharmacotherapy. The ultimate goal must be to develop therapies with curative potential by achieving an organ without signs of parenchymal cell destruction and without signs of immune cell infiltration. In the case of the pancreas, this means regenerated and well-preserved beta cells in the islets without activated infiltrating immune cells. Recent research has opened up the prospect of successful antibody combination therapy for autoimmune diabetes with curative potential. This goal cannot be achieved with monotherapies. The requirements for the implementation of such a therapy with curative potential for the benefit of patients with T1DM and LADA (latent autoimmune diabetes in adults) are considered.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of molecular histology \n Type I Diabetes Mellitus impairs cytotoxic immunity through CEACAM5 upregulation in colorectal cancer : Exploring the intersection of autoimmune dysfunction and cancer progression: the role of NF-\u03baB p65 in colorectal cancer. \n Type 1 diabetes (T1D) is characterized by an autoimmune-mediated destruction of pancreatic beta cells and a chronic inflammatory state, which may influence the progression of colorectal cancer (CRC) through immune system dysregulation and enhanced tumor immune evasion. This study aims to elucidate the role of p65 in modulating the tumor microenvironment in CRC within the context of T1D and to determine how this modulation affects tumor growth, immune cell infiltration, and the expression of immune evasion molecules such as CEACAM5. NOD mice, which model T1D, were inoculated with MC38 colon carcinoma cells engineered to knock down p65. Tumor growth was monitored, and the tumor microenvironment was analyzed using flow cytometry to assess the infiltration of immune cells. The expression of Ki-67 and CEACAM5 in tumor cells was also evaluated. Additionally, in vitro assays were conducted to study the proliferation and activation of T cells co-cultured with tumor cells. Knockdown of p65 in tumor cells significantly inhibited tumor growth in NOD mice. This was accompanied by an increased infiltration of cytotoxic CD8+ T cells and no significant change in CD4+\u2009or Foxp3\u2009+ T regulatory cells within the tumor microenvironment. There was a notable reduction in the expression of Ki-67 and CEACAM5, indicating decreased proliferation and potential immune evasion capabilities of the tumor cells. Our findings demonstrate that the NF-\u03baB p65 subunit plays a crucial role in promoting tumor growth and modulating the immune microenvironment in CRC, particularly in the context of T1D. Knocking down p65 not only reduces tumor progression but also enhances the anti-tumor immune response by decreasing immune evasion mechanisms. These results suggest that targeting the NF-\u03baB pathway may be a viable strategy to improve the efficacy of cancer immunotherapy, especially in patients with autoimmune diseases like T1D. Physical activity enhances the effect of immune checkpoint blockade by inhibiting the intratumoral HIF1-\u03b1/CEACAM5 axis.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Antiviral research \n Vemurafenib inhibits the replication of diabetogenic enteroviruses in intestinal epithelial and pancreatic beta cells. \n Enteroviruses, which infect via the gut, have been implicated in type 1 diabetes (T1D) development. Prolonged faecal shedding of enterovirus has been associated with islet autoimmunity. Additionally, enteroviral proteins and viral RNA have been detected in the pancreatic islets of individuals with recent-onset T1D, implicating their possible role in beta cell destruction. Despite this, no approved antiviral drugs currently exist that specifically target enterovirus infections for utilisation in disease interventions. Drug repurposing allows for the discovery of new clinical uses for existing drugs and can expedite drug discovery. Previously, the cancer drug Vemurafenib demonstrated unprecedented antiviral activity against several enteroviruses. In the present study, we assessed the efficacy of Vemurafenib and an analogue thereof in preventing infection or reducing the replication of enteroviruses associated with T1D. We tested Vemurafenib in intestinal epithelial cells (IECs) and insulin-producing beta cells. Additionally, we established a protocol for infecting human stem cell-derived islets (SC-islets) and used Vemurafenib and its analogue in this model. Our studies revealed that Vemurafenib exhibited strong antiviral properties in IECs and a beta cell line. The antiviral effect was also seen with the Vemurafenib analogue. SC-islets expressed the viral receptors CAR and DAF, with their highest expression in insulin- and glucagon-positive cells, respectively. SC-islets were successfully infected by CVBs and the antiviral activity of Vemurafenib and its analogue was confirmed in most SC-islet batches. In summary, our observations suggest that Vemurafenib and its analogue warrant further exploration as potential antiviral agents for the treatment of enterovirus-induced diseases, including T1D.",
- "labels": [
- 1
- ]
- },
- {
- "text": "The lancet. Diabetes & endocrinology \n Continuous glucose sensor accuracy: beyond the headline metric. \n The promotion of continuous glucose monitoring (CGM) to standard of care for type 1 diabetes and insulin-treated type 2 diabetes reflects a robust and wide evidence base for the technology's effectiveness supported by real-world efficacy data. Multiple CGM devices are available worldwide and are marketed, in part, based on accuracy data. In this Viewpoint, we argue that accuracy metrics are no longer a point of difference between CGM devices as almost all exceed an acceptable threshold. We also argue that domains of standardisation, clinical outcomes, and sustainability should now be given primacy as CGM devices seek to be implemented for new indications. These domains are key for the success of the next generation of CGM devices. Additionally, we discuss the need to address inequalities in accessing clinically impactful technologies.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Diabetes care \n Eighteen-Month Hybrid Closed-Loop Use in Very Young Children With Type 1 Diabetes: A Single-Arm Multicenter Trial. \n Use of the Cambridge hybrid CL system led to sustained improvements in glycemic control lasting more than 18 months in very young children with T1D.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Scientific reports \n Clinical importance of cytokine (IL-6, IL-8, and IL-10) and vitamin D levels among patients with Type-1 diabetes. \n Type-1 diabetes (T1D) is an autoimmune disorder characterized by impaired insulin release by islet \u03b2 cells. It has been shown that proinflammatory cytokines released during the disease can exacerbate the condition, while anti-inflammatory cytokines offer protection. This study analyzed the clinical role of interleukin (IL)-6, -8, -10, and vitamin D levels in T1D patients compared to healthy controls. The levels of IL-6, IL-8, IL-10, and vitamin D in the participants' serum samples were analyzed using ELISA. The findings showed that T1D patients had significantly increased levels (p\u2009<\u20090.0001) of fasting blood glucose, HbA1c, systolic blood pressure, low-density lipoprotein, triglycerides, cholesterol, and very low-density lipoprotein and decreased levels of high-density lipoprotein and vitamin D (p\u2009<\u20090.0001) compared to healthy controls. Moreover, the levels of IL-6, IL-8, and IL-10 were also significantly greater (p\u2009<\u20090.0001) in T1D patients. The study also determined the significance of these cytokines among T1D patients and healthy controls using ROC curves. Furthermore, we found that smokers had significantly higher levels of IL-6 (p\u2009=\u20090.01) and IL-8 (p\u2009=\u20090.003) than non-smokers. These results showed that elevated levels of IL-6, IL-8, and IL-10, decreased vitamin D levels, and smoking among T1D participants could contribute to the worsening of T1D disease and could serve as predictive indicators.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Acta paediatrica (Oslo, Norway : 1992) \n Low-carbohydrate diet proved effective and safe for youths with type 1 diabetes: A randomised trial. \n Both diets improved glycaemic outcomes in adolescents and youths with type 1 diabetes, without increasing hypoglycaemia or cardiovascular risk factors, indicating comparable safety and efficacy.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Use of continuous glucose monitoring and hybrid closed-loop therapy in pregnancy. \n Continuous glucose monitoring (CGM) has led to a paradigm shift in the management of pregnant women with type 1 diabetes (T1D), with improved glycaemic control, less hypoglycaemia and fewer pregnancy complications. Data on CGM use in pregnant women with type 2 diabetes (T2D) are limited. A large randomized controlled trial (RCT) on CGM use in people with T2D in pregnancy is ongoing. Small studies on CGM use in women with gestational diabetes (GDM) have suggested improved glycaemic control and better qualification when insulin is needed. However, none of these studies was powered to evaluate pregnancy outcomes. Several large RCTs are ongoing in women with GDM. In addition to CGM, other technologies, such as advanced hybrid closed-loop (AHCL) systems have further improved glycaemic management in people with T1D. AHCL therapy adapts insulin delivery via a predictive algorithm integrated with CGM and an insulin pump. A large RCT with the AHCL CamAPS\u00ae FX demonstrated a 10% increase in time in range compared to standard insulin therapy in a pregnant population with T1D. Recently, an RCT of an AHCL system not approved for use in pregnancy (780G MiniMed) has also demonstrated additional benefits of AHCL therapy compared to standard insulin therapy, with improved time in range overnight, less hypoglycaemia and improved treatment satisfaction. More evidence is needed on the impact of AHCL therapy on maternal and neonatal outcomes and on which glycaemic targets with CGM should be used in pregnant women with T2D and GDM. We review the current evidence on the use of CGM and AHCL therapy in pregnancy.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Frontiers in immunology \n TNF-\u03b1 inhibitors for type 1 diabetes: exploring the path to a pivotal clinical trial. \n Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing \u03b2-cells in the pancreas. This destruction leads to chronic hyperglycemia, necessitating lifelong insulin therapy to manage blood glucose levels. Typically diagnosed in children and young adults, T1D can, however, occur at any age. Ongoing research aims to uncover the precise mechanisms underlying T1D and to develop potential interventions. These include efforts to modulate the immune system, regenerate \u03b2-cells, and create advanced insulin delivery systems. Emerging therapies, such as closed-loop insulin pumps, stem cell-derived \u03b2-cell replacement and disease-modifying therapies (DMTs), offer hope for improving the quality of life for individuals with T1D and potentially moving towards a cure. Currently, there are no disease-modifying therapies approved for stage 3 T1D. Preserving \u03b2-cell function in stage 3 T1D is associated with better clinical outcomes, including lower HbA1c and decreased risk of hypoglycemia, neuropathy, and retinopathy. Tumor Necrosis Factor alpha (TNF-\u03b1) inhibitors have demonstrated efficacy at preserving \u03b2-cell function by measurement of C-peptide in two clinical trials in people with stage 3 T1D. However, TNF-\u03b1 inhibitors have yet to be evaluated in a pivotal trial for T1D. To address the promising clinical findings of TNF-\u03b1 inhibitors in T1D, Breakthrough T1D convened a panel of key opinion leaders (KOLs) in the field. The workshop aimed to outline an optimal clinical path for moving TNF-\u03b1 inhibitors to a pivotal clinical trial in T1D. Here, we summarize the evidence for the beneficial use of TNF-\u03b1 inhibitors in T1D and considerations for strategies collectively identified to advance TNF-\u03b1 inhibitors beyond phase 2 clinical studies for stage 3 T1D.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Frontiers in endocrinology \n Clinical perspective on innovative insulin delivery technologies in diabetes management. \n The present study highlights that physicians are generally supportive of utilizing new technology. The questionnaires and the open discussion revealed the expectation that the Smart MDI technology provides better control, primarily by identifying missed boluses, while expressing concerns on the use of the technology by teenagers and children, who might forget the device and be reluctant to use in public, and by the older population, who might be challenged by the technology.",
- "labels": [
- 0,
- 1
- ]
- },
- {
- "text": "Journal of pediatric gastroenterology and nutrition \n Is HLA-DQ typing useful in screening for celiac disease among Arabs with type 1 diabetes? A case-control study. \n Only 4% of Saudi patients with T1D carry DQ-genotypes at no risk to develop CD, which supports the European guidelines that recommend celiac serology test as the most cost-effective screening method. We identified the risk gradient associated with DQ-genotypes to develop CD in our population which could help in counseling patients for the risk to develop CD and planning follow-up serology tests.",
- "labels": [
- 1
- ]
- },
- {
- "text": "International journal of molecular sciences \n Unravelling the Role of Gut and Oral Microbiota in the Pediatric Population with Type 1 Diabetes Mellitus. \n Type 1 Diabetes Mellitus (T1DM) is a chronic autoimmune disease that results in the destruction of pancreatic \u03b2 cells, leading to hyperglycaemia and the need for lifelong insulin therapy. Although genetic predisposition and environmental factors are considered key contributors to T1DM, the exact causes of the disease remain partially unclear. Recent evidence has focused on the relationship between the gut, the oral cavity, immune regulation, and systemic inflammation. In individuals with T1DM, changes in the gut and oral microbial composition are commonly observed, indicating that dysbiosis may contribute to immune dysregulation. Gut dysbiosis can influence the immune system through increased intestinal permeability, altered production of short chain fatty acids (SCFAs), and interactions with the mucosal immune system, potentially triggering the autoimmune response. Similarly, oral dysbiosis may contribute to the development of systemic inflammation and thus influence the progression of T1DM. A comprehensive understanding of these relationships is essential for the identification of biomarkers for early diagnosis and monitoring, as well as for the development of therapies aimed at restoring microbial balance. This review presents a synthesis of current research on the connection between T1DM and microbiome dysbiosis, with a focus on the gut and oral microbiomes in pediatric populations. It explores potential mechanisms by which microbial dysbiosis contributes to the pathogenesis of T1DM and examines the potential of microbiome-based therapies, including probiotics, prebiotics, synbiotics, and faecal microbiota transplantation (FMT). This complex relationship highlights the need for longitudinal studies to monitor microbiome changes over time, investigate causal relationships between specific microbial species and T1DM, and develop personalised medicine approaches.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Nutrients \n Nutrition and Glycemic Control in Children and Adolescents with Type 1 Diabetes Mellitus Attending Diabetes Camps. \n ",
- "labels": [
- 1
- ]
- },
- {
- "text": "BMC oral health \n Genetic and therapeutic for oral lichen planus and diabetes mellitus: a comprehensive study. \n The study highlighted a complex interplay between diabetes and OLP, underscoring the efficacy of integrated therapeutic strategies that target both conditions. The findings suggest that both pharmaceutical and herbal treatments can effectively manage the clinical manifestations of OLP and associated metabolic challenges. This holistic approach to treatment could significantly enhance patient outcomes by addressing the interconnected aspects of these chronic conditions.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Nature communications \n TGF-\u03b2-mediated crosstalk between TIGIT \n Type 1 diabetes (T1D) is a chronic autoimmune condition characterized by hyperglycemia resulting from the destruction of insulin-producing \u03b2-cells that is traditionally deemed irreversible, but partial remission (PR) with temporary reversal of hyperglycemia is sometimes observed. Here we use single-cell RNA sequencing to delineate the immune cell landscape across patients in different T1D stages. Together with cohort validation and functional assays, we observe dynamic changes in TIGIT",
- "labels": [
- 1
- ]
- },
- {
- "text": "Computers in biology and medicine \n Riemannian manifold-based geometric clustering of continuous glucose monitoring to improve personalized diabetes management. \n This study demonstrates the utility of UMAP in enhancing the analysis of CGM data for diabetes management. We revealed distinct clustering of glycemic profiles between healthy individuals and diabetics on daily insulin indicating that in most instances insulin does not restore a normal glycemic phenotype. In addition, the SS quantifies day by day the degree of this continued dysglycemia and therefore potentially offers a novel approach for personalized diabetes care.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Diabetologia \n Quantitative analysis of islet prohormone convertase 1/3 expression in human pancreas donors with diabetes. \n Our high-resolution histomorphological analysis of human pancreatic islets from donors with and without diabetes has uncovered details of the cellular origin of islet prohormone peptide processing defects. Reduced beta cell PC1/3 and increased alpha cell PC1/3 in islets from donors with type 1 diabetes pinpointed the functional deterioration of beta cells and the concomitant potential increase in PC1/3 usage for prohormone processing in alpha cells during the pathogenesis of type 1 diabetes. Our finding of PC1/3 loss in beta cells may inform the discovery of new prohormone biomarkers as indicators of beta cell dysfunction, and the finding of elevated PC1/3 expression in alpha cells may encourage the design of therapeutic targets via leveraging alpha cell adaptation in diabetes.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Italian journal of pediatrics \n Promising predictors of diabetic peripheral neuropathy in children and adolescents with type 1 diabetes mellitus. \n Despite limited research in pediatrics, MNSI and serum NSE are promising predictive tools for DPN in children and adolescents with T1DM, even when they are asymptomatic. Poor glycemic control and lipid profile changes may play a critical role in the development of DPN in these patients, despite conflicting results in various studies.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Cell transplantation \n Xenogenic Engraftment of Human-Induced Pluripotent Stem Cell-Derived Pancreatic Islet Cells in an Immunosuppressive Diabetic G\u00f6ttingen Mini-Pig Model. \n In the development of cell therapy products, immunocompromised animal models closer in size to humans are valuable for enhancing the translatability of ",
- "labels": [
- 1
- ]
- },
- {
- "text": "Frontiers in immunology \n Enhancing human islet xenotransplant survival and function in diabetic immunocompetent mice through LRH-1/NR5A2 pharmacological activation. \n The intricate etiology of type 1 diabetes mellitus (T1D), characterized by harmful interactions between the immune system and insulin-producing beta cells, has hindered the development of effective therapies including human islet transplantation, which requires strong immunosuppressants that impair beta cell survival and function. As such alternative immunomodulating therapies are required for successful transplantation. The discovery that pharmacological activation of the nuclear receptor LRH-1/NR5A2 can reverse hyperglycemia in mouse models of T1D by altering, and not suppressing the autoimmune attack, prompted us to investigate whether LRH-1/NR5A2 activation could improve human islet function/survival after xenotransplantation in immunocompetent mice. Human islets were transplanted under the kidney capsule of streptozotocin (STZ)-induced diabetic mice, and treatment with BL001 (LRH-1/NR5A2 agonist) or vehicle was administered one week post-transplant. Our study, encompassing 3 independent experiments with 3 different islet donors, revealed that mice treated for 8 weeks with BL001 exhibited lower blood glucose levels correlating with improved mouse survival rates as compared to vehicle-treated controls. Human C-peptide was detectable in BL001-treated mice at both 4 and 8 weeks indicating functional islet beta cells. Accordingly, in mice treated with BL001 for 8 weeks, the beta cell mass was preserved, while a significant decrease in alpha cells was observed compared to mice treated with BL001 for only 4 weeks. In contrast, vehicle-treated mice exhibited a reduction in insulin-expressing cells at 8 weeks compared to those at 4 weeks. These results suggest that BL001 significantly enhances the survival, engraftment, and functionality of human islets in a STZ-induced diabetic mouse model.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Frontiers in endocrinology \n Exploring the influencing factors of non-insulin drug prescriptions in discharged patients with type 1 diabetes. \n We identified notable factors that influence discharge prescriptions in patients with T1D. In order to enhance the treatment outcome for the patient, clinicians ought to have a special focus on these indicators or factors.",
- "labels": [
- 1
- ]
- },
- {
- "text": "The Israel Medical Association journal : IMAJ \n Hospitalization Outcomes of Patients with Type 2 Diabetes Mellitus Complicated with Diabetic Ketoacidosis. \n Our findings underscore the importance of recognizing DKA as a substantial complication in diabetic patients, particularly those with T2DM. Vigilance in management, adherence to DKA guidelines, and awareness of triggers such as SGLT2 inhibitors are crucial for improving outcomes in this population.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences \n [Fulminant type 1 diabetes mellitus with acute pancreatitis: A case report and literature review]. \n The objective was to report a relatively rare case of fulminant type 1 diabetes (FT1DM) complicated with acute pancreatitis (AP), to summarize the characteristics as well as experience of diagnosis and treatment, and to explore its pathogenesis. Clinical data of a case of FT1DM complicated with AP in the Department of Endocrinology of our hospital were analyzed retrospectively. A 66-year-old male presented with acute fever and abdominal pain, accompanying with the significantly elevated pancreatic enzymes, and his abdominal CT scan showed exudation around the pancreas. The clinical manifestations mentioned above were consistent with the diagnosis of AP. Five days after onset, the patient developed clinical symptoms, such as obvious thirst, polyuria, polyasthenia and fatigue. Meanwhile, his plasma glucose increased significantly and the diabetic ketoacidosis (DKA) occurred. The patient's fasting and postprandial 2 hours C peptide decreased significantly (all 0.02 \u03bcg/L), glycated hemoglobin level was not high (6%), and his islet-related autoantibodies were undetectable. Thus, the patient could be diagnosed with FT1DM. After the treatment of fasting, fluid replacement, anti-infection, somatostatin, anticoagulation and intravenous insulin sequential subcutaneous insulin pump, the patient gained the alleviation of pancreatitis, restoration of oral intake, and relatively stable blood glucose levels. Summarizing the characte-ristics of this case and reviewing the literature, FT1DM complicated with AP was relatively rare in FT1DM. Its common characteristics were described below: (1) Most cases started with AP and the blood glucose elevated within 1 week, or some cases had the simultaneously onset of AP and FT1DM. (2) The clinical course of AP was short and relieved no more than 1 week; Pancreatic imaging could completely return to normal within 1 to 4 weeks after onset. (3) The etiology of AP most was idiopathic; The elevation of pancreatic enzyme level was slight and the recovery was rapidly compared with AP of other etiologies. FT1DM could be complicated with AP, which was different from the physiological manifestations of pancreatic disease in general FT1DM patients. Virus infection mignt be the common cause of AP and FT1DM, and AP might be the early clinical manifestation of some FT1DM. The FT1DM patients developed with abdominal pain was easy to be missed, misdiagnosed and delayed, which should receive more attention in clinic.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Experimental eye research \n Hyperglycemia-depleted glutamine contributes to the pathogenesis of diabetic corneal endothelial dysfunction. \n Diabetic mellitus (DM) causes various complications, including the corneal endothelial dysfunction that leads to corneal edema and vision loss, especially in the DM patients with intraocular surgeries. However, the pathogenic mechanism of hyperglycemia-caused corneal endothelial dysfunction remains incomplete understood. Here we firstly screened and identified the glutamine contents of aqueous humor (AH) were significantly reduced in the type 2 diabetic patients and type 1 and type 2 diabetic mice. To explore the potential therapeutic effects of glutamine (Gln) supplement on the protection of diabetic corneal endothelial dysfunction, we performed the anterior chamber perfusion with the addition of L-alanyl-L-glutamine (Ala-Gln), and confirmed that Ala-Gln supplement not only accelerated the resolution of corneal edema and recovery of corneal thickness, but also preserved the regular arrangement and barrier-pump function of cornea. Mechanistically, we revealed that the supplements of Ala-Gln protect corneal endothelial cells (CECs) from the deleterious effects of high glucose-induced oxidative stress, mitochondrial dysfunction, and cell apoptosis. Overall, these results indicate the Gln depletion plays an important role in the diabetic corneal endothelial dysfunction, while the Ala-Gln supplement during intraocular surgery provide an effective prevention strategy through regulating the redox homeostasis and mitochondrial function of corneal endothelium.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Immunity \n Autoimmune CD4 \n Self-reactive T\u00a0cells experience chronic antigen exposure but do not exhibit signs of exhaustion. Here, we investigated the mechanisms for sustained, functioning autoimmune CD4",
- "labels": [
- 1
- ]
- },
- {
- "text": "Brain research \n Ferroptosis-associated alterations in diabetes following ischemic stroke: Insights from RNA sequencing. \n Our bulk RNA sequencing and bioinformatics analyses show that altered ferroptosis signaling pathway was associated with the exacerbation of experimental stroke injury under diabetic condition. Especially, additional investigation into the mechanisms of SLC25A28 and SCP2 in diabetes-exacerbated stroke will be explored in the future study.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Contemporary clinical trials \n DiaBetter Together: Clinical trial protocol for a strengths-based Peer Mentor intervention for young adults with type 1 diabetes transitioning to adult care. \n The goal of this research is to evaluate a developmentally appropriate, supportive intervention that can improve T1D self-management and successful transfer of care during the difficult young adult years and promote optimal T1D health outcomes.",
- "labels": [
- 1
- ]
- },
- {
- "text": "Journal of medical Internet research \n Characterization of Telecare Conversations on Lifestyle Management and Their Relation to Health Care Utilization for Patients with Heart Failure: Mixed Methods Study. \n Our approach and findings offer novel perspectives on the content, structure, and clinical associations of telehealth conversations on lifestyle management for patients with HF. Hence, our study could inform ways to enhance telehealth programs for self-care management in chronic conditions.",
- "labels": [
- 2
- ]
- },
- {
- "text": "JAMA network open \n Cardiovascular Risks With SGLT2 Inhibitors in Clinical Practice Among Patients With Type 2 Diabetes. \n In this cohort study of patients with T2D, the use of SGLT2is vs DPP4is was associated with reduced total cardiovascular burden, suggesting that long-term use of this therapy may optimize treatment benefit among patients with chronic CVD. The SGLT2i-associated benefit among patients with high risk of CVD encourages the prioritization of SGLT2i use for these vulnerable individuals.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Arquivos brasileiros de cardiologia \n Causal Relationship between Television Viewing Time, Cardiovascular Diseases, and Potential Mechanisms. \n An overview of the effect of television viewing time on cardiovascular diseases and biomarkers of cardiometabolic risk.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of molecular endocrinology \n The role of mu-opioid receptors in pancreatic islet \u03b1-cells. \n Diabetes is a complex disease that impacts more than 500 million people across the world. Many of these individuals will develop diabetic neuropathy as a comorbidity, which is historically treated with exogenous opioids, such as morphine, oxycodone, or tramadol. Although these opioids are effective analgesics, growing evidence indicates that they may directly impact the endocrine pancreas function in patients. One common feature of these exogenous opioid ligands is their preference for the mu-opioid receptor (MOPR), so we aimed to determine whether endogenous MOPRs directly regulate pancreatic islet metabolism and hormone secretion. We show that pharmacological antagonism of MOPRs enhances glucagon secretion, but not insulin secretion, from human islets under high-glucose conditions. This increased secretion is accompanied by increased cAMP signaling. mRNA expression of MOPRs is robust in nondiabetic human islets but downregulated in islets from T2D donors, suggesting a link between metabolism and MOPR expression. Conditional genetic knockout of MOPRs in murine \u03b1-cells increases glucagon secretion under high-glucose conditions without increasing glucagon content. Consistent with downregulation of MOPRs during metabolic disease, conditional MOPR knockout mice treated with a high-fat diet show impaired glucose tolerance, increased glucagon secretion, increased insulin content, and increased islet size. Together, these results demonstrate a direct mechanism of action for endogenous opioid regulation of endocrine pancreas.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Endokrynologia Polska \n Identification of fibrosis-associated lncRNAs in diabetic cardiomyopathy patients. \n Our study disclosed a subset of lncRNAs and mRNAs that are implicated in diabetic cardiomyopathy and myocardial fibrosis, thereby presenting themselves as promising biomarkers and therapeutic targets for the management of both diabetic cardiomyopathy and myocardial fibrosis.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Endokrynologia Polska \n The correlation between S-nitrosylation and type 2 diabetes mellitus: a review. \n Type 2 diabetes mellitus (T2DM) represents a chronic metabolic disorder, constituting over 90% of all diabetes cases. Its primary characteristics include insulin deficiency and insulin resistance. The aetiology of T2DM is complex, which is attributed to a convergence of genetic and environmental factors. Moreover, it can engender various complications such as diabetes retinopathy, diabetes nephropathy, and diabetes neuropathy. T2DM cannot be cured fundamentally, it can only delay the development of the disease by controlling the blood sugar level. If the blood sugar is at a high level for a long time, it will aggravate the disease progress, and even lead to death in serious cases. Therefore, understanding the pathogenesis of diabetes, early detection, and intervention are the main means of treatment. S-nitrosylation (SNO), a post-translational modification of proteins based on redox, possesses the capacity to regulate a variety of physiological and pathological processes, and it is also involved in the occurrence and development of T2DM. However, the relationship between the dysregulation of SNO homeostasis and the occurrence of diabetes is not fully understood. This article reviews the correlation between SNO and T2DM, elucidating the mechanism by which SNO contributes to T2DM, encompassing diminishing insulin secretion, inducing insulin resistance, and affecting glucokinase activity. Understanding the correlation between SNO and T2DM provides a new research direction for the pathogenesis and treatment targets of diabetes.",
- "labels": [
- 2
- ]
- },
- {
- "text": "British journal of hospital medicine (London, England : 2005) \n Advances in Research on the Anticancer Properties and Mechanisms of Metformin in Lung Cancer. \n Lung cancer is a leading cause of death globally with high mortality and morbidity. Patients are often diagnosed at an advanced stage. Metformin has become a primary medication used in the clinical management of type 2 diabetes mellitus (T2DM) due to its relative safety, low cost, and effectiveness, mainly exerting its hypoglycemic effect by inhibiting hepatic gluconeogenesis and insulin resistance. Research data indicate that metformin extends the distant metastasis-free survival (DMFS) and progression-free survival (PFS) of diabetic patients with lung cancer, improving overall survival rates. Metformin lowers the risk of tumour development through various mechanisms, including the adenosine 5'-monophosphate-activated protein kinase/liver kinase B1/mechanistic target of rapamycin (AMPK/LKB1/mTOR) pathway, insulin-like growth factor-1 receptor pathway, apoptosis, and autophagy. However, research findings are not entirely consistent. This article reviews the research progress of metformin in terms of lung cancer treatment within the past few years, aiming to provide a more comprehensive understanding of how metformin exerts its anti-cancer impact and how it can be clinically applied, as well as provide new insights for lung cancer treatment.",
- "labels": [
- 2
- ]
- },
- {
- "text": "British journal of hospital medicine (London, England : 2005) \n Impact of Co-Management Mode on Diagnosis and Treatment Compliance in Community-Level Diabetic Patients with Retinopathy. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "The British journal of nutrition \n Perspective on the health effects of unsaturated fatty acids and commonly consumed plant oils high in unsaturated fat. \n Epidemiological and clinical trial evidence indicates that ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medical decision making : an international journal of the Society for Medical Decision Making \n Using QALYs as an Outcome for Assessing Global Prediction Accuracy in Diabetes Simulation Models. \n Diabetes simulation models are currently validated by examining their ability to predict the incidence of individual events (e.g., myocardial infarction, stroke, amputation) or composite events (e.g., first major adverse cardiovascular event).We introduce Q",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "Nederlands tijdschrift voor geneeskunde \n [Acute blindness in a patient with metformin-associated lactic acidosis]. \n Lactic acidosis is a rare metabolic complication that can occur in patients with diabetes mellitus type 2 who use metformin. We discuss a 79-year old woman with metformin-associated lactic acidosis (MALA) and acute kidney injury based on gastroenteritis. Patient reported acute blindness which in literature is described as a rare presentation of a metabolic acidosis (regardless of its underlying cause). Immediate treatment with hemodialysis led to improvement of the acidosis and complete recovery of the vision. It is important that patients who use metformin are instructed to consult their health care provider and/or discontinue metformin in case of intercurrent diseases.",
- "labels": [
- 2
- ]
- },
- {
- "text": "AIDS (London, England) \n Hepatic steatosis-insulin resistance and type 2 diabetes in people with HIV at diagnosis: effect of initial antiretroviral therapy. \n We evaluated the impact of hepatic steatosis-insulin resistance (HS-IR) and liver fibrosis (LF) on type 2 diabetes mellitus (DM2) using triglyceride-glucose (TyG) and Fibrosis-4 (FIB-4). The incidence of DM2 was 12.9 [95% confidence interval (CI), 16.9-9.7] and 9.8 (95% CI, 6.9-13.6) per 1000 person-years in HS-IR and LF. The prevalence of HS-IR was significantly lower at 12 and 24\u200amonths with TDF + (3TC or FTC) + RPV [hazard ratio (HR) 0.5 [95% CI, 0.3-0.8], P\u200a<\u200a0.01 at 12\u200amonths; 0.6 [0.4-0.9], P\u200a=\u200a0.01 at 24\u200amonths].",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Cost-utility analysis of once-weekly insulin icodec and once-daily insulin glargine in patients with type 2 diabetes receiving basal-bolus insulin therapy in China. \n The conclusion drawn from this study is that, with insulin glargine as the cost reference, the economic cost of insulin icodec for Chinese type 2 diabetes patients is expected to range from $784.90 to $1145.96, providing a reference basis for clinical decision-making and healthcare policy formulation.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of diabetes research \n Impact of Vitamin E Supplementation on High-Density Lipoprotein in Patients With Haptoglobin Genotype-Stratified Diabetes: A Systematic Review of Randomized Controlled Trials. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of diabetes research \n Adipocytokines and Inflammation in Patients and a Gerbil Model: Implications for Obesity-Related and Nonobese Diabetes. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetic medicine : a journal of the British Diabetic Association \n The effect of high-fibre diets on glycaemic control in women with diabetes in pregnancy: A systematic review and meta-analysis. \n High-quality dietary intervention studies in pregnancy are lacking. Our results suggest that high-fibre diets improve fasting and postprandial glycaemia and reduce the likelihood of requiring insulin in women with diabetes in pregnancy.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Gut microbes \n Exercise-changed gut mycobiome as a potential contributor to metabolic benefits in diabetes prevention: an integrative multi-omics study. \n Our findings suggest that intense exercise training significantly remodels the human fungal microbiome composition. Changes in gut fungal composition are associated with the metabolic benefits of exercise, indicating gut mycobiome is a possible molecular transducer of exercise. Moreover, baseline gut fungal signatures predict exercise responsiveness for diabetes prevention, highlighting that targeting the gut mycobiome emerges as a prospective strategy in tailoring personalized training for diabetes prevention.",
- "labels": [
- 2
- ]
- },
- {
- "text": "BMC endocrine disorders \n Association between the soluble receptor for advanced glycation end products and diabetes mellitus: systematic review and meta-analysis. \n CRD42024521252.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "BMC psychiatry \n Association of antipsychotic drugs on type 2 diabetes mellitus risk in patients with schizophrenia: a population-based cohort and in vitro glucose homeostasis-related gene expression study. \n This study demonstrates the impact of schizophrenia and APs and the risk of developing T2DM in Asian populations. Unmeasured confounding risk factors for T2DM may not have been included in the study. These findings may help psychiatric practitioners identify patients at risk of developing T2DM.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nature communications \n Identification of gut microbiome features associated with host metabolic health in a large population-based cohort. \n The complex relationship between the gut microbiome and host metabolic health has been an emerging research area. Several recent studies have highlighted the potential effects of the microbiome's diversity, composition and metabolic production capabilities on Body Mass Index (BMI), liver health, glucose homeostasis and Type-2 Diabetes (T2D). The majority of these studies were constrained by relatively small cohorts, mostly focusing on individuals with metabolic disorders, limiting a comprehensive understanding of the microbiome's role in metabolic health. Leveraging a large-scale, comprehensive cohort of nearly 9000 individuals, measured using Continuous Glucose Monitoring (CGM), Dual-energy X-ray absorptiometry (DXA) scan and liver Ultrasound (US) we examined the functional profile of the gut microbiome, and its relation to 38 metabolic health measures. We identified 145 unique bacterial pathways significantly correlated with metabolic health measures, with 86.9% of these showing significant associations with more than one metabolic health measure. Furthermore, 87,678 unique bacterial gene families were found to be significantly associated with at least one metabolic health measure. Notably, \"key\" bacterial pathways such as purine ribonucleosides degradation and anaerobic energy metabolism demonstrated multiple robust associations across various metabolic health measures, highlighting their potential roles in regulating metabolic processes. Our results remained largely unchanged after adjustments for nutritional habits and for BMI they were replicated in a geographically independent cohort. These insights pave the way for future research and potentially the development of microbiome-targeted interventions to enhance metabolic health.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nature communications \n Heterogeneous enhancer states orchestrate \u03b2 cell responses to metabolic stress. \n Obesity-induced \u03b2 cell dysfunction contributes to the onset of type 2 diabetes. Nevertheless, elucidating epigenetic mechanisms underlying islet dysfunction at single cell level remains challenging. Here we profile single-nuclei RNA along with enhancer marks H3K4me1 or H3K27ac in islets from lean or obese mice. Our study identifies distinct gene signatures and enhancer states correlating with \u03b2 cell dysfunction trajectory. Intriguingly, while many metabolic stress-induced genes exhibit concordant changes in both H3K4me1 and H3K27ac at their enhancers, expression changes of specific subsets are solely attributable to either H3K4me1 or H3K27ac dynamics. Remarkably, a subset of H3K4me1",
- "labels": [
- 2
- ]
- },
- {
- "text": "Clinica chimica acta; international journal of clinical chemistry \n HPLC-MS/MS method for simultaneous analysis of plasma 2-hydroxybutyrate and 2-hydroxyisobutyrate: Development and clinical significance. \n Recent studies have identified relationships between diabetes mellitus and short-chain fatty acids, including 2-hydroxybutyrate (2-HB) and 2-hydroxyisobutyrate (2-HiB); 2-HB has been associated to the early stages of insulin resistance, while 2-HiB with the risk and progression of complications of Type 1 diabetes. Their metabolism and pathophysiological role in humans are not fully clarified. The possible association between 2-HB and 2-HiB and diabetes mellitus was investigated with a novel mass spectrometry-based assay, capable of discriminating plasma 2-HiB and 2-HB from their HB isomers. Accuracy and precision (RSD%) were always in the range 99-102% and 0.7-3.5%, respectively. The study involved samples from subjects with normal glucose tolerance (NGT) and Type 2 diabetes (T2D), originally included in a multicenter study investigating mechanisms involved in atherothrombosis. NGT subjects exhibited concentrations of 2-HB and 2-HiB of 61 (36) and 3.1 (1.9) \u00b5mol/L, median (interquartile range), respectively, that were significantly lower than those of the T2D patients, whose values were 74 (4.0) and 3.8 (2.9) \u00b5mol/L, respectively. The pattern of association of these molecules with clinical and metabolic variables is partially different: both compounds were directly related to male sex, BMI, HbA",
- "labels": [
- 2
- ]
- },
- {
- "text": "The journal of nutrition, health & aging \n Spatiotemporal trends of Type 2 diabetes due to low physical activity from 1990 to 2019 and forecasted prevalence in 2050: A Global Burden of Disease Study 2019. \n LPA significantly impacts T2DM, particularly in low SDI regions. Promotion of physical activity is crucial to reduce this burden, particularly in regions where the disease's impact is most severe.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Geriatric nursing (New York, N.Y.) \n Impact of a motor-cognitive intervention on cognitive function in middle-aged and older patients with type 2 diabetes. \n This study evaluated the impact of a motor-cognitive intervention on cognitive function in patients with type 2 diabetes mellitus (T2DM). A single-group design with repeated measures was used, with twenty-six middle-aged and older patients with T2DM (aged 68.58 \u00b1 6.15 years) tested on two occasions four weeks apart to establish a baseline before participating in the exercise programme (55-60 min per session; 3 x week) for eight weeks. Participants were then tested again immediately after the training programme. Except for phonemic fluency error scores, the baseline data remained unchanged. After the training programme, statistical tests showed a significant improvement in some variables of executive function and attention demand, (p < 0.017, Bonferroni adjustment to compensate for multiple comparisons), as well as a positive effect on information processing speed, and dual-task performance. Combining physical and cognitive stimulation can have a positive impact on the cognitive functioning of participants with T2DM.",
- "labels": [
- 2
- ]
- },
- {
- "text": "International immunopharmacology \n Tirzepatide's role in targeting adipose tissue macrophages to reduce obesity-related inflammation and improve insulin resistance. \n Tirzepatide's potential as a therapeutic strategy for addressing metabolic diseases associated with obesity and T2DM by targeting ATM activity and mitigating obesity-associated inflammation.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of managed care & specialty pharmacy \n Social determinants of health and newer glucose-lowering drugs adoption among US Medicare beneficiaries with type 2 diabetes. \n We identified key contextual-level SDOH associated with real-world adoption of newer GLDs and explored their geographic variation through spatially explicit, data-driven analytical approaches. Identifying areas of strong association between SDOH and newer GLD initiation is crucial for policymakers to allocate resources and develop interventions that address structural inequities.",
- "labels": [
- 2
- ]
- },
- {
- "text": "ACS nano \n Engineering Supramolecular Nanofiber Depots from a Glucagon-Like Peptide-1 Therapeutic. \n Diabetes and obesity have emerged as major global health concerns. Glucagon-like peptide-1 (GLP-1), a natural incretin hormone, stimulates insulin production and suppresses glucagon secretion to stabilize and reduce blood glucose levels and control appetite. The therapeutic use of GLP-1 receptor agonists (e.g., semaglutide) has transformed the standard of care in recent years for treating type 2 diabetes and reversing obesity. The native GLP-1 sequence has a very short half-life, and therapeutic advances have come from molecular engineering to alter the pharmacokinetic profile of synthetic GLP-1 receptor agonists to enable once-weekly administration, reduce the frequency of injection, and improve adherence. Efforts to further extend this profile would offer additional convenience or enable entirely different treatment modalities. Here, an injectable GLP-1 receptor agonist depot is engineered through integration of a prosthetic self-assembling peptide motif to enable supramolecular nanofiber formation and hydrogelation. This supramolecular GLP-1 receptor agonistic (PA-GLP1) offers sustained release in vitro for multiple weeks, supporting long-lasting therapy. Moreover, in a rat model of type 2 diabetes, a single injection of the supramolecular PA-GLP1 formulation achieved sustained serum concentrations for at least 40 days, with an overall reduction in blood glucose levels and reduced weight gain, comparing favorably to daily injections of semaglutide. The general and modular approach is also extensible to other next-generation peptide therapies. Accordingly, the formation of supramolecular nanofiber depots offers a more convenient and long-lasting therapeutic option to manage diabetes and treat metabolic disorders.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Neuromolecular medicine \n Distinct Hippocampal Expression Profiles of lncRNAs in Obese Type 2 Diabetes Mice Exhibiting Cognitive Impairment. \n Cognitive dysfunction has been accepted as a possible complication of type 2 diabetes (T2D), but few studies revealed the potential roles of Long non\u2011coding RNAs (lncRNAs) in cognitive dysfunction in T2D. The current research aims to demonstrate the specific expression patterns of lncRNA-mRNA in the hippocampi of T2D db/db mice exhibiting cognitive impairment. In this study, the results from behavioral tests showed that T2D db/db mice displayed short-term and spatial working memory deficits compared to db/m mice. Furthermore, western blot analysis demonstrated that compared with db/m mice, p-GSK3\u03b2 (ser9) protein levels were markedly elevated in T2D db/db mice (P\u2009<\u20090.01). In addition, though not statistically significant, the ratio of p-Tau (Ser396) to Tau 46, \u03b1-Synuclein expression, and p-GSK3\u03b1 (ser21) expression were also relatively higher in T2D db/db mice than in db/m mice. The microarray profiling revealed that 75 lncRNAs and 26 mRNAs were dysregulated in T2D db/db mice (>\u20092.0 fold change, P\u2009<\u20090.05). GO analysis demonstrated that the differentially expressed mRNAs participated in immune response, extracellular membrane-bounded organelle, and extracellular region. KEGG analysis revealed that the differentially expressed mRNAs were mainly involved in one carbon pool by folate, glyoxylate and dicarboxylate metabolism, autophagy, glycine, serine and threonine metabolism, and B cell receptor signaling pathway. A lncRNA\u2011mRNA coexpression network containing 71 lncRNAs and 26 mRNAs was built to investigate the interaction between lncRNA and mRNA. Collectively, these results revealed the differential hippocampal expression profiles of lncRNAs in T2D mice with cognitive dysfunction, and the findings from this study provide new clues for exploring the potential roles of lncRNAs in the pathogenesis of cognitive dysfunction in T2D.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicine \n Metformin: Diverse molecular mechanisms, gastrointestinal effects and overcoming intolerance in type 2 Diabetes Mellitus: A review. \n Metformin, the first line treatment for patients with type 2 diabetes mellitus, has alternative novel roles, including cancer and diabetes prevention. This narrative review aims to explore its diverse mechanisms, effects and intolerance, using sources obtained by searching Scopus, PubMed and Web of Science databases, and following Scale for the Assessment of Narrative Review Articles reporting guidelines. Metformin exerts it actions through duration influenced, and organ specific, diverse mechanisms. Its use is associated with inhibition of hepatic gluconeogenesis targeted by mitochondria and lysosomes, reduction of cholesterol levels involving brown adipose tissue, weight reduction influenced by growth differentiation factor 15 and novel commensal bacteria, in addition to counteraction of meta-inflammation alongside immuno-modulation. Interactions with the gastrointestinal tract include alteration of gut microbiota, enhancement of glucose uptake and glucagon like peptide 1 and reduction of bile acid absorption. Though beneficial, they may be linked to intolerance. Metformin related gastrointestinal adverse effects are associated with dose escalation, immediate release formulations, gut microbiota alteration, epigenetic predisposition, inhibition of organic cation transporters in addition to interactions with serotonin, histamine and the enterohepatic circulation. Potentially effective measures to overcome intolerance encompasses carefully objective targeted dose escalation, prescription of fixed dose combination, microbiome modulators and prebiotics, in addition to use of extended release formulations.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Hepatology communications \n Clinical care guidance in patients with diabetes and metabolic dysfunction-associated steatotic liver disease: A joint consensus. \n Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide, affecting >30% of the global population. Metabolic dysregulation, particularly insulin resistance and its subsequent manifestation as type 2 diabetes mellitus, serves as the fundamental pathogenesis of metabolic liver disease. Clinical evidence of the recent nomenclature evolution is accumulating. The interaction and impacts are bidirectional between MASLD and diabetes in terms of disease course, risk, and prognosis. Therefore, there is an urgent need to highlight the multifaceted links between MASLD and diabetes for both hepatologists and diabetologists. The surveillance strategy, risk stratification of management, and current therapeutic achievements of metabolic liver disease remain the major pillars in a clinical care setting. Therefore, the Taiwan Association for the Study of the Liver (TASL), Taiwanese Association of Diabetes Educators, and Diabetes Association of the Republic of China (Taiwan) collaboratively completed the first guidance in patients with diabetes and MASLD, which provides practical recommendations for patient care.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of diabetes \n Association of systolic blood pressure variability with cognitive decline in type 2 diabetes: A post hoc analysis of a randomized clinical trial. \n A greater visit-to-visit systolic BPV was significantly associated with an increased risk of cognitive decline measured by DSST and an increase in white matter lesion volume in patients with type 2 diabetes.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of biochemical and molecular toxicology \n Sesamol Alleviated Lipotoxicity-Induced Dysfunction in MIN6 Cells via Facilitating Cellular Senescence Caused by Endoplasmic Reticulum Stress. \n Obesity is found to be a significant risk factor for type 2 diabetes mellitus (T2DM), attributed to lipotoxicity-induced \u03b2-cell dysfunction. However, the specific mechanism involved in the process remains incompletely unclarified. The current study demonstrated lipotoxicity resulted in the activation of ER stress, which increased the protein level of TXNIP, thereby inducing senescence-assiciated dysfunction in MIN6 cells under high fat environment. And we also found sesamol, a natural functional component extracted from sesame, was able to alleviate senescence-associated \u03b2-cell dysfunction induced by lipotoxicity by inhibiting ER stress and TXNIP. Our findings provided novel insights into senescence-related T2DM and propose innovative therapeutic approaches for utilizing sesamol in the treatment of T2DM in the obese elderly population.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Frontiers in endocrinology \n Tracing links between micronutrients and type 2 diabetes risk: the singular role of selenium. \n Our study presents novel evidence of a positive correlation between selenium intake and T2D risk, underscoring the importance of micronutrients in diabetes prevention and treatment strategies. Further research is necessary to confirm these findings and to clarify the specific biological mechanisms through which selenium influences diabetes risk.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Sheng li xue bao : [Acta physiologica Sinica] \n [Resistance exercise regulates hippocampal microglia polarization through TREM2/NF-\u03baB/STAT3 signal pathway to improve cognitive dysfunction in T2DM mice]. \n The study aimed to explore the effect and mechanism of resistance exercise (RE) on cognitive dysfunction in type 2 diabetes mellitus (T2DM) mice. Six 8-week-old male m/m mice were used as control (Con) group, and db/db mice of the matched age were randomly divided into model control (db/db) group and db+RE group, with 6 mice in each group. The db+RE group was given 8 weeks of resistance climbing ladder exercise intervention. The fasting blood glucose and body weight of the mice were measured weekly. After the intervention, the spatial learning and memory of the mice were detected by Morris water maze, and the neuronal damage in the hippocampus of the mice was detected by Nissl staining. The protein expression levels of PSD93, PSD95, BDNF, CREB, p-CREB, IL-6, IL-1\u03b2, TNF-\u03b1, Iba-1, iNOS, CD206, Arg1, triggering receptor expressed on myeloid cells 2 (TREM2), NF-\u03baB, p-STAT3, and STAT3 were detected by Western blot. The mRNA expression levels of inflammatory factors and TREM2 in hippocampus were evaluated by qRT-PCR, and the expression and localization of Iba-1, CD206, CD86, and TREM2 were determined by immunofluorescence staining. The results showed that the spatial learning and memory of the db/db group were significantly declined, the neurons in the hippocampus were damaged, the protein levels of PSD93, PSD95, BDNF, CD206, Arg1, TREM2 and the ratio of p-CREB/CREB were significantly down-regulated, the mRNA and protein expression levels of IL-6, IL-1\u03b2 and TNF-\u03b1 were significantly up-regulated, and the protein levels of iNOS, Iba-1, NF-\u03baB and the ratio of p-STAT3/STAT3 were significantly increased compared with the Con group. However, the 8-week RE improved the spatial learning and memory of db/db mice, alleviated the damage of hippocampal neurons, promoted the polarization of M2 microglia, and inhibited the neuroinflammation. The above results suggest that RE can improve cognitive dysfunction in T2DM mice, and its mechanism may be related to regulating microglia polarization via TREM2/NF-\u03baB/STAT3 signaling pathway.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Age and ageing \n Assessing 1-year sodium-glucose co-transporter-2 inhibitor tolerance in older adults. \n No clinically meaningful differences in SGLT2 inhibitor intolerance were observed in patients up to 84\u00a0years. Our findings support having closer follow-up when initiating in patients 85\u00a0years and older.",
- "labels": [
- 2
- ]
- },
- {
- "text": "BMC endocrine disorders \n Lipids as the link between central obesity and diabetes: perspectives from mediation analysis. \n In central obesity-related diabetes risk, most lipids, especially lipid ratio parameters, play a significant mediating role. Given these findings, we advocate for increased efforts in multifactorial risk monitoring and joint management of diabetes. The evaluation of lipids, particularly lipid ratio parameters, may be holds substantial value in the prevention and management of diabetes risk under close monitoring of central obesity.",
- "labels": [
- 0,
- 2
- ]
- },
- {
- "text": "Cardiovascular diabetology \n The effect of empagliflozin on circulating endothelial progenitor cells in patients with diabetes and stable coronary artery disease. \n Empagliflozin treatment in patients with DM and stable CAD increases cEPC levels and function, implying a cardioprotective mechanism. These findings highlight the potential of SGLT2i in treating cardiovascular diseases, warranting further research to explore these effects and their long-term implications.",
- "labels": [
- 2
- ]
- },
- {
- "text": "BMC endocrine disorders \n To analyse the correlation between UAER and eGFR and the risk factors for reducing eGFR in patients with type 2 diabetes. \n Peripheral vascular disease, systolic blood pressure, fatty liver, and beta-2-microglobulin are risk factors for decreased eGFR levels in patients with T2DM, which should be applied for control DKD. HDL and fasting CP have important effects on maintaining eGFR, and blood pressure and fasting CP can be used as new targets for subsequent diabetic kidney disease treatment.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Visit-to-visit HbA1c variability and risk of potentially avoidable hospitalisations in adults with type 2 diabetes receiving outpatient care at a tertiary hospital. \n In individuals receiving care at specialist outpatient clinics of a tertiary hospital, HbA1c variability is associated with a higher risk of PAH. Comprehensive diabetes management strategies addressing both glycaemic control and variability may offer benefits.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Effect of spironolactone wash-out on albuminuria after long-term treatment in individuals with type 2 diabetes and high risk of kidney disease-An observational follow-up of the PRIORITY study. \n UACR did not change after discontinuation of long-term treatment with spironolactone. However, an increase in eGFR was observed supporting a haemodynamic effect of spironolactone in the kidneys.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Scientific reports \n Cardiometabolic risk factor clusters in older adults using latent class analysis on the Bushehr elderly health program. \n Metabolic syndrome (MetS), comprising obesity, insulin resistance, hypertension, and dyslipidemia, increases the risk of type II diabetes mellitus and cardiovascular disease. This study aimed to identify the prevalence and determinants of specific clusters of the MetS components and tobacco consumption among older adults in Iran. The current study was conducted in the second stage of the Bushehr Elderly Health (BEH) program in southern Iran-a population-based cohort including 2424 subjects aged\u2009\u2265\u200960 years. Latent class analysis (LCA) was used to identify MetS and tobacco consumption patterns. Multinomial logistic regression was conducted to investigate factors associated with each MetS class, including sociodemographic and behavioral variables. Out of 2424 individuals, the overall percentage of people with one or more components of MetS or current tobacco use was 57.8% and 20.8%, respectively. The mean (SD) age of all participants was 69.3(6.4) years. LCA ascertained the presence of four latent classes: class 1 (\"low risk\"; with a prevalence of 35.3%), class 2 (\"MetS with medication-controlled diabetes\"; 11.1%), class 3 (\"high risk of MetS and associated medication use\"; 27.1%), and class 4 (\"central obesity and treated hypertension\"; 26.4%). Compared to participants with a body mass index (BMI)\u2009<\u200930, participants with BMI\u2009\u2265\u200930 were more likely to belong to class 3 (OR 1.91, 95% CI 1.31-2.79) and class 4 (OR 1.49, 95% CI 1.06-2.08). Polypharmacy was associated with membership in class 2 (OR 2.07, 95% CI 1.12-3.81), class 3 (OR 9.77, 95% CI 6.12-15.59), and class 4 (OR 1.76, 95% CI 1.07-2.91). The elevated triglyceride-glucose index was associated with membership in class 2 (OR 12.33, 95% CI 7.75-19.61) and class 3 (OR 12.04, 95% CI 8.31-17.45). Individuals with poor self-related health were more likely to belong to class 3 (OR 1.43; 95% CI 1.08-1.93). Four classes were identified among older adults in Iran with distinct patterns of cardiometabolic risk factors. Segmenting elderly individuals into these cardiometabolic categories has the potential to enhance the monitoring and management of cardiometabolic risk factors. This strategy may help reduce the severe outcomes of metabolic syndrome in this susceptible population.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nature communications \n Transcriptome-wide Mendelian randomization during CD4 \n Immunity has shown potentials in informing drug development for cardiometabolic diseases, such as type 2 diabetes (T2D) and coronary artery disease (CAD). Here, we performed a transcriptome-wide Mendelian randomization (MR) study to estimate the putative causal effects of 11,021 gene expression profiles during CD4",
- "labels": [
- 2
- ]
- },
- {
- "text": "Heart failure reviews \n Sodium-glucose cotransporter-2 inhibitors in acute myocardial infarction: a systematic review and meta-analysis of randomized controlled trials. \n We aimed to assess the efficacy and safety of sodium-glucose cotransporter-2 inhibitors (SGLT2i) versus placebo, initiated within the hospitalization period, in addition to habitual treatment, for treating adult patients with confirmed acute myocardial infarction (AMI). We also conducted subgroup analysis by diabetes mellitus (DM) status and type of AMI. We systematically searched PubMed, Embase, and Cochrane Library for randomized controlled trials (RCTs). The primary outcome was hospitalization for heart failure (HF). The secondary outcomes were all-cause death, cardiovascular death, and serious adverse events (AEs). We pooled risk ratios (RR) with a 95% confidence interval (CI) for binary outcomes. The between-study variance was assessed using tau",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetologia \n Autoimmune diseases and the risk and prognosis of latent autoimmune diabetes in adults. \n We confirm that several common ADs confer an excess risk of LADA, especially LADA with higher GADA levels, but having such a comorbidity does not appear to affect the risk of diabetic retinopathy.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Diabetologia \n Exposure to antibiotics and risk of latent autoimmune diabetes in adults and type 2 diabetes: results from a Swedish case-control study (ESTRID) and the Norwegian HUNT study. \n We found no evidence that exposure to broad-spectrum antibiotics up to 10 years prior to diagnosis increases the risk of LADA. There was some indication of increased LADA risk with exposure to narrow-spectrum antibiotics, which warrants further investigation.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "PloS one \n Associations of the TyG index with albuminuria and chronic kidney disease in patients with type 2 diabetes. \n The TyG index is positively associated with albuminuria and CKD in patients with T2DM and may be a marker for predicting the occurrence of early kidney injury in patients with T2DM. Clinicians should test this indicator early to detect lesions and improve patient prognosis.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Subphenotypes of adult-onset diabetes: Data-driven clustering in the population-based KORA cohort. \n T2D subphenotyping based on its sample's own clinical characteristics leads to stable categorization and adequately reflects T2D heterogeneity.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetes, obesity & metabolism \n Dietary potassium intake and its interaction with sodium intake on risk of developing cardiovascular disease in persons with type 2 diabetes: The Japan Diabetes Complication and its Prevention Prospective study (JDCP study 12). \n Low potassium intake in conjunction with high sodium intake was significantly associated with increased incident CVD in persons with T2DM. However, CVD incidence was not related to high potassium intake, regardless of sodium intake.",
- "labels": [
- 2
- ]
- },
- {
- "text": "The science of diabetes self-management and care \n Characteristics and Correlates of Health Information Literacy Among Patients With Type 2 Diabetes and Metabolic Syndrome: A Cross-Sectional Study. \n Overall, the health information literacy among Chinese patients with type 2 diabetes coexisting with metabolic syndrome is suboptimal. Study findings demonstrated that personal and social contextual resources factors are significantly related to health information literacy. Health care professionals should consider strategies to enhance people's health information literacy level and promote individuals' health problem-solving, enhance chronic illness resources, and improve self-management knowledge when developing tailored interventions.",
- "labels": [
- 2
- ]
- },
- {
- "text": "The science of diabetes self-management and care \n Exploring Type 2 Diabetes Self-Management Practices Among African Americans in Rural Counties: A Qualitative Study. \n The decision-making involved in glycemic level management emerges as a complex developmental process influenced by disease trajectory and cultural and environmental factors. These findings may inform a conceptual framework to guide future inquiries and provide insights for primary care clinicians and diabetes care and education specialists to better understand the complexities of T2D management among African American individuals in rural settings.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicine \n Effect of glucagon-like peptide-1 receptor agonists on prostate cancer: A review. \n Glucagon-like peptide-1 receptor agonist (GLP-1RA) is widely used in the treatment of type 2 diabetes mellitus (T2DM) for its significant hypoglycemic effect, weight loss and small side effects. Some studies have shown that GLP-1RA has an inhibitory effect on prostate cancer, and its application will produce adverse effects associated with an increased or decreased risk of some tumors. GLP-1R is widely expressed by various types of cells and tissues in the human body, so GLP-1RA has attracted wide clinical attention to the occurrence, development and prognosis of tumors, which brings more new directions and hopes for the treatment of prostate cancer. This paper describes the expression of glucagon-like peptide-1 receptor (GLP-1R) in prostate cancer and the effects of glucagon-like peptide-1 receptor agonist (GLP-1RA) on prostate cancer.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicine \n Association of metformin use with asthma development and adverse outcomes: A systematic review and meta-analysis. \n In most outcome indicators, it cannot be assumed that the use of metformin can reduce asthma-related adverse events. However, the conclusion is not so certain, and longer observation and more evidence are still required. Metformin still shows some potential in the intervention of respiratory diseases.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Epidemiology and psychiatric sciences \n Mediating pathways between attention deficit hyperactivity disorder and type 2 diabetes mellitus: evidence from a two-step and multivariable Mendelian randomization study. \n These findings suggest a potentially causal, positive relationship between ADHD liability and T2D, with mediation through higher BMI, more TV watching and lower EA. Intervention on these factors may thus have beneficial effects on T2D risk in individuals with ADHD.",
- "labels": [
- 2
- ]
- },
- {
- "text": "The British journal of nutrition \n Type 2 diabetes prevention: genetic association analysis of dried fruit intake and disease risk. \n Prior research has suggested an inverse correlation between dried fruit intake and type 2 diabetes mellitus (T2DM), yet the causal link remains uncertain. This study seeks to investigate the potential causal impact of dried fruit intake on T2DM, covering cases both with and without various complications, as well as glycaemic traits, using a two-sample Mendelian randomisation (MR) approach. Using MR analysis with genome-wide association study summary statistics, the primary analysis investigated the causal relationship between dried fruit intake and T2DM, both with and without complications, as well as glycaemic traits, employing the inverse variance weighted method. Supplementary analyses were conducted using MR-Egger and the weighted median method. Heterogeneity and intercept tests were utilised to evaluate the robustness of the study outcomes. The results show a significant association between dried fruit intake and T2DM without complications, as well as fasting insulin. Sensitivity analyses confirmed the robustness of the results and the independence from multicollinearity. However, no association was found between dried fruit intake and T2DM with various complications or other glycaemic traits. The significant association between dried fruit intake and T2DM without complications and fasting insulin persisted even after adjusting for BMI. This study offers genetic evidence endorsing the protective effects of dried fruit intake against T2DM, specifically for cases without complications, and in regulating fasting insulin. These findings suggest that dried fruit intake might serve as a primary preventive strategy for T2DM.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Trials \n Effectiveness of specialist involvement in case discussion conferences with primary healthcare providers on the management of type 2 diabetes patients: a study protocol for a cluster randomized controlled trial. \n Chinese Clinical Trial Registry ChiCTR2300078829. Registered on December 19, 2023. https://www.chictr.org.cn/showproj.html?proj=210293.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Alzheimer's research & therapy \n Molecular landscape of the overlap between Alzheimer's disease and somatic insulin-related diseases. \n Alzheimer's disease (AD) is a multifactorial disease with both genetic and environmental factors contributing to its etiology. Previous evidence has implicated disturbed insulin signaling as a key mechanism that plays a role in both neurodegenerative diseases such as AD and comorbid somatic diseases such as diabetes mellitus type 2 (DM2). In this study, we analysed available genome-wide association studies (GWASs) of AD and somatic insulin-related diseases and conditions (SID), i.e., DM2, metabolic syndrome and obesity, to identify genes associated with both AD and SID that could increase our insights into their molecular underpinnings. We then performed functional enrichment analyses of these genes. Subsequently, using (additional) GWAS data, we conducted shared genetic etiology analyses between AD and SID, on the one hand, and blood and cerebrospinal fluid (CSF) metabolite levels on the other hand. Further, integrating all these analysis results with elaborate literature searches, we built a molecular landscape of the overlap between AD and SID. From the landscape, multiple functional themes emerged, including insulin signaling, estrogen signaling, synaptic transmission, lipid metabolism and tau signaling. We also found shared genetic etiologies between AD/SID and the blood/CSF levels of multiple metabolites, pointing towards \"energy metabolism\" as a key metabolic pathway that is affected in both AD and SID. Lastly, the landscape provided leads for putative novel drug targets for AD (including MARK4, TMEM219, FKBP5, NDUFS3 and IL34) that could be further developed into new AD treatments.",
- "labels": [
- 2
- ]
- },
- {
- "text": "BMC gastroenterology \n Effect of diabetes mellitus type 2 and sulfonylurea on colorectal cancer development: a case-control study. \n This study found an insignificant association between type 2 diabetes and the chance of CRC development in an adjusted state. Sulfonylurea consumption was also associated with a higher chance of CRC development among patients with T2D. These findings have implications for clinical practice and public health strategies in CRC prevention for patients with T2D.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Swiss medical weekly \n Recommendations for early identification of heart failure in patients with diabetes: Consensus statement of the Swiss Society of Endocrinology and Diabetology and the Heart Failure Working Group of the Swiss Society of Cardiology. \n Diabetes is a well-recognised risk factor for the development of heart failure, with a prevalence higher than 30% in patients with diabetes aged over 60 years. Heart failure often emerges as the primary cardiovascular manifestation in patients with type 2 diabetes and appears to be even more prevalent in type 1 diabetes. In Switzerland, there are approximately 500,000 individuals with diabetes, and the number of affected people has been steadily rising in recent years. Therefore, the consequences of heart failure will affect an increasing number of patients, further straining the Swiss healthcare system. Early lifestyle modification and initiation of appropriate treatment can prevent or at least significantly delay the onset of symptomatic heart failure by several years. These facts underscore the urgent need for early detection of individuals with subclinical heart failure, which often remains undiagnosed until the first episode of acute heart failure requiring hospital admission occurs. To address this issue, the European Society of Cardiology, the American Diabetes Association (ADA) and other international professional societies have published recommendations on heart failure screening, diagnosis and management. To address this issue in Switzerland, experts from the Swiss Society of Endocrinology and Diabetology, the Swiss Society of Cardiology and the General Internal Medicine specialty met and prepared a consensus report including a simple diagnostic algorithm for use in everyday practice.",
- "labels": [
- 1,
- 2
- ]
- },
- {
- "text": "Scientific reports \n Dietary acid load adopts the effect of ApoB ins/del genetic variant (rs11279109) on obesity trait, cardiovascular markers, lipid profile, and serum leptin level among patients with diabetes: a cross-sectional study. \n ApoB insertion/deletion (ins/del) genetic variant (rs11279109) is thought to be related to cardio-metabolic markers and obesity. This association has the potential to be modified by dietary patterns. Since the majority of studies concerned the role of dietary acid load (DAL) or ApoB in type 2 diabetes mellitus\u00a0(T2DM) and its complications independently, and due to the insufficient data regarding the possible interactions between ApoB genetic variants and DAL on anthropometric and metabolic markers, we aimed to study the interaction between this genetic variant and dietary acid load (DAL) on cardio-metabolic markers, along with leptin among Iranian individuals with T2DM. 700 T2DM patients were randomly recruited. A validated semi-quantitative food frequency questionnaire was used for DAL calculation including potential renal acid load (PRAL) and net-endogenous acid production (NEAP). The polymerase chain reaction was used for genotyping the ApoB ins/del (rs11279109). The general linear model was applied to find the interactions in the crude and adjusted models. Patients with del/del genotype (rs11279109) with high PRAL intake have lower low-density lipoprotein cholesterol (LDL-C) (P",
- "labels": [
- 2
- ]
- },
- {
- "text": "PeerJ \n Association analysis of MTHFR (rs1801133 and rs1801131) gene polymorphism towards the development of type 2 diabetes mellitus in Dali area population from Yunnan Province, China. \n Our study suggests that the genetic variations of MTHFR C677T and A1298C are significantly associated with T2DM susceptibility in the population of the Dali area of Yunnan Province, China.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Romanian journal of ophthalmology \n Correlations between dyslipidemia and retinal parameters measured with Angio-OCT in type II diabetics without diabetic retinopathy. \n Type II diabetes patients tend to have elevated serum lipid levels compared to normal subjects, but the impact of dyslipidemia on the onset and progression of DR is incompletely elucidated.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of the Academy of Nutrition and Dietetics \n Randomized Controlled Feasibility Trial of Late 8-Hour Time-Restricted Eating for Adolescents With Type 2 Diabetes. \n Recruitment and retention rates suggest a trial of lTRE in adolescents with T2D was feasible. lTRE was seen as acceptable by participants and adherence was high. A revised intervention, building on the successful elements of this pilot alongside adapting implementations strategies to augment adherence and engagement, should therefore be considered.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Frontiers in endocrinology \n Risk of bone fracture by using dipeptidyl peptidase-4 inhibitors, glucagon-like peptide-1 receptor agonists, or sodium-glucose cotransporter-2 inhibitors in patients with type 2 diabetes mellitus: a network meta-analysis of population-based cohort studies. \n https://www.crd.york.ac.uk/prospero/, identifier CRD42023448720.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Acta medica Indonesiana \n Effectiveness and Safety of DLBS3233 in Newly Diagnosed Type 2 Diabetes Mellitus: A 12-week Clinical Trial. \n DLBS3233 showed potential for improving postprandial glucose control in newly diagnosed T2DM individuals. Although significant changes were limited, the study suggests that DLBS3233 could enhance glycemic regulation. The safety evaluation indicated no adverse effects on vital parameters. Further research with larger samples and more prolonged duration is warranted to comprehensively explore DLBS3233's potential in T2DM management.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of diabetes \n Stratum corneum hydration levels are negatively correlated with HbA1c levels in the elderly Chinese. \n Highlights Stratum corneum hydration levels are negatively correlated with HbA1c levels and positively correlated with skin surface pH. Individuals with type 2 diabetes display lower levels of stratum corneum hydration. Because low stratum corneum hydration levels can increase circulating levels of proinflammatory cytokines, which are linked to the pathogenesis of type 2 diabetes, improvement in stratum corneum hydration can be an alternative approach in the management of type 2 diabetes.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Clinical breast cancer \n Effective Strategies for the Prevention and Mitigation of Phosphatidylinositol-3-Kinase Inhibitor-Associated Hyperglycemia: Optimizing Patient Care. \n Hyperglycemia is a common adverse event (AE) associated with phosphatidylinositol-3-kinase inhibitors (PI3Kis) and considered an on-target effect. Presence of hyperglycemia is associated with poor outcomes in patients with cancer, and there is need for further refinement of hyperglycemia prevention and mitigation strategies in patients receiving PI3Kis. In this review, the authors highlight effective strategies for preventing PI3Ki-induced hyperglycemia before and during treatment as well as hyperglycemia management. Prior to initiating treatment with PI3Ki, identify baseline risk factors of patients at increased risk for developing hyperglycemia, which include older age, obesity, and glycosylated hemoglobin (HbA1c) 5.7%-6.4% (prediabetes or Type 2 diabetes). To prevent new-onset hyperglycemia, optimize blood glucose, and recommend a low-carbohydrate (60-130 g/day) diet along with regular exercise to all patients prior to initiating the PI3Ki. Prophylactic metformin may be considered in all patients starting a PI3Ki with HbA1c \u22646.4%. Although existing recommendations support monitoring fasting blood glucose (FBG) once weekly (twice-weekly for intermediate-risk, daily for high-risk patients) and HbA1c every 3 months upon initiation of PI3Ki, more frequent FBG monitoring may be considered for prompt detection of hyperglycemia. Experts also recommend considering postprandial glucose monitoring because it is an early indicator of glucose intolerance. If hyperglycemia develops, metformin (first-line) and/or sodium glucose co-transporter 2 inhibitors or thiazolidinediones (second-/third-line) are the preferred agents; consider early referral to an endocrinologist. In conclusion, hyperglycemia is a common but manageable AE associated with PI3Kis. Multidisciplinary approach to the prevention, monitoring, and management of hyperglycemia optimizes patient care and allows patients to maintain therapy on PI3Ki.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi \n [Functional study of amine oxidase copper-containing 1 (AOC1) in lipid metabolism]. \n Amine oxidase copper-containing 1 (AOC1) is a key member of copper amine oxidase family, which is responsible for deamination oxidation of histamine and putrescine. In recent years, AOC1 has been reported to be associated with various cancers, with its expression levels significantly elevated in certain cancer cells, suggesting its potential role in cancer progression. However, its function in lipid metabolism still remains unclear. Through genetic analysis, we have discovered a potential relationship between AOC1 and lipid metabolism. To further investigate, we generated ",
- "labels": [
- 2
- ]
- },
- {
- "text": "The journal of medical investigation : JMI \n Characteristics of storage and voiding symptoms in adult patients with type 2 diabetes with lower urinary tract symptoms. \n Our analysis of diabetic patients with LUTS revealed differences in the characteristics of storage and voiding symptoms. These findings provide evidence that the features of LUTS associated with diabetes may have different pathogenic origins. J. Med. Invest. 71 : 237-245, August, 2024.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Drug discoveries & therapeutics \n Effect of switching from dulaglutide to tirzepatide on blood glucose and renal function. \n The case reports a woman in her 70s, with type 2 diabetes and chronic kidney disease in G4 stage. The patient had elevated HbA1c, and she was switched from linagliptin, a dipeptidyl peptidase 4 inhibitor, to dulaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA). Thereafter, the HbA1c level decreased; however, since the dulaglutide supply became a problem, the patient was switched to tirzepatide, a glucose-dependent insulinotropic polypeptide (GIP)/GLP-1RA. To date, no clinical studies have evaluated the efficacy and safety of switching from GLP-1RA to GIP/GLP-1RA, but we report this case because efficacy was observed in this patient. The therapeutic effects after switching to tirzepatide included decrease in HbA1c, increase in eGFR, and decrease in BUN, when compared to when dulaglutide was used. A change from dulaglutide to tirzepatide, could inhibit renal impairment progression and improve renal function.",
- "labels": [
- 2
- ]
- },
- {
- "text": "BMC cardiovascular disorders \n Pattern and outcome of the first manifestation of cardiovascular disease among patients with type 2 diabetes mellitus in Cameroon: a cross-sectional study. \n Not applicable.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Scientific reports \n DII modulates the relationship between SVD3 and NAFLD prevalence, rather than liver fibrosis severity, in hospitalized T2DM population. \n Type 2 diabetes (T2DM) patients are at high risk for non-alcoholic fatty liver disease (NAFLD). Studies show SVD3 and dietary inflammatory index (DII) are associated with NAFLD. It's unknown if they interact in T2DM patients with NAFLD. We collected data from 110 hospitalized T2DM patients, measured physiological and biochemical indicators, conducted dietary surveys, and converted data into DII and NFS, FIB-4, and BARD indices. We used logistic regression, mediation effect analysis, and moderation effect analysis to explore the relationship between DII and SVD3 with NAFLD and liver fibrosis in T2DM patients. DII was not significant in either NAFLD incidence in T2DM patients or liver fibrosis in NAFLD patients. SVD3 was positively correlated with NAFLD incidence in T2DM patients, but this correlation became insignificant as DII increased towards pro-inflammation. SVD3 is positively correlated with NAFLD incidence in T2DM patients, but this correlation becomes less significant as DII increases towards pro-inflammation.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Scientific reports \n HbA1c and leukocyte mtDNA levels as major factors associated with post-COVID-19 syndrome in type 2 diabetes patients. \n Post-COVID-19 syndrome (PCS) is an emerging health problem in people recovering from COVID-19 infection within the past 3-6 months. The current study aimed to define the predictive factors of PCS development by assessing the mitochondrial DNA (mtDNA) levels in blood leukocytes, inflammatory markers and HbA1c in type 2 diabetes patients (T2D) with regard to clinical phenotype, gender, and biological age. In this case-control study, 65 T2D patients were selected. Patients were divided into 2 groups depending on PCS presence: the PCS group (n\u2009=\u200944) and patients who did not develop PCS (n\u2009=\u200921) for up to 6 months after COVID-19 infection. HbA1c and mtDNA levels were the primary factors linked to PCS in different models. We observed significantly lower mtDNA content in T2D patients with PCS compared to those without PCS (1.26\u2009\u00b1\u20090.25 vs. 1.44\u2009\u00b1\u20090.24; p\u2009=\u20090.011). In gender-specific and age-related analyses, the mt-DNA amount did not differ significantly between the subgroups. According to the stepwise multivariate logistic regression analysis, low mtDNA content and HbA1c were independent variables associated with PCS development, regardless of oxygen, glucocorticoid therapy and COVID-19 severity. The top-performing model for PCS prediction was the gradient boosting machine (GBM). HbA1c and mtDNA had a notably greater influence than the other variables, indicating their potential as prognostic biomarkers.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Scientific reports \n One-year outcomes of a digital twin intervention for type 2 diabetes: a retrospective real-world study. \n This retrospective observational study, building on prior research that demonstrated the efficacy of the Digital Twin (DT) Precision Treatment Program over shorter follow-up periods\u200b\u200b, aimed to examine glycemic control and reduced anti-diabetic medication use after one-year in a DT commercial program. T2D patients enrolled had adequate hepatic and renal function and no recent cardiovascular events. DT intervention powered by artificial intelligence utilizes precision nutrition, activity, sleep, and deep breathing exercises. Outcome measures included HbA1c change, medication reduction, anthropometrics, insulin markers, and continuous glucose monitoring (CGM) metrics. Of 1985 enrollees, 132 (6.6%) were lost to follow-up, leaving 1853 participants who completed one-year. At one-year, participants exhibited significant reductions in HbA1c [mean change: -1.8% (SD 1.7%), p\u2009<\u20090.001], with 1650 (89.0%) achieving HbA1c below 7%. At baseline, participants were on mean 1.9 (SD 1.4) anti-diabetic medications, which decreased to 0.5 (SD 0.7) at one-year [change: -1.5 (SD 1.3), p\u2009<\u20090.001]. Significant reductions in weight [mean change: -4.8\u00a0kg (SD 6.0\u00a0kg), p\u2009<\u20090.001], insulin resistance [HOMA2-IR: -0.1 (SD 1.2), p\u2009<\u20090.001], and improvements in \u03b2-cell function [HOMA2-B: +21.6 (SD 47.7), p\u2009<\u20090.001] were observed, along with better CGM metrics. These findings suggest that DT intervention could play a vital role in the future of T2D care.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Obesity surgery \n Eight Year Follow-Up After Gastric Bypass and Sleeve Gastrectomy in a Brazilian Cohort: Weight Trajectory and Health Outcomes. \n Patients undergoing RYGB showed greater weight loss and less weight regain 8\u00a0years after bariatric surgery compared to those undergoing SG.",
- "labels": [
- 2
- ]
- },
- {
- "text": "BMJ open \n Healthy Eating and Active Lifestyles for Diabetes (HEAL-D) Online: a mixed methods evaluation exploring the feasibility of implementing a virtual culturally tailored diabetes self-management programme for African and Caribbean communities. \n This evaluation demonstrates the feasibility of delivering HEAL-D using an online platform, with its ability to achieve similar goals compared with its face-to-face counterpart. Challenges were identified around the identification, recruitment and referral of eligible patients into the programme, which need to be addressed for successful implementation on a wider scale.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Neuroscience letters \n Neurometabolic substrate transport across brain barriers in diabetes mellitus: Implications for cognitive function and neurovascular health. \n Neurometabolic homeostasis in the brain depends on the coordinated transport of glucose and other essential substrates across brain barriers, primarily the blood-brain barrier and the blood-cerebrospinal fluid barrier. In type 2 diabetes mellitus (T2DM), persistent hyperglycemia disrupts these processes, leading to neurovascular dysfunction and cognitive impairment. This review examines how T2DM alters glucose and neurometabolite transport, emphasizing the role of glucose transporters and the astrocyte-neuron lactate shuttle in maintaining cerebral energy balance. Reduced expression of glucose transporters and impaired neurovascular coupling are key contributors to cognitive decline in T2DM. Additionally, the review highlights insulin's pivotal role in the hippocampus, where it enhances neuro-glial coupling and modulates astrocyte glucose uptake to support neuronal energy demands. Synthesizing current findings, we underscore the importance of therapeutic strategies aimed at correcting glucose transport dysregulation to alleviate diabetes-associated cognitive decline.",
- "labels": [
- 2
- ]
- },
- {
- "text": "The lancet. Diabetes & endocrinology \n Younger-onset compared with later-onset type 2 diabetes: an analysis of the UK Prospective Diabetes Study (UKPDS) with up to 30 years of follow-up (UKPDS 92). \n National Institute of Health and Care Research's Biomedical Research Centre.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of diabetes and its complications \n Effects of moderate-intensity aerobic training on cardiac structure and function in type 2 mellitus diabetic rats: Based on echocardiography and speckle tracking. \n LS-STE was a sensitive method to assess subclinical myocardial changes in T2DM rats. MIAT had the benefit of reversing cardiac systolic subclinical dysfunction in T2DM rats.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Diabetologia \n Intermittently scanned continuous glucose\u00a0monitoring compared with blood glucose monitoring is associated with lower HbA \n This study shows that Swedish adults with type 2 diabetes on insulin who are using isCGM have a significantly reduced HbA",
- "labels": [
- 2
- ]
- },
- {
- "text": "Journal of diabetes investigation \n Association between malnutrition and adverse renal outcomes in patients with type 2 diabetes. \n We observed an association between poor nutritional status, assessed by GNRI, and adverse outcomes in patients with type 2 diabetes. Nutritional status assessment has potential utility as a prognostic tool for individuals with type 2 diabetes.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Pharmacotherapy \n ECLIPSES: Early initiation of sodium glucose cotransporter-2 inhibitors for cardiovascular protection in patients with type 2 diabetes following acute coronary syndrome and subsequent coronary artery bypass graft surgery. \n Early initiation of SGLT2i use was not associated with a reduction in MACE in patients with T2DM who experienced ACS and underwent subsequent CABG surgery. However, no apparent safety concerns were identified. Adequately powered trials are required to confirm this finding.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicina (Kaunas, Lithuania) \n Age-Related Changes in Insulin Resistance and Muscle Mass: Clinical Implications in Obese Older Adults. \n The older segment of the global population is increasing at a rapid pace. Advancements in public health and modern medicine lengthened life expectancy and reduced the burden of disease in communities worldwide. Concurrent with this demographic change is the rise in overweight people and obesity, which is evident in all age groups. There is also an aging-related reduction in muscle mass and function, or sarcopenia, that is exacerbated by sedentary lifestyle and poor nutrition. The coexistence of muscle loss and elevated body mass index, termed \"sarcopenic obesity\", has particularly deleterious consequences in older individuals. Worsening insulin resistance and a proinflammatory state operate at the pathophysiologic level and lead to adverse health outcomes such as a proclivity to cardiovascular disease, type 2 diabetes, and even cognitive dysfunction. Although the concept of sarcopenic obesity as a disease construct is being increasingly recognized, a clearer understanding is warranted in order to define its components and health impact. Research is needed at the molecular-cellular level to tie together derangements in insulin action, cytokines, myokines, and endothelial dysfunction with clinical outcomes. Lifestyle modifications as well as targeted nonpharmacologic approaches, such as supplements and antioxidants, appear to have a promising role in reducing the chronic burden of this emerging disorder. Breakthroughs in drug therapies that retard or even reverse the underlying dynamics of sarcopenia and obesity in older persons are being actively explored.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicina (Kaunas, Lithuania) \n Scoring Health Behaviors of Patients with Type 2 Diabetes. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicina (Kaunas, Lithuania) \n Beyond Blood Sugar: Low Awareness of Kidney Disease among Type 2 Diabetes Mellitus Patients in Dalmatia-Insights from the First Open Public Call. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicina (Kaunas, Lithuania) \n Impact of the COVID-19 Pandemic on Lifestyle Behavior and Clinical Care Pathway Management in Type 2 Diabetes: A Retrospective Cross-Sectional Study. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Medicina (Kaunas, Lithuania) \n Cardiovascular Risk Factors as Independent Predictors of Diabetic Retinopathy in Type II Diabetes Mellitus: The Development of a Predictive Model. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Molecules (Basel, Switzerland) \n Identification of Novel PPAR\u03b3 Partial Agonists Based on Virtual Screening Strategy: In Silico and In Vitro Experimental Validation. \n Thiazolidinediones (TZDs) including rosiglitazone and pioglitazone function as peroxisome proliferator-activated receptor gamma (PPAR\u03b3) full agonists, which have been known as a class to be among the most effective drugs for the treatment of type 2 diabetes mellitus (T2DM). However, side effects of TZDs such as fluid retention and weight gain are associated with their full agonistic activities toward PPAR\u03b3 induced by the AF-2 helix-involved \"locked\" mechanism. Thereby, this study aimed to obtain novel PPAR\u03b3 partial agonists without direct interaction with the AF-2 helix. Through performing virtual screening of the Targetmol L6000 Natural Product Library and utilizing molecular dynamics (MD) simulation, as well as molecular mechanics Poisson-Boltzmann surface area (MM-PBSA) analysis, four compounds including tubuloside b, podophyllotoxone, endomorphin 1 and paliperidone were identified as potential PPAR\u03b3 partial agonists. An in vitro TR-FRET competitive binding assay showed podophyllotoxone displayed the optimal binding affinity toward PPAR\u03b3 among the screened compounds, exhibiting IC",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n Exploring the Interplay of Genetics and Nutrition in the Rising Epidemic of Obesity and Metabolic Diseases. \n ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n The Contribution of Postprandial Glucose Levels to Hyperglycemia in Type 2 Diabetes Calculated from Continuous Glucose Monitoring Data: Real World Evidence from the DIALECT-2 Cohort. \n Both PPG and FPG contribute to hyperglycemia, with PPG playing a larger role in patients with better glycemic control, especially after breakfast. Targeting PPG may be crucial for optimizing glucose management.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n Development of a Diabetes Dietary Quality Index: Reproducibility and Associations with Measures of Insulin Resistance, Beta Cell Function, and Hyperglycemia. \n We identified a questionnaire-derived Diabetes Dietary Quality index that was reproducible and inversely associated with a number of type 2 diabetes mellitus and metabolic risk factors, like 2 h post-meal glucose, Hba1c and LDL, and total cholesterol. Once relative validity has been established, the Diabetes Dietary Quality index could be used by health care professionals to identify individuals with diets adversely related to development of type 2 diabetes.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n Does Online Social Support Affect the Eating Behaviors of Polish Women with Insulin Resistance? \n Our study indicates a relationship between participation in online support groups and dietary behaviors and the subjective assessment of nutrition knowledge. Future research should focus on elucidating the mechanisms behind these influences and exploring how these communities can be optimized for broader public health initiatives.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n Microbiota Transplantation in Individuals with Type 2 Diabetes and a High Degree of Insulin Resistance. \n The objective of this study was to determine the results of fecal microbiota transplantation (FMT) from healthy lean subjects in patients with type 2 diabetes (T2D); Methods: We designed a phase II, randomized, single-blind, parallel-arm clinical trial. Twenty-one subjects (12 men [57.1%] and 9 women [42.9%]), who had previously signed an informed consent were randomized to FMT from lean donors, a probiotic (",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n Experiences of Postpartum Follow-Up and Participation in a Lifestyle Intervention after Gestational Diabetes: A Qualitative Study. \n The study findings can help support the development of future intervention programmes for women who have experienced gestational diabetes.",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n Harnessing Prebiotics to Improve Type 2 Diabetes Outcomes. \n The gut microbiota, a complex ecosystem of microorganisms in the human gastrointestinal tract (GI), plays a crucial role in maintaining metabolic health and influencing disease susceptibility. Dysbiosis, or an imbalance in gut microbiota, has been linked to the development of type 2 diabetes mellitus (T2DM) through mechanisms such as reduced glucose tolerance and increased insulin resistance. A balanced gut microbiota, or eubiosis, is associated with improved glucose metabolism and insulin sensitivity, potentially reducing the risk of diabetes-related complications. Various strategies, including the use of prebiotics like inulin, fructooligosaccharides, galactooligosaccharides, resistant starch, pectic oligosaccharides, polyphenols, \u03b2-glucan, and ",
- "labels": [
- 2
- ]
- },
- {
- "text": "Nutrients \n \n Overall, Akk appears to be effective at reducing the onset of type 2 diabetes and diet-induced obesity. Long-term studies with larger sample sizes are needed to confirm these beneficial effects, as the current animal studies were of short duration (less than 20 weeks).",
- "labels": [
- 2
- ]
- },
- {
- "text": "International journal of environmental research and public health \n Stakeholder Perspectives on the Acceptability, Design, and Integration of Produce Prescriptions for People with Type 2 Diabetes in Australia: A Formative Study. \n Produce prescription programs can benefit both individuals and health systems; however, best practices for integrating such programs into the Australian health system are yet unknown. This study explored stakeholders' perspectives on the acceptability, potential design and integration of produce prescription programs for adults with type 2 diabetes in Australia. Purposive sampling was used to recruit 22 participants for an online workshop, representing six stakeholder groups (government, healthcare service, clinician, food retailer, consumer, non-government organisation). Participant responses were gathered through workshop discussions and a virtual collaboration tool (Mural). The workshop was video-recorded and transcribed verbatim, and thematic analysis was conducted using a deductive-inductive approach. Stakeholders recognised produce prescription as an acceptable intervention; however, they identified challenges to implementation related to contextuality, accessibility, and sustainability. Stakeholders were vocal about the approach (e.g., community-led) and infrastructure (e.g., screening tools) needed to support program design and implementation but expressed diverse views about potential funding models, indicating a need for further investigation. Aligning evaluation outcomes with existing measures in local, State and Federal initiatives was recommended, and entry points for integration were identified within and outside of the Australian health sector. Our findings provide clear considerations for future produce prescription interventions for people with type 2 diabetes.",
- "labels": [
- 2
- ]
- },
- {
- "text": "International journal of environmental research and public health \n Impact of Oral Hygiene Practices in Reducing Cardiometabolic Risk, Incidence, and Mortality: A Systematic Review. \n Cardiometabolic diseases share many modifiable risk factors. However, periodontitis, a chronic inflammatory condition of the gums, is a risk factor that is rarely publicized. This systematic review aims to evaluate the impact of oral hygiene practices on the risk, incidence, and/or mortality rate of cardiovascular disease (CVD), type 2 diabetes mellitus (T2DM), and chronic kidney disease (CKD). Searches were conducted using MEDLINE, Embase, Scopus, and CINHAL. Randomized controlled trials (RCTs), quasi-RCTs, and observational studies were included. Eligible studies reported on associations of toothbrushing, interdental cleaning, mouthwash, or toothpaste use, either alone or in combination with CVD, CKD, and/or T2DM outcomes in adults \u2265 18 years. Fifty-five studies were included. Cochrane's risk of bias tool and the Newcastle-Ottawa Scale were used for quality assessment. Data synthesis is narratively presented. Toothbrushing and interdental cleaning were associated with lower risk of developing T2DM or hypertension HR 0.54 [",
- "labels": [
- 2
- ]
- },
- {
- "text": "International journal of environmental research and public health \n Diabetes Distress and Health-Related Quality of Life among Patients with Type 2 Diabetes-Mediating Role of Experiential Avoidance and Moderating Role of Post-Traumatic Growth. \n These findings underscore the importance of Acceptance and Commitment Therapy as it can potentially decrease the experiential avoidance behaviour of patients. Moreover, intervention should also target the facilitation of PTG due to its beneficial effects in reducing the negative effects of diabetes distress on health and recovery.",
- "labels": [
- 2
- ]
- },
- {
- "text": "International journal of molecular sciences \n Sexual Dimorphism in Impairment of Acetylcholine-Mediated Vasorelaxation in Zucker Diabetic Fatty (ZDF) Rat Aorta: A Monogenic Model of Obesity-Induced Type 2 Diabetes. \n Several reports, including our previous studies, indicate that hyperglycemia and diabetes mellitus exert differential effects on vascular function in males and females. This study examines sex differences in the vascular effects of type 2 diabetes (T2D) in an established monogenic model of obesity-induced T2D, Zucker Diabetic Fatty (ZDF) rats. Acetylcholine (ACh) responses were assessed in phenylephrine pre-contracted rings before and after apocynin, a NADPH oxidase (NOX) inhibitor. The mRNA expressions of aortic endothelial NOS (eNOS), and key NOX isoforms were also measured. We demonstrated the following: (1) diabetes had contrasting effects on aortic vasorelaxation in ZDF rats, impairing relaxation to ACh in females while enhancing it in male ZDF rats; (2) inhibition of NOX, a major source of superoxide in vasculature, restored aortic vasorelaxation in female ZDF rats; and (3) eNOS and NOX4 mRNA expressions were elevated in female (but not male) ZDF rat aortas compared to their respective leans. This study highlights sexual dimorphism in ACh-mediated vasorelaxation in the aorta of ZDF rats, suggesting that superoxide may play a role in the impaired vasorelaxation observed in female ZDF rats.",
- "labels": [
- 2
- ]
- },
- {
- "text": "International journal of molecular sciences \n Glucagon-like Peptide 1 Receptor Agonists in Cardio-Oncology: Pathophysiology of Cardiometabolic Outcomes in Cancer Patients. \n Cancer patients, especially long cancer survivors, are exposed to several cardio-metabolic diseases, including diabetes, heart failure, and atherosclerosis, which increase their risk of cardiovascular mortality. Therapy with glucagon-like peptide 1 (GLP1) receptor agonists demonstrated several beneficial cardiovascular effects, including atherosclerosis and heart failure prevention. Cardiovascular outcome trials (CVOTs) suggest that GLP-1 RA could exert cardiorenal benefits and systemic anti-inflammatory effects in patients with type-2 diabetes through the activation of cAMP and PI3K/AkT pathways and the inhibition of NLRP-3 and MyD88. In this narrative review, we highlight the biochemical properties of GLP-1 RA through a deep analysis of the clinical and preclinical evidence of the primary prevention of cardiomyopathies. The overall picture of this review encourages the study of GLP-1 RA in cancer patients with type-2 diabetes, as a potential primary prevention strategy against heart failure and atherosclerosis.",
- "labels": [
- 2
- ]
- },
- {
- "text": "International journal of molecular sciences \n Regulation of Mitochondrial and Peroxisomal Metabolism in Female Obesity and Type 2 Diabetes. \n Obesity and type 2 diabetes (T2D) are widespread metabolic disorders that significantly impact global health today, affecting approximately 17% of adults worldwide with obesity and 9.3% with T2D. Both conditions are closely linked to disruptions in lipid metabolism, where peroxisomes play a pivotal role. Mitochondria and peroxisomes are vital organelles responsible for lipid and energy regulation, including the \u03b2-oxidation and oxidation of very long-chain fatty acids (VLCFAs), cholesterol biosynthesis, and bile acid metabolism. These processes are significantly influenced by estrogens, highlighting the interplay between these organelles' function and hormonal regulation in the development and progression of metabolic diseases, such as obesity, metabolic dysfunction-associated fatty liver disease (MAFLD), and T2D. Estrogens modulate lipid metabolism through interactions with nuclear receptors, like peroxisome proliferator-activated receptors (PPARs), which are crucial for maintaining metabolic balance. Estrogen deficiency, such as in postmenopausal women, impairs PPAR regulation, leading to lipid accumulation and increased risk of metabolic disorders. The disruption of peroxisomal-mitochondrial function and estrogen regulation exacerbates lipid imbalances, contributing to insulin resistance and ROS accumulation. This review emphasizes the critical role of these organelles and estrogens in lipid metabolism and their implications for metabolic health, suggesting that therapeutic strategies, including hormone replacement therapy, may offer potential benefits in treating and preventing metabolic diseases.",
- "labels": [
- 2
- ]
- }
-]
\ No newline at end of file
diff --git a/model/gpt-test.py b/models/LLM/ChatGpt/gpt-test.py
similarity index 100%
rename from model/gpt-test.py
rename to models/LLM/ChatGpt/gpt-test.py
diff --git a/model/claude.py b/models/LLM/Claude/claude.py
similarity index 100%
rename from model/claude.py
rename to models/LLM/Claude/claude.py
diff --git a/model/cohereCommand.py b/models/LLM/Cohere/cohereCommand.py
similarity index 100%
rename from model/cohereCommand.py
rename to models/LLM/Cohere/cohereCommand.py
diff --git a/model/doc/cohere.md b/models/LLM/Cohere/doc/cohere.md
similarity index 100%
rename from model/doc/cohere.md
rename to models/LLM/Cohere/doc/cohere.md
diff --git a/model/doc/gemini.md b/models/LLM/Gemini/doc/gemini.md
similarity index 100%
rename from model/doc/gemini.md
rename to models/LLM/Gemini/doc/gemini.md
diff --git a/model/gemini.py b/models/LLM/Gemini/gemini.py
similarity index 100%
rename from model/gemini.py
rename to models/LLM/Gemini/gemini.py
diff --git a/model/llama.py b/models/LLM/Llama/llama.py
similarity index 100%
rename from model/llama.py
rename to models/LLM/Llama/llama.py
diff --git a/model/HuggingFace/HuggingFace.md b/models/ZeroShotClassifier/HuggingFace/doc/HuggingFace.md
similarity index 100%
rename from model/HuggingFace/HuggingFace.md
rename to models/ZeroShotClassifier/HuggingFace/doc/HuggingFace.md
diff --git a/model/doc/facebookBartLargeMnli.md b/models/ZeroShotClassifier/HuggingFace/doc/facebookBartLargeMnli.md
similarity index 100%
rename from model/doc/facebookBartLargeMnli.md
rename to models/ZeroShotClassifier/HuggingFace/doc/facebookBartLargeMnli.md
diff --git a/model/HuggingFace/zero_shot_classification.py b/models/ZeroShotClassifier/HuggingFace/zero_shot_classification.py
similarity index 100%
rename from model/HuggingFace/zero_shot_classification.py
rename to models/ZeroShotClassifier/HuggingFace/zero_shot_classification.py
diff --git a/model/doc/source.md b/models/ZeroShotClassifier/doc/source.md
similarity index 100%
rename from model/doc/source.md
rename to models/ZeroShotClassifier/doc/source.md
diff --git a/model/BiomedBERT.py b/old/BiomedBERT.py
similarity index 98%
rename from model/BiomedBERT.py
rename to old/BiomedBERT.py
index a47b9dcb74028332b6a6d20c2af3d0af6f0f7ec6..a65476a958d701e4c78edd2b4255534ef1e8865d 100644
--- a/model/BiomedBERT.py
+++ b/old/BiomedBERT.py
@@ -4,7 +4,7 @@ import os
# Ajouter le répertoire parent au chemin de recherche
sys.path.append(os.path.abspath(os.path.join(os.path.dirname(__file__), "../")))
-from api.pubmedApi import getPubmedData
+from dataSources.PubMed.pubmedApi import getPubmedData
from transformers import AutoTokenizer, AutoModelForSequenceClassification
import time
import json
diff --git a/api/model/img/GptClassificationResult.png b/old/GptClassificationResult.png
similarity index 100%
rename from api/model/img/GptClassificationResult.png
rename to old/GptClassificationResult.png
diff --git a/api/main.py b/old/main.py
similarity index 87%
rename from api/main.py
rename to old/main.py
index ab6f9a5d24660018a9e09b26085b348690dcaa6c..db2c53795a61caf9298aae212e5b7dbd0999c849 100644
--- a/api/main.py
+++ b/old/main.py
@@ -1,6 +1,6 @@
-from parser.jsonParser import parseJsonFile
-from parser.xlsxParser import parseXlsxFile
-from whoApi import getCountriesList
+from parsers.jsonParser import parseJsonFile
+from parsers.xlsxParser import parseXlsxFile
+from dataSources.WHO.whoApi import getCountriesList
if __name__ == "__main__":
print("\nKeywords:\n")
diff --git a/api/model/models.md b/old/models.md
similarity index 98%
rename from api/model/models.md
rename to old/models.md
index adcd11f1e78a978ee75e8213366ec4f7ad187cfb..afdeedc7fd205714f34607a81065473eb81ba8b2 100644
--- a/api/model/models.md
+++ b/old/models.md
@@ -23,4 +23,4 @@ Voici un texte : Cardiovascular events are frequent among individuals with predi
#### Résultat
-
\ No newline at end of file
+
\ No newline at end of file
diff --git a/api/model/tars.py b/old/tars.py
similarity index 100%
rename from api/model/tars.py
rename to old/tars.py
diff --git a/api/parser/jsonParser.py b/parsers/jsonParser.py
similarity index 100%
rename from api/parser/jsonParser.py
rename to parsers/jsonParser.py
diff --git a/api/parser/xlsxParser.py b/parsers/xlsxParser.py
similarity index 100%
rename from api/parser/xlsxParser.py
rename to parsers/xlsxParser.py
diff --git a/api/parser/xmlParser.py b/parsers/xmlParser.py
similarity index 100%
rename from api/parser/xmlParser.py
rename to parsers/xmlParser.py
diff --git a/rapport.md b/rapports/rapport.md
similarity index 100%
rename from rapport.md
rename to rapports/rapport.md
diff --git a/model/dataset/cancer.json b/testModel/dataset/cancer.json
similarity index 100%
rename from model/dataset/cancer.json
rename to testModel/dataset/cancer.json
diff --git a/model/dataset/cardiovascular_diseases.json b/testModel/dataset/cardiovascular_diseases.json
similarity index 100%
rename from model/dataset/cardiovascular_diseases.json
rename to testModel/dataset/cardiovascular_diseases.json
diff --git a/model/dataset/chronic_respiratory_disease.json b/testModel/dataset/chronic_respiratory_disease.json
similarity index 100%
rename from model/dataset/chronic_respiratory_disease.json
rename to testModel/dataset/chronic_respiratory_disease.json
diff --git a/model/create_test_data.py b/testModel/dataset/create_test_data.py
similarity index 96%
rename from model/create_test_data.py
rename to testModel/dataset/create_test_data.py
index 398ea24456a9030721477c4695b2582e66232a86..c618a35a221026f143e70e46554cb38d0612dbdd 100644
--- a/model/create_test_data.py
+++ b/testModel/dataset/create_test_data.py
@@ -6,7 +6,7 @@ import time
# Ajouter le répertoire parent au chemin de recherche
sys.path.append(os.path.abspath(os.path.join(os.path.dirname(__file__), "../")))
-from api.pubmedApi import getPubmedData
+from folders.dataSources.PubMed.pubmedApi import getPubmedData
LABELS = [
"Noncommunicable Diseases",
diff --git a/model/dataset/diabetes.json b/testModel/dataset/diabetes.json
similarity index 100%
rename from model/dataset/diabetes.json
rename to testModel/dataset/diabetes.json
diff --git a/model/dataset/diabetes_type_1.json b/testModel/dataset/diabetes_type_1.json
similarity index 100%
rename from model/dataset/diabetes_type_1.json
rename to testModel/dataset/diabetes_type_1.json
diff --git a/model/dataset/diabetes_type_2.json b/testModel/dataset/diabetes_type_2.json
similarity index 100%
rename from model/dataset/diabetes_type_2.json
rename to testModel/dataset/diabetes_type_2.json
diff --git a/model/dataset/mental_health.json b/testModel/dataset/mental_health.json
similarity index 100%
rename from model/dataset/mental_health.json
rename to testModel/dataset/mental_health.json
diff --git a/model/dataset/noncommunicable_diseases.json b/testModel/dataset/noncommunicable_diseases.json
similarity index 100%
rename from model/dataset/noncommunicable_diseases.json
rename to testModel/dataset/noncommunicable_diseases.json
diff --git a/docImg/smallTextPredictions.png b/testModel/doc/img/smallTextPredictions.png
similarity index 100%
rename from docImg/smallTextPredictions.png
rename to testModel/doc/img/smallTextPredictions.png
diff --git a/model/doc/small_text_test.md b/testModel/doc/small_text_test.md
similarity index 94%
rename from model/doc/small_text_test.md
rename to testModel/doc/small_text_test.md
index dfe16a827f3bf6a043533f3132d9b1a4158d3501..1e6d3c23f53341e6b2cc1c2ac7972afefb34b5f7 100644
--- a/model/doc/small_text_test.md
+++ b/testModel/doc/small_text_test.md
@@ -15,6 +15,6 @@ For an entrie that have:
- Results: 'Diabetes type 2' -> 0.7203449606895447 (~ 72%)
Results for the 5 entries:
-
+
I saw that the lenght of the text didn't really have an impact on the acuracy of the prediction.
\ No newline at end of file
diff --git a/model/multi_label_test.py b/testModel/multi_label_test.py
similarity index 96%
rename from model/multi_label_test.py
rename to testModel/multi_label_test.py
index 525799826f4c4001244e6af91d53edae23aeb9ba..1660e9c5cc1e921a9a705c59aa44ef25f22e337e 100644
--- a/model/multi_label_test.py
+++ b/testModel/multi_label_test.py
@@ -4,7 +4,7 @@ import os
# Ajouter le répertoire parent au chemin de recherche
sys.path.append(os.path.abspath(os.path.join(os.path.dirname(__file__), "../")))
-from model.HuggingFace.zero_shot_classification import create_classifier, classify
+from models.ZeroShotClassifier.HuggingFace.zero_shot_classification import create_classifier, classify
labels = [
"Diabetes",
diff --git a/model/results/cohere/v1.txt b/testModel/results/cohere/v1.txt
similarity index 100%
rename from model/results/cohere/v1.txt
rename to testModel/results/cohere/v1.txt
diff --git a/model/results/gemini/v1.txt b/testModel/results/gemini/v1.txt
similarity index 100%
rename from model/results/gemini/v1.txt
rename to testModel/results/gemini/v1.txt
diff --git a/model/results/gemini/v2.txt b/testModel/results/gemini/v2.txt
similarity index 100%
rename from model/results/gemini/v2.txt
rename to testModel/results/gemini/v2.txt
diff --git a/model/results/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/v1/facebook-bart_large_mnli.txt b/testModel/results/v1/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/v1/facebook-bart_large_mnli.txt
rename to testModel/results/v1/facebook-bart_large_mnli.txt
diff --git a/model/results/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/results/v2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/v2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/v2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/v2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/v2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/v2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/v2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/v2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/v2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/v2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/v2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/v2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/v2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/v2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/v2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/v2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/v2/facebook-bart_large_mnli.txt b/testModel/results/v2/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/v2/facebook-bart_large_mnli.txt
rename to testModel/results/v2/facebook-bart_large_mnli.txt
diff --git a/model/results/v2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/v2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/v2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/v2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/results/v3/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/v3/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/v3/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/v3/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/v3/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/v3/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/v3/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/v3/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/v3/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/v3/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/v3/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/v3/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/v3/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/v3/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/v3/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/v3/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/v3/facebook-bart_large_mnli.txt b/testModel/results/v3/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/v3/facebook-bart_large_mnli.txt
rename to testModel/results/v3/facebook-bart_large_mnli.txt
diff --git a/model/results/v3/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/v3/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/v3/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/v3/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/results/v4/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/v4/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/v4/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/v4/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/v4/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/v4/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/v4/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/v4/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/v4/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/v4/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/v4/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/v4/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/v4/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/v4/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/v4/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/v4/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/v4/facebook-bart_large_mnli.txt b/testModel/results/v4/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/v4/facebook-bart_large_mnli.txt
rename to testModel/results/v4/facebook-bart_large_mnli.txt
diff --git a/model/results/v4/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/v4/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/v4/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/v4/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/results/v5_1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/v5_1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/v5_1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/v5_1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/v5_1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/v5_1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/v5_1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/v5_1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/v5_1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/v5_1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/v5_1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/v5_1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/v5_1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/v5_1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/v5_1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/v5_1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/v5_1/facebook-bart_large_mnli.txt b/testModel/results/v5_1/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/v5_1/facebook-bart_large_mnli.txt
rename to testModel/results/v5_1/facebook-bart_large_mnli.txt
diff --git a/model/results/v5_1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/v5_1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/v5_1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/v5_1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/results/v5_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/v5_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/v5_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/v5_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/v5_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/v5_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/v5_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/v5_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/v5_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/v5_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/v5_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/v5_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/v5_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/v5_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/v5_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/v5_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/v5_2/facebook-bart_large_mnli.txt b/testModel/results/v5_2/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/v5_2/facebook-bart_large_mnli.txt
rename to testModel/results/v5_2/facebook-bart_large_mnli.txt
diff --git a/model/results/v5_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/v5_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/v5_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/v5_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/results/v6_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/v6_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/v6_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/v6_2/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/v6_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/v6_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/v6_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/v6_2/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/v6_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/v6_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/v6_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/v6_2/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/v6_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/v6_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/v6_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/v6_2/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/v6_2/facebook-bart_large_mnli.txt b/testModel/results/v6_2/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/v6_2/facebook-bart_large_mnli.txt
rename to testModel/results/v6_2/facebook-bart_large_mnli.txt
diff --git a/model/results/v6_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/v6_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/v6_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/v6_2/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/results/zero_shot/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt b/testModel/results/zero_shot/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
similarity index 100%
rename from model/results/zero_shot/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
rename to testModel/results/zero_shot/v1/MoritzLaurer-DeBERTa_v3_base_mnli_fever_anli.txt
diff --git a/model/results/zero_shot/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt b/testModel/results/zero_shot/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
similarity index 100%
rename from model/results/zero_shot/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
rename to testModel/results/zero_shot/v1/MoritzLaurer-bge_m3_zeroshot_v2_0.txt
diff --git a/model/results/zero_shot/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt b/testModel/results/zero_shot/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
similarity index 100%
rename from model/results/zero_shot/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
rename to testModel/results/zero_shot/v1/MoritzLaurer-deberta_v3_base_zeroshot_v1_1_all_33.txt
diff --git a/model/results/zero_shot/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt b/testModel/results/zero_shot/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
similarity index 100%
rename from model/results/zero_shot/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
rename to testModel/results/zero_shot/v1/MoritzLaurer-multilingual_MiniLMv2_L6_mnli_xnli.txt
diff --git a/model/results/zero_shot/v1/facebook-bart_large_mnli.txt b/testModel/results/zero_shot/v1/facebook-bart_large_mnli.txt
similarity index 100%
rename from model/results/zero_shot/v1/facebook-bart_large_mnli.txt
rename to testModel/results/zero_shot/v1/facebook-bart_large_mnli.txt
diff --git a/model/results/zero_shot/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt b/testModel/results/zero_shot/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
similarity index 100%
rename from model/results/zero_shot/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
rename to testModel/results/zero_shot/v1/microsoft-BiomedNLP_BiomedBERT_base_uncased_abstract.txt
diff --git a/model/smallTextTest.py b/testModel/smallTextTest.py
similarity index 100%
rename from model/smallTextTest.py
rename to testModel/smallTextTest.py
diff --git a/model/test_cohere.py b/testModel/test_cohere.py
similarity index 97%
rename from model/test_cohere.py
rename to testModel/test_cohere.py
index 66cc9cb566666ca97b62f93d9599b672a350e837..8b9024518ec34407095836516d10383bdfabb7eb 100644
--- a/model/test_cohere.py
+++ b/testModel/test_cohere.py
@@ -4,10 +4,10 @@ import os
# Ajouter le répertoire parent au chemin de recherche
sys.path.append(os.path.abspath(os.path.join(os.path.dirname(__file__), "../")))
-from api.parser.jsonParser import parseJsonFile
+from parsers.jsonParser import parseJsonFile
import time
-from model.cohereCommand import cohere_classify
+from models.LLM.Cohere.cohereCommand import cohere_classify
LABELS = [
"Noncommunicable Diseases",
diff --git a/model/test_gemini.py b/testModel/test_gemini.py
similarity index 97%
rename from model/test_gemini.py
rename to testModel/test_gemini.py
index 4964469aa5f7113f5b05b409f8711b69a9b90708..5cd68459e06c26a72a0de129406301200308006a 100644
--- a/model/test_gemini.py
+++ b/testModel/test_gemini.py
@@ -4,10 +4,10 @@ import os
# Ajouter le répertoire parent au chemin de recherche
sys.path.append(os.path.abspath(os.path.join(os.path.dirname(__file__), "../")))
-from api.parser.jsonParser import parseJsonFile
+from parsers.jsonParser import parseJsonFile
import time
-from model.gemini import gemini_classify, gemini_start_chat
+from models.LLM.Gemini.gemini import gemini_classify, gemini_start_chat
LABELS = [
"Noncommunicable Diseases",
diff --git a/model/test_model.py b/testModel/test_model.py
similarity index 97%
rename from model/test_model.py
rename to testModel/test_model.py
index ce084a8f0a775b93b5911c598f0912bccdf96c2e..183f9f202e9813131ee5825eecf6f20e7e07d8ae 100644
--- a/model/test_model.py
+++ b/testModel/test_model.py
@@ -4,11 +4,11 @@ import os
# Ajouter le répertoire parent au chemin de recherche
sys.path.append(os.path.abspath(os.path.join(os.path.dirname(__file__), "../")))
-from api.parser.jsonParser import parseJsonFile
+from parsers.jsonParser import parseJsonFile
import time
import statistics
-from model.HuggingFace.zero_shot_classification import create_classifier, classify, MODELS
+from models.ZeroShotClassifier.HuggingFace.zero_shot_classification import create_classifier, classify, MODELS
TRESHOLD = 0.7