Diabetes最新文献

{"title":"Comparative Analysis of the Sensitivity, Specificity, Concordance, and 5-Year Predictive Power of Diabetes-Related Autoantibody Assays.","authors":"Jeffrey P Krischer, Sarah Muller, Lu You, Peter Achenbach, Elena Bazzigaluppi, Cristina Brigatti, Vito Lampasona, Anu Mathew, Peter Robinson, David Seftel, George Sigal, Cheng-Ting Tsai, Mingyue Wang, Liping Yu","doi":"10.2337/db24-0814","DOIUrl":"10.2337/db24-0814","url":null,"abstract":"<p><strong>Article highlights: </strong>Interassay concordance and 5-year diabetes prediction of islet cell autoantibody detection using the radiobinding assay (TrialNet), two independently developed multiplex electrochemiluminescence detection methods, the luciferase immune precipitation system, detection by agglutination-PCR, and truncated GADA, and IA2βA radiobinding assays are reported. There was considerable discordance that varied by type of autoantibody across the assays. Type 1 diabetes prediction was relatively high and uniform, implying confirmation of increased diabetes risk among those who are multiple autoantibody positive, although substantial false positive rates need to be considered when autoantibodies alone are used for screening to identify high diabetes risk.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"1535-1546"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Type 1 Diabetes Autoantibodies in Acute, Recurrent Acute, and Chronic Pancreatitis.","authors":"Clive H Wasserfall, Chris E Forsmark, Shuang Li, Liang Li, Phil A Hart, Mark O Goodarzi, Yogish C Kudva, Melena D Bellin, Dhiraj Yadav, Darwin L Conwell, Jose Serrano, Dana K Andersen, William Fisher, Anna Casu, Ken Cusi, Steven J Hughes, Evan Fogel, Walter Park, Stephen K Van Den Eeden","doi":"10.2337/db24-0931","DOIUrl":"10.2337/db24-0931","url":null,"abstract":"<p><strong>Article highlights: </strong>Type 1 diabetes-associated autoimmune mechanisms have not been thoroughly examined in pancreatitis-associated diabetes. We assessed the prevalence of four islet autoantibodies in serum from a large prospective cohort of patients with acute, recurrent acute, or chronic pancreatitis. Diabetes was present in 11 (12%) of 94 participants with acute pancreatitis, 69 (27%) of 273 with recurrent acute pancreatitis, and 235 (43%) of 560 with chronic pancreatitis. Excluding those with only insulin autoantibody positivity, which is confounded by insulin treatment, islet autoantibodies were identified in 51 (5.5%) of 927 participants, and 30 (3.2%) of 297 were positive for two or more autoantibodies. Our findings suggest pancreatitis may elicit islet autoimmunity in a subset of patients, necessitating prospective longitudinal follow-up.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"1603-1612"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes Genetic Clusters and Clinical Outcomes in American Indians.","authors":"Kaylia M Reynolds, Quan Sun, Ying Zhang, Jason Umans, Shelley A Cole, Andrew P Morris, Nora Franceschini","doi":"10.2337/db25-0322","DOIUrl":"10.2337/db25-0322","url":null,"abstract":"<p><p>Diabetes has a large medical and public health impact in American Indians. Studies have used genetic data to distinguish type 1 diabetes (T1D) and type 2 diabetes (T2D) and uncover biologic mechanisms underlying T2D clinical heterogeneity. We applied a T1D polygenic score (PS) to 3,084 American Indians (mean age 56 years, 58% women, 39% diabetes). We also calculated partitioned PS for eight clusters of T2D-associated variants and evaluated their association with 20 cardiometabolic traits and five clinical outcomes. The profile of T1D PS for individuals with diabetes was consistent with T2D. A total T2D PS was significantly associated with early age of T2D onset (P = 3.5 × 10-11). Partitioned PS for T2D clusters were significantly associated with cardiometabolic traits for the obesity cluster (increased measures of body fat and total triglycerides but lower HDL cholesterol), while the lipodystrophy cluster was associated with increased fasting insulin, waist-to-hip ratio, triglycerides, and blood pressure, and lower body fat percentage and HDL cholesterol. T2D clusters were not associated with cardiovascular and kidney outcomes. Our findings support a relationship of cluster-specific T2D partitioned PS with cardiometabolic traits described in other populations, but there are opportunities for developing improved clustering methods using genetic variation from American Indians.</p><p><strong>Article highlights: </strong>Diabetes is highly prevalent in American Indians and a main cause of morbidity and mortality, and its clinical heterogeneity can be uncovered using genetic data. We are interested in identifying type 1 versus type 2 diabetes in American Indians with diabetes and identifying biological mechanisms for type 2 diabetes that are related to clinical outcomes using genetic data. Using genetic data, we found a high probability of participants having type 2 diabetes. We identified similar associations of type 2 diabetes genetic clusters, that are related to biological mechanisms, with cardiometabolic traits as previously described in other populations, but no associations of genetic clusters with cardiovascular and kidney outcomes. Our findings support type 2 diabetes as the main cause of diabetes in our American Indian cohort and provide insights into improvements using genetic data to uncover type 2 biological mechanisms.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Dual Stable Isotope Study of the Effect of Altitude and Simulated Flight on Glucose Metabolism in Type 1 Diabetes: A Randomized Crossover Study.","authors":"Ka Siu Fan, Fariba Shojaee-Moradie, Fereshteh Jeivad, Antonios Manoli, Ahmad Haidar, Monique Borg Inguanez, Fiona Sammut, Gerd Koehler, Victoria Edwards, Vivienne Lee, Agnieszka Falinska, Zosanglura Bawlchhim, Julia K Mader, A Margot Umpleby, David Russell-Jones","doi":"10.2337/db25-0004","DOIUrl":"10.2337/db25-0004","url":null,"abstract":"<p><p>The impact of atmospheric pressure changes on glucose metabolism encountered in aviation on people with type 1 diabetes is controversial. A dual-isotope study was performed in a hypobaric chamber to simulate pressure changes experienced on commercial flights. The fasting and postprandial glucose kinetics of individuals with type 1 diabetes were evaluated across simulated in-flight cabin pressures (550 mmHg; experimental arm) and ground level (750 mmHg; control arm). The impact of ambient pressure on glucose disposal (Rd), endogenous glucose production (EGP), meal glucose appearance (Ra), and insulin concentrations were evaluated. Six male participants, aged 20-61 years, with a median BMI of 26.6 kg/m2, were studied. Baseline glucose Rd, EGP, and meal Ra values were not affected by ambient pressure changes. Postprandial glucose Rd was higher in hypobaric conditions than ground, the percent change in postprandial glucose concentration was lower, but postprandial EGP and meal Ra were not affected. Insulin concentration between 120 and 180 min was higher in the hypobaric simulation. The observed increase in glucose Rd for individuals with type 1 diabetes who were using insulin pumps may be related to the hypoxia and pressure changes experienced during flight. Because glucose profiles were unaffected, there is no evidence that insulin pump therapy is a risk factor in flight.</p><p><strong>Article highlights: </strong>The effects of acute atmospheric pressure changes on glucose metabolism in type 1 diabetes remain controversial and may have safety implications for pilots and travelers alike. What are the differences in glucose kinetics and hormones between ground and simulated flight environments? Glucose disposal and insulin concentration are increased in response to a meal during flight, without associated changes in endogenous glucose production or meal glucose appearance rates. Pressure-related changes in insulin pump performance and hypoxia may explain these findings. Because glucose concentrations were unaffected, there is no evidence that insulin pump therapy is a risk factor in flight.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"1367-1373"},"PeriodicalIF":0.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Insulin-Positive Cell Clusters Precedes the Decrease in Islet Frequency and β-Cell Area in Type 1 Diabetes.","authors":"Denise M Drotar, Giovanni J A Vazquez Ramos, MacKenzie D Williams, Surya T David, Caitlyn Luce, Justin A Smith, Amanda L Posgai, Rhonda Bacher, Martha Campbell-Thompson, Irina Kusmartseva, Maigan A Brusko, Mark A Atkinson, Clive H Wasserfall","doi":"10.2337/db25-0326","DOIUrl":"https://doi.org/10.2337/db25-0326","url":null,"abstract":"<p><p>In type 1 diabetes (T1D), insulin (INS) deficiency results from immune-mediated destruction of β-cells. The majority of functional β-cell mass is typically lost within months to years of disease diagnosis, but the timing and nature of this loss, particularly in early disease stages, remain unclear. We developed a whole-slide scanned image analysis pipeline for semiautomated quantitation of endocrine area, islet frequency, interislet distance, and endocrine object size distribution in 145 human pancreata from 60 donors without diabetes, 19 donors with single autoantibody positivity, 10 with multiple autoantibody positivity (mAAb+), and 16 with recent-onset (duration 0-1 year), 23 with medium-duration (1-7 years), and 17 with long-duration T1D (7+ years). We observed age-related differences in endocrine composition and islet frequency in pancreata from donors without diabetes. Age-corrected data revealed decreased islet frequency and greater interislet distance in the T1D pancreas. INS+ single cells (≤10 μm), cell clusters (>10 to <35 μm), small- and medium-sized islets (35-100 and 100-200 μm, respectively) were significantly lost at T1D onset, whereas large INS+ islets (>200 μm) were preserved. Moreover, changes in endocrine composition also occurred in pancreata from mAAb+ donors, including a significant decrease in the INS+ islet fraction. These data suggest preferential loss of INS+ small endocrine objects early in T1D development.</p><p><strong>Article highlights: </strong>Understanding the timing and nature of β-cell loss is essential for developing effective strategies to interrupt type 1 diabetes progression. Which types of islets, in terms of size and cellular composition, are lost first during disease development? Insulin-positive single cells and cell clusters are lost before large islets during disease development. Insulin-positive single cells and cell clusters might be more susceptible to destruction in type 1 diabetes.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin Boosts Intestinal Lipid Sensing via GIP to Suppress Feeding.","authors":"Rachel Kuah, Melissa T Wang, Zeyu Yang, Grace Back, Rosa J W Li, Kyla Bruce, Jessica N LoChoy, Jacqueline L Beaudry, Daniel R Barros, Song-Yang Zhang, Tony K T Lam","doi":"10.2337/db25-0100","DOIUrl":"https://doi.org/10.2337/db25-0100","url":null,"abstract":"<p><p>An acute increase of lipids in the upper small intestine (USI) of rodents and humans triggers lipid-sensing pathways to reduce food intake. However, USI lipid sensing does not reduce feeding in high-fat (HF) fed conditions, and the underlying mechanism remains elusive. Here, we report that HF feeding in male rats impaired USI lipid infusion to stimulate glucose-dependent insulinotropic polypeptide (GIP) secretion and decrease refeeding, and the defects of USI lipid sensing were restored by metformin. Next, we found that infusion of GIP receptor (GIPR) agonist in the nucleus of the solitary tract (NTS), but not mediobasal hypothalamus or area postrema, resulted in decreased refeeding in chow-fed rats. The anorectic effect of NTS GIPR agonist remained intact in HF rats and was inhibited by a genetic knockdown of GIPR. Finally, an inhibition of NTS GIPR also negated the ability of USI lipid sensing with metformin to decrease refeeding despite an increase in plasma GIP levels in HF rats. Thus, USI lipid sensing in HF rats is enhanced by metformin to trigger an endocrine GIP to NTS GIPR axis to reduce food intake, thereby unveiling small intestinal lipid-sensing pathways as potential targets to enhance GIP action and reduce weight in obesity.</p><p><strong>Article highlights: </strong>High-fat (HF) feeding in rats impairs upper small intestine (USI) lipid sensing to increase plasma glucose-dependent insulinotropic polypeptide (GIP) levels and reduce feeding. Metformin enhances USI lipids to increase GIP and reduce feeding in HF-fed rats. GIP activates the GIP receptor (GIPR) in the nucleus of the solitary tract (NTS), which reduces food intake in HF-fed rats. GIPR in the NTS is required for small intestinal lipids with metformin to reduce feeding.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144692815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liraglutide Treatment Reverses Unconventional Cellular Defects in Induced Pluripotent Stem Cell-Derived β-Cells Harboring a Partially Functional WFS1 Variant.","authors":"Silvia Torchio, Gabriel Siracusano, Federica Cuozzo, Valentina Zamarian, Silvia Pellegrini, Fabio Manenti, Riccardo Bonfanti, Giulio Frontino, Valeria Sordi, Raniero Chimienti, Lorenzo Piemonti","doi":"10.2337/db24-0720","DOIUrl":"10.2337/db24-0720","url":null,"abstract":"<p><p>Wolfram syndrome 1 (WS1) is a rare genetic disorder caused by WFS1 variants that disrupt wolframin, an endoplasmic reticulum-associated protein essential for cellular stress responses, Ca2+ homeostasis, and autophagy. Here, we investigated how the c.316-1G>A and c.757A>T WFS1 mutations, which yield partially functional wolframin, affect the molecular functions of β-cells and explored the therapeutic potential of the glucagon-like peptide 1 receptor (GLP-1R) agonist liraglutide. Pancreatic β-cells obtained from patient-derived induced pluripotent stem cells (iPSCs) carrying this WFS1 variant exhibited reduced insulin processing and impaired secretory granule maturation, as evidenced by proinsulin accumulation and decreased prohormone convertase PC1/3. Moreover, they exhibited dysregulated Ca2+ fluxes due to altered transcription of Ca2+-related genes, including CACNA1D, and significantly reduced SNAP25 levels, leading to uncoordinated oscillations and poor glucose responsiveness. Affected cells also showed increased autophagic flux and heightened susceptibility to inflammatory cytokine-induced apoptosis. Notably, liraglutide treatment rescued these defects by normalizing Ca2+ handling, enhancing insulin processing and secretion, and reducing apoptosis, likely through modulation of the unfolded protein response. These findings underscore the importance of defining mutation-specific dysfunctions in WS1 and support targeting the GLP-1/GLP-1R axis as a therapeutic strategy.</p><p><strong>Article highlights: </strong>The molecular basis of WFS1-related mutations remains poorly investigated, and no definitive therapies exist for Wolfram syndrome 1. We dissected the molecular defects associated with c.316-1G>A and c.757A>T WFS1 mutations in patient-derived induced pluripotent stem cell islets and analyzed whether they are potential therapeutic targets of the glucagon-like peptide 1 receptor agonist liraglutide. We found impaired insulin granule maturation, altered Ca2+ fluxes, increased autophagic activity, and heightened susceptibility to inflammatory apoptosis in mutated cells. Liraglutide restored critical β-cell functions suggesting a route for personalized therapy based on WFS1 mutations.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"1273-1288"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12185971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143813245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Type 1 Diabetes Depends on CD4-Driven Expression of the Transcriptional Repressor Bcl6.","authors":"Dudley H McNitt, Jonathan M Williams, Joseph G Santitoro, Jacob Kim, James W Thomas, Rachel H Bonami","doi":"10.2337/db23-0709","DOIUrl":"10.2337/db23-0709","url":null,"abstract":"<p><p>High-affinity islet autoantibodies predict type 1 diabetes in mice and humans and implicate germinal centers (GCs) in disease pathogenesis. T follicular helper (Tfh) cells are increased in individuals with type 1 diabetes and alterations in Tfh-like cells in the peripheral blood predicted individual responses to abatacept. Tfh cells support GC responses and depend on the transcriptional repressor BCL6 for their maturation. Therefore, we hypothesized that CD4-driven deletion of Bcl6 would disrupt essential T- and B-cell interactions in GCs to prevent type 1 diabetes. To test this hypothesis, we generated Bcl6fl/fl-CD4.Cre.NOD mice and found they were completely protected against diabetes. Insulitis severity and tertiary lymphoid structure organization were preserved in the pancreas of Bcl6fl/fl-CD4.Cre.NOD mice, which did not show decreases in CD4+, CD8+, and B-cell numbers in the pancreas and draining lymph nodes, relative to control Bcl6fl/fl.NOD mice. CD4-driven loss of functional BCL6 resulted in significantly reduced GC B-cell and Tfh-cell numbers in the pancreatic lymph nodes and pancreas at late prediabetic intervals. Spontaneous anti-insulin autoantibody was blunted in Bcl6fl/fl-CD4.Cre.NOD mice. These data highlight BCL6 as a novel therapeutic target in type 1 diabetes.</p><p><strong>Article highlights: </strong>Germinal center B cells and CD4+ T follicular helper cells are implicated in the pathogenesis of type 1 diabetes and depend upon the transcriptional repressor BCL6 for their maturation. This study tests the dependence of type 1 diabetes development on BCL6 expression in CD4+ cells. Data presented here show that CD4-driven loss of Bcl6 blocks germinal center formation, spontaneous insulin autoantibody production, and type 1 diabetes in nonobese diabetic mice, despite normal tertiary lymphoid structure formation in pancreatic islets. This study highlights BCL6 as a potential immunomodulatory target in type 1 diabetes.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"921-932"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diroximel Fumarate Acts Through Nrf2 to Attenuate Methylglyoxal-Induced Nociception in Mice and Decrease ISR Activation in DRG Neurons.","authors":"Muhammad Saad Yousuf, Marisol Mancilla Moreno, Brodie J Woodall, Vikram Thakur, Jiahe Li, Lucy He, Rohita Arjarapu, Danielle Royer, Jennifer Zhang, Munmun Chattopadhyay, Peter M Grace, Theodore J Price","doi":"10.2337/db23-1025","DOIUrl":"10.2337/db23-1025","url":null,"abstract":"<p><p>Diabetic neuropathic pain is associated with elevated plasma levels of methylglyoxal (MGO). MGO is a metabolite of glycolysis that causes pain hypersensitivity in mice by stimulating the phosphorylation of eukaryotic initiation factor 2α (p-eIF2α) and subsequently activating the integrated stress response (ISR). We first established that Zucker diabetic fatty rats have enhanced MGO signaling, engage ISR, and develop pain hypersensitivity. Since nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the expression of antioxidant proteins that neutralize MGO, we hypothesized that fumarates, like diroximel fumarate (DRF), will stimulate Nrf2 signaling, and prevent MGO-induced ISR and pain hypersensitivity. DRF (100 mg/kg) treated animals were protected from developing MGO (20 ng) induced mechanical and cold hypersensitivity. Mechanistically, DRF treatment protected against MGO-induced increase in p-eIF2α levels in the sciatic nerve and reduced loss of intraepidermal nerve fiber density. Using Nrf2 knockout mice, we demonstrate that Nrf2 is necessary for the antinociceptive effects of DRF. Cotreatment of MGO (1 µmol/L) with monomethyl fumarate (10, 20, and 50 µmol/L), the active metabolite of DRF, prevented ISR in both mouse and human dorsal root ganglia neurons. Our data show that targeting Nrf2 with DRF is a strategy to potentially alleviate pain associated with elevated MGO levels.</p><p><strong>Article highlights: </strong></p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"827-837"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143461277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Of Mice and Men: Toward a Better Model of Diabetic Cardiomyopathy With Application in Female Animals.","authors":"Jordan S F Chan, John R Ussher","doi":"10.2337/dbi25-0010","DOIUrl":"https://doi.org/10.2337/dbi25-0010","url":null,"abstract":"","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":"74 5","pages":"689-690"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}