Diabetes最新文献

{"title":"Phase I Clinical Trial of Islet Antigen-Specific Plasmid Coexpressing Tolerogenic Proteins Demonstrates Safety in Adults With Type 1 Diabetes.","authors":"Carla J Greenbaum, S Alice Long, Stephen E Gitelman, Jason L Gaglia, Mark Daniels, Todd M Brusko, Sandra Lord, Brian N Bundy, Jeffrey P Krischer, Michael J Haller, Andrea K Steck, Linda A DiMeglio, Carmella Evans-Molina, Antoinette Moran, Priya Prahalad, Darrell M Wilson, William E Russell, Jennifer L Sherr, Philip Raskin, Mark A Clements, Wayne V Moore, Ingrid Libman, Karsten Wassermann, Matthias von Herrath, Regine Bergholdt, Hanne Hastrup, Sarah E Kobernat, Anna M Kus, Lin Wei Tung, Robin S Goland, Kevan C Herold","doi":"10.2337/db25-0777","DOIUrl":"10.2337/db25-0777","url":null,"abstract":"<p><p>There is significant interest in antigen-specific approaches to delaying type 1 diabetes in preclinical stages and supporting tolerance after diagnosis. We conducted a phase I trial of a nonintegrating DNA plasmid constructed to secrete the type 1 diabetes antigen preproinsulin (PPI) and the immune modulatory cytokines transforming growth factor-β1 (TGF-β1), interleukin-10 (IL-10), and IL-2. In this placebo-controlled, double-masked study of 47 adults with stage 3 type 1 diabetes, we showed that the drug is safe and well tolerated, with most reported adverse events (AEs) categorized as grade 1 and with no clinically significant difference in AEs among treatment groups. There were no untoward metabolic or immune effects. We found pharmacodynamic evidence of treatment, as demonstrated by a dose-dependent type 1 interferon (IFN) signature. Plasmid DNA, representing a pharmocokinetic measure, was detected in the two highest dosing groups. We did not find global or antigen-specific immune cell changes following treatment with a DNA plasmid expressing PPI, IL-2, IL-10, and TGF-β1, and we did not detect immune changes driven by IL-2, IL-10, or TGF-β1. Our results support further trials of this novel tolerizing antigen construct.</p><p><strong>Article highlights: </strong>Antigen-specific therapy is needed to induce tolerance in type 1 diabetes at early disease stages or in combination with immunotherapy. We conducted a phase I trial in type 1 diabetes of a novel plasmid construct expressing the islet antigen preproinsulin (PPI) and immunomodulatory cytokines transforming growth factor-β1 (TGF-β1), interleukin-10 (IL-10), and IL-2. The therapy was safe and well tolerated. Dose-dependent changes in DNA plasmid levels and type 1 interferon signatures were detected; however, global and antigen-specific immune changes to PPI, IL-2, IL-10, or TGF-β1 were not observed. Further trials are needed to assess efficacy.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"506-518"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12889172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021078","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":"Integrating SMRT and Bulk RNA Sequencing With Metabolic Phenotyping to Examine Reduced Skeletal Muscle Mitochondrial Respiration in Type 2 Diabetes.","authors":"Martin Schön, Daniel Oehler, Iryna Yurchenko, Alexander Lang, Nina Trinks, Bedair Dewidar, Lucia Mastrototaro, Oana P Zaharia, Kálmán B Bódis, Yanislava Karusheva, Frederico G S Toledo, Volker Burkart, Cesare Granata, Ralf Westenfeld, Amin Polzin, Malte Kelm, Robert Wagner, Michael Roden, Julia Szendroedi","doi":"10.2337/db25-0625","DOIUrl":"10.2337/db25-0625","url":null,"abstract":"<p><p>Recent advances in RNA sequencing (RNA-seq) techniques allow the identification of tissue-specific alternative splicing and can thereby provide new insights into molecular mechanisms of energy metabolism. Full-length transcriptomics based on single-molecule real-time sequencing (SMRT-seq) enable precise detection of isoforms with 99% accuracy in an unbiased manner. In this proof-of-concept study, we integrated SMRT-seq, bulk RNA-seq, and comprehensive metabolic phenotyping to investigate reduced mitochondrial function in the skeletal muscle of individuals with type 2 diabetes. Muscle biopsies were taken from nine individuals with type 2 diabetes and nine age- and BMI-matched glucose-tolerant men. Whole-body insulin sensitivity (WBIS) was assessed by hyperinsulinemic-euglycemic clamps, and muscle mitochondrial respiration was assessed by high-resolution respirometry. In muscle samples, SMRT-seq was used to create full-length reads and isoforms, which were mapped to the genome. Short-read sequencing was used to compare isoform expression between the groups. Participants with diabetes exhibited lower WBIS and fatty acid-driven and complex I-linked respiration compared with control participants. SMRT-seq revealed ∼67,000 isoforms originating from ∼14,000 unique genes. Although isoform numbers per gene did not differ, SMRT-seq-based mapping enabled refined data set clustering compared with conventional short-read sequencing and identified four splicing variants of the ATP5F1A gene encoding a subunit for ATP synthase. Among these, two novel transcripts were expressed exclusively in control participants. This study identified splicing variants of ATP synthase that were differentially expressed between participants with type 2 diabetes and those with normal glucose tolerance, which may contribute to the reduced fatty acid oxidation in diabetes.</p><p><strong>Article highlights: </strong>In our study, we developed a pipeline to integrate single-molecule real-time sequencing (SMRT-seq) with comprehensive metabolic phenotyping to examine reduced mitochondrial respiration in the skeletal muscle of individuals with type 2 diabetes. SMRT-seq revealed ∼67,000 isoforms originating from ∼14,000 unique genes; the isoform numbers per gene did not differ between participants with diabetes and matched control participants. Our data identified novel alternative splicing events, including two variants of the ATP5F1A gene encoding a subunit for ATP synthase. Among these, two novel transcripts were expressed exclusively in control participants. Our findings link transcriptomic changes to impaired mitochondrial respiration in type 2 diabetes, with the potential of providing novel therapeutic targets to improve metabolic health.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"571-581"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146013712","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":"Paracrine Hormonal Signals From Islet α-Cells Regulate Microtubule Dynamics in β-Cells to Promote Insulin Secretion in Mouse and Human Islets.","authors":"Kung-Hsien Ho, Syed N Barmaver, Shannon E Gibson, Ruiying Hu, Mahircan Yagan, Hamida K Ahmed, Appakalai N Balamurugan, David A Jacobson, Irina Kaverina, Guoqiang Gu","doi":"10.2337/db24-1025","DOIUrl":"10.2337/db24-1025","url":null,"abstract":"<p><p>The microtubule network in β-cells attenuates insulin secretion by pulling insulin secretory granules away from the plasma membrane. Thus, high-glucose-induced microtubule remodeling is required for robust glucose-stimulated insulin secretion. We now demonstrate that hormones secreted by α-cells regulate microtubule dynamics in β-cells through receptors for glucagon (GcgR) and glucagon-like peptide 1 (GLP-1R). Activation of GcgR or GLP-1R destabilizes microtubules in β-cells, accompanied by increased insulin secretion. In contrast, inhibiting these receptors attenuates high-glucose-induced microtubule destabilization and decreases secretion. Supporting the physiological significance of this regulation, β-cells in islets with a higher α-cell-to-β-cell ratio exhibit more dynamic microtubules than those with a lower ratio, and a high-fat diet challenge in mice, which can compromise β-cell secretion, attenuates this effect in their islets. Within individual islets, β-cells located near α-cells show faster microtubule remodeling upon glucose stimulation than those more distant from α-cells. Consequently, islets with a higher α-cell-to-β-cell ratio secrete more insulin in response to glucose stimulation and plasma membrane depolarization, results recapitulated by exogenous glucagon stimulation or chemically induced microtubule destabilization in islets with lower α-cell-to-β-cell ratios. These combined results suggest that α-cells use glucagon-mediated and/or GLP-1-mediated paracrine signaling to fine-tune β-cell secretion via microtubule remodeling.</p><p><strong>Article highlights: </strong>Glucagon/glucagon-like peptide 1 sensitizes glucose-induced microtubule remodeling in β-cells. Microtubule density in islets inversely correlates with the α-cell-to-β-cell ratio. Glucose-stimulated insulin secretion levels in single islets positively correlate with their α-cell-to-β-cell ratio. Glucagon and microtubule destabilization mobilize the same granule pool.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"494-505"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145936863","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":"Amino Acid Sensing by the α-Cell Mitochondrial Phosphoenolpyruvate Cycle Regulates Intracellular Ca2+ Levels Without Affecting Glucagon Secretion.","authors":"Erli Jin, Hannah R Foster, Evgeniy Potapenko, Shih Ming Huang, Xinhang Dong, Jing W Hughes, Matthew J Merrins","doi":"10.2337/db25-0510","DOIUrl":"10.2337/db25-0510","url":null,"abstract":"<p><p>Pancreatic islet α-cells are increasingly recognized as amino acid sensors for the organism. Building on our prior work in β-cells, we sought to determine whether the mitochondrial phosphoenolpyruvate (PEP) cycle is involved in α-cell amino acid sensing. Three different methods were used to probe the PEP cycle, including pyruvate kinase activators (TEPP-46), and mice with α-cell-specific deletion (KO) of pyruvate kinase M (PKM1/2-αKO) or mitochondrial PEP carboxykinase (PCK2-αKO). The mitochondrial fuel leucine, in the presence of glutamine, antagonized alanine/arginine-stimulated Ca2+ influx and glucagon secretion under hypoglycemic conditions. Both PKM1/2 and PCK2 deletion prevented leucine from closing α-cell KATP channels. The Ca2+ response to amino acids was suppressed by pyruvate kinase activation with TEPP-46 and enhanced by α-cell deletion of PKM1/2 or PCK2-all without changing glucagon secretion. Using diazoxide/KCl to probe the pathways downstream of membrane depolarization, we identified a further role of the PEP cycle in homeostatically regulating Ca2+ levels. In sum, α-cell pyruvate kinase and the mitochondrial PEP cycle senses leucine and inhibits KATP channels similarly to β-cells, while restricting amino acid-stimulated membrane depolarization and Ca2+ influx. However, none of the amino acids tested, including alanine/arginine, regulate glucagon secretion by modulating membrane depolarization or Ca2+ influx.</p><p><strong>Article highlights: </strong>Our studies identify a role for the α-cell phosphoenolpyruvate cycle in sensing amino acids under hypoglycemic conditions. Leucine, in the presence of glutamine, opposes alanine/arginine-stimulated Ca2+ influx and glucagon secretion. Pyruvate kinase and phosphoenolpyruvate carboxykinase 2 are required for leucine to close α-cell KATP channels and limit Ca2+ influx. All of the amino acids tested regulate glucagon secretion, but none do so by modulating membrane depolarization or intracellular Ca2+ levels.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"483-493"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145954594","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":"Identifying Insulin Autoantibodies With Differential Risk in Type 1 Diabetes With a Novel Bridging ELISA.","authors":"Xiaofan Jia, Caiguo Zhang, Kathleen Waugh, Dongmei Miao, Aaron W Michels, Marian J Rewers, Liping Yu","doi":"10.2337/db25-0696","DOIUrl":"10.2337/db25-0696","url":null,"abstract":"<p><p>Insulin autoantibodies (IAAs) are commonly measured by radiobinding assays (RBAs), which detect both high- and low-affinity binding. Improved assays that preferentially detect high-affinity IAA are likely to provide greater specificity and thereby increase the diagnostic accuracy of IAA for early-stage type 1 diabetes (T1D). This study aimed to develop and validate a novel bridging ELISA for IAA detection. The bridging ELISA detects IAAs by their bivalent cross-linking of two proinsulin moieties in fluid phase. Validation was performed by using samples from 227 patients with newly diagnosed stage 3 T1D and 1,021 control participants. Additionally, 202 children positive for IAA by RBA from general population screening were tested by the bridging ELISA and electrochemiluminescence (ECL) assay. At 99.5% specificity, ELISA detected IAA in 65.2% of patients with stage 3 T1D vs. 60.8% by RBA. Among children identified as having RBA-positive IAA in general population screening, 80.3% of those with multiple islet autoantibodies and 48.1% of those with a single IAA had ELISA-IAA positive findings (P < 0.0001). For children with a single IAA by RBA, ELISA detected 78.9% of those with ECL-IAA-positive findings vs. 27.9% of those with ECL-IAA negative findings (P < 0.0001). Samples that were IAA negative by ELISA showed lower antibody affinity. The ELISA-IAA assay demonstrates high sensitivity and specificity and could become a practical tool for T1D population screening and clinical diagnosis across laboratories.</p><p><strong>Article highlights: </strong>In global type 1 diabetes (T1D) population screening studies, there is an urgent need for a highly sensitive and specific insulin autoantibody (IAA) assay that can be implemented across multiple laboratories. This study aimed to develop and characterize a novel ELISA-based platform for IAA detection. We established a new bridging ELISA for IAA and validated it in cohorts of patients with stage 3 T1D, children positive for multiple and single islet antibodies, and control children negative for islet autoantibodies. The bridging ELISA-IAA assay demonstrates excellent sensitivity and specificity, preferentially identifies high-risk individuals, and offers a practical, scalable solution for T1D population screening and clinical diagnosis across laboratories.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"519-525"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145954542","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":"Toward Scientific Rigor: Setting Standards for Indirect Calorimetry Analysis and Reporting.","authors":"Elizabeth L Lieu, Mark A Herman, Sean M Hartig","doi":"10.2337/db25-0998","DOIUrl":"10.2337/db25-0998","url":null,"abstract":"<p><p>Indirect calorimetry determines energy expenditure by measuring respiratory gas exchange. The approach is based on the principle that nutrient metabolism consumes O2 and produces CO2 and water in predictable ratios that can be compared with heat production. Due to the impracticality and high cost of direct calorimetry, indirect calorimetry is the major approach for modern metabolic studies in preclinical models. Despite the broad adoption of this method in rodent phenotyping, the field has lacked standardized methods for analyzing, representing, and sharing these data, limiting scientific progress. The recent review in Nature Metabolism by the International Indirect Calorimetry Consensus Committee (IICCC) addresses the lack of standardized methods by providing updated guidelines for data processing and representation and emphasizes the importance of shared data repositories tailored to these studies. These expert consensus standards aim to improve transparency, facilitate data sharing and archiving, and enhance cross-study comparability. We encourage authors submitting to Diabetes to adopt the IICCC guidelines to strengthen rigor and reproducibility in the field.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"401-402"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145770336","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":"GLP-1, Pancreatic β-Cells, and Insulin Secretion: What We Know and Where We Need to Go.","authors":"Éverton L Vogt, Alicia J Kowaltowski","doi":"10.2337/db25-0695","DOIUrl":"10.2337/db25-0695","url":null,"abstract":"<p><p>GLP-1 receptor agonists have emerged as key pharmacological tools in the treatment of type 2 diabetes and obesity. While their anorexigenic effects are well characterized, the mechanisms by which GLP-1 modulates pancreatic β-cell function remain only partially understood. In this article, we argue that GLP-1 receptor agonists should be viewed as integrative regulators of β-cell function and explore the multifaceted actions of GLP-1 analogs on β-cell signaling. GLP-1 influences key secretagogues and intracellular mediators (calcium, glutamate, γ-aminobutyric acid, serotonin, and urocortin-3), with complex roles in insulin exocytosis. Additionally, we discuss the interplay between calcium and cAMP, and how GLP-1 modulates both pathways to coordinate insulin secretion. Emerging evidence suggests that GLP-1 analogs affect mitochondrial morphology and redox homeostasis. Considering the relatively low expression of classical antioxidant enzymes in β-cells, and their reliance on both glycolytic and mitochondrial metabolism to sustain insulin secretion, the influence of GLP-1 on mitochondrial dynamics and reactive oxygen species may play a central role in sustaining cell function and viability. Despite recent advances, critical gaps persist in the literature, particularly regarding organelle cross talk, intracellular calcium stores, and the modulation of vesicular content. Drawing on current evidence, we propose that three mechanistic dimensions (intracellular neurotransmitters, mitochondrial remodeling, and redox control) represent key areas where clarifying GLP-1 actions could most effectively advance the field. Further investigation into these mechanisms is essential for a comprehensive understanding of GLP-1 actions in β-cells. This knowledge may help refine current incretin-based therapies and identify novel molecular targets for the treatment of metabolic disorders.</p><p><strong>Article highlights: </strong>GLP-1 and its analogs enhance insulin secretion, but the specific intracellular mechanisms in β-cells remain unclear. Key intracellular mediators including calcium, glutamate, γ-aminobutyric acid, serotonin, and urocortin-3 are modulated by GLP-1 signaling with variable and sometimes contradictory effects. GLP-1 may affect mitochondrial dynamics and redox balance in β-cells, both critical for function and survival. Gaps in knowledge remain regarding cross talk between classical secretagogues and GLP-1 pathways. Further investigation is needed to clarify how GLP-1 integrates metabolic, signaling, and organelle-based processes in insulin secretion.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"403-413"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145954589","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":"Integrating Polygenic Scores and Family History for Type 2 Diabetes Prediction in an East Asian Population: Insights From the Taiwan Biobank.","authors":"Wen-Ling Liao, Chun-Wen Cheng, Ya-Wen Chang, Mei-Chen Lin, Chi-Fung Cheng, Shih-Feng Tsai, Chih-Cheng Hsu, Shi-Heng Wang","doi":"10.2337/db25-0357","DOIUrl":"10.2337/db25-0357","url":null,"abstract":"<p><p>Type 2 diabetes is a complex disease influenced by both genetic and environmental factors. Although polygenic risk scores (PRS) and family history (FH) are established predictors, their combined utility in East Asian populations remains unclear. In this study, we analyzed 111,899 unrelated participants from the Taiwan Biobank with linkage to nationwide health registry data. We constructed transancestry, East Asian-specific, and European-derived PRS and assessed their associations with type 2 diabetes. The transancestry PRS improved the explained variance in disease risk compared with ancestry-specific PRS and FH. FH, particularly sibling history, also showed a strong association with type 2 diabetes. When combined, PRS and FH contributed independently and additively, improving predictive performance. These findings demonstrate that PRS and FH are independent yet complementary risk indicators and support the application of transancestry PRS models in East Asian populations. Incorporating both genetic and familial risk factors may enhance early detection and facilitate more personalized prevention strategies for type 2 diabetes.</p><p><strong>Article highlights: </strong>Type 2 diabetes is influenced by genetic and environmental factors. Although polygenic risk scores (PRS) and family history (FH) are established predictors, their combined utility in East Asian populations is unclear. We evaluated the predictive performance of PRS and the independent and joint effects of PRS and FH on diabetes risk in an East Asian population. The transancestry PRS explained more variance than ancestry-specific PRS and FH. PRS and FH were independently predictive, and their combination improved prediction, with stronger effects in men. Sibling history showed the strongest familial association. Integrating PRS and FH may enhance diabetes risk prediction in East Asian populations.</p>","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":" ","pages":"582-590"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145859701","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":"Diabetes Spotlight: Jay M. Sosenko, MD-Diabetic Neuropathy and Prevention Strategies for Type 1 Diabetes.","authors":"Benjamin Page","doi":"10.2337/dbi25-0051","DOIUrl":"https://doi.org/10.2337/dbi25-0051","url":null,"abstract":"","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":"75 2","pages":"227-228"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146108926","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":"Urinary Dickkopf-3 Reveals Tubular Fibrosis and Hidden Progression in Diabetic Kidney Disease.","authors":"Ming-Cheng Lin, Shiuan-Chih Chen","doi":"10.2337/db25-0992","DOIUrl":"10.2337/db25-0992","url":null,"abstract":"","PeriodicalId":93977,"journal":{"name":"Diabetes","volume":"75 2","pages":"e1-e2"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146013697","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}