Diabetes最新文献

{"title":"Intrasplenic Transplantation of Islets With a Platelet-Shielding System Restores Glycemic Control","authors":"Lin Song, Chunyan Liu, Anqi Yang, Xiaohai Zhang, Xintong Wang, Yanjiao Teng, Decheng Lu, Xiaocong Kuang, Chunming Wang, Junfeng Zhang, Xuyong Sun, Lei Dong","doi":"10.2337/db24-0856","DOIUrl":"https://doi.org/10.2337/db24-0856","url":null,"abstract":"Intraportal islet transplantation to treat insulin-dependent diabetes has been clinically validated. However, the hypoxic environment and sinusoidal architecture of the liver are unsuitable for the long-term survival of transplanted islets, leading to the loss of therapeutic effects within 1 year. The spleen has oxygen levels that meet islet needs, but intense instant blood-mediated inflammatory reactions (IBMIRs) and low extracellular matrix (ECM) concentrations hinder islet engraftment and survival. In this study, we developed constructs of islets encapsulated by hepatocytes and fibroblasts. The hepatocytes and fibroblasts create a protective coating that reduces IBMIRs because of the low expression of von Willebrand factor in hepatocytes and supports normal islet survival through ECM production by fibroblasts. These constructs can be easily injected into the mouse spleen. The hepatocyte–fibroblast encapsulation significantly reduces islet mortality during the posttransplantation stress period, enabling rapid engraftment and vascularization in the spleen. The high-oxygen environment of the spleen then supports long-term (>1 year) islet survival and sustained glycemic regulation. Additionally, this method significantly lowers the critical islet dose required for transplantation. The live cell–shielding strategy developed in this study represents a novel approach in islet transplantation and functional regeneration, demonstrating promising clinical potential. ARTICLE HIGHLIGHTS Instant blood-mediated inflammatory reactions (IBMIRs) and low extracellular matrix (ECM) concentrations hinder islet implantation and survival in the spleen. Islets were encapsulated in hepatocytes and fibroblasts. The low expression of von Willebrand factor in hepatocytes enables them to form a protective coating with fibroblasts. This coating reduces IBMIRs and supports islet survival through ECM production by fibroblasts. The hepatocyte–fibroblast encapsulation significantly reduces islet mortality during the posttransplantation stress period, enabling rapid engraftment and vascularization in the spleen.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"49 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Splanchnic and Leg Glucagon Metabolism in Healthy and Type 1 Diabetes: First in Human Study Using [13C9, 15N1]-Glucagon","authors":"F.N.U. Ruchi, Michele Schiavon, Yogesh Yadav, Chiara Dalla Man, Claudio Cobelli, Akhilesh Pandey, Luke Wilkins, Rita Basu, Ananda Basu","doi":"10.2337/db24-1064","DOIUrl":"https://doi.org/10.2337/db24-1064","url":null,"abstract":"Circulating glucagon concentrations differ between individuals with no diabetes (ND) and those with type 1 diabetes (T1D). We combined isotope dilution technique using stable tracers [6,22 13C9, 15N1]-glucagon and [6,14,19,22 13C9, 15N1]-glucagon with splanchnic and leg catheterization in participants with ND (n = 8; age 23.1 ± 2.9 years, BMI 26.6 ± 3.5 kg/m2, HbA1c 5.0 ± 0.2% [31 ± 2 mmol/mol]) and T1D (n = 6; 29.0 ± 8.8 years, BMI 26.3 ± 5.0 kg/m2, HbA1c 7.9 ± 0.8% [63 ± 8 mmol/mol]) in the overnight fasted state. After baseline period, exogenous glucagon was infused at rates designed to achieve plasma glucagon concentrations spanning the physiological ranges, to determine the effects of rising glucagon concentrations on splanchnic and leg glucagon balance. At baseline, splanchnic glucagon extraction (SGE) was similar (30.7 ± 2.7 vs. 29.1 ± 2.9%) but leg glucagon extraction (LGE) was lower (27.0 ± 4.2 vs. 40.6 ± 3.1%) in participants with T1D versus those with ND. However, with increasing plasma glucagon concentrations, while SGE remained unchanged within and between groups, LGE fell in participants with ND (41 vs. 31 vs. 24%) but did not change in those with T1D. Despite a numerically lower net splanchnic glucagon production in participants with T1D than in those with ND, no changes were observed with increasing glucagon concentrations within the physiological range in both groups. This is the first human study applying novel glucagon isotopes that describes regional glucagon metabolism in participants with ND and T1D. Our observations provide translational relevance for dual hormone closed loop systems and provide tools for probing the effects of GLP-1, dual, and triple receptor agonists on pancreatic α-cell functions. ARTICLE HIGHLIGHTS This study was conducted to assess splanchnic and leg glucagon metabolism in humans using stable glucagon isotopes. We wanted to evaluate whether splanchnic and leg glucagon metabolism differed between participants with no diabetes (ND) and those with type 1 diabetes (T1D) at glucagon concentrations spanning the physiological range. Whereas splanchnic glucagon extraction did not differ between participants with ND and those with T1D, leg glucagon extraction fell in those with ND but did not change in those with T1D as glucagon concentrations increased. Net splanchnic glucagon production did not change with exogenous glucagon infusion. Our study has implications for dual hormone closed loop control in T1D where glucagon is infused for prevention of hypoglycemia and for investigating the effects of emerging GLP-1, glucose-dependent insulinotropic polypeptide, and glucagon receptor agonists on endogenous glucagon secretion and clearance.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"6 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucose-Dependent Insulinotropic Polypeptide Is Involved in Postprandial Regulation of Splanchnic Blood Supply","authors":"Rasmus S. Rasmussen, Ludvig S. Langberg, Frederikke Østergaard, Sophie W. Nielsen, Mark B. Vestergaard, Kirsa Skov-Jeppesen, Bolette Hartmann, Helle Hjorth Johannesen, Jens J. Holst, Bryan Haddock, Henrik B. W. Larsson, Mette M. Rosenkilde, Ali Asmar, Ulrik B. Andersen, Lærke S. Gasbjerg","doi":"10.2337/db25-0149","DOIUrl":"https://doi.org/10.2337/db25-0149","url":null,"abstract":"Gastrointestinal hormones are essential for nutrient handling and regulation of glucose metabolism and may affect postprandial blood redistribution. In a randomized cross-over design in 10 healthy men, the involvement of glucose-dependent insulinotropic polypeptide (GIP) in splanchnic blood flow regulation was investigated using an infusion of GIP receptor antagonist (GIPR-An) GIP(3-30)NH2 during ingestion of oral glucose (75 g). In five separate sessions, we investigated GIP(1-42), GIPR-An with and without oral glucose, oral glucose alone, and a control saline infusion. Blood flow was assessed by phase contrast MRI, hepatic oxygen consumption by T2*, and plasma glucose, insulin, C-peptide, glucagon, GIP, GIPR-An, glucagon-like peptide 2, and bone metabolism markers by frequent blood sampling during all sessions. We found GIP(1-42) to stimulate blood flow in the superior mesenteric artery by ∼10% in the fasting state. Oral glucose alone increased mean blood flow in the superior mesenteric artery by ∼70% and portal vein by ∼40% of baseline. During oral glucose ingestion with concurrent infusion of GIPR-An, blood flow in the superior mesenteric artery was ∼22% lower. The hormone infusions did not affect blood flow in the hepatic artery and the celiac artery. Infusion of GIPR-An during oral glucose ingestion resulted in lower insulin secretion and higher levels of carboxy-terminal collagen crosslinks (bone resorption biomarker) compared with saline infusion, whereas glucagon levels were unaffected by both the injection of GIP and the GIPR-An infusions. We conclude that endogenous GIP increases splanchnic blood flow and contributes to postprandial intestinal hyperemia in healthy men. ARTICLE HIGHLIGHTS Administration of the gut hormone glucose-dependent insulinotropic polypeptide (GIP) increases splanchnic blood flow. We investigated the role of endogenous GIP in splanchnic blood flow regulation using a receptor antagonist in humans. Oral glucose ingestion increased blood flow in the superior mesenteric artery by ∼70%, and the increase was significantly lower during concurrent infusion of the GIP receptor antagonist. Thus, endogenous GIP contributed ∼22% of the postprandial increase in superior mesenteric artery blood flow. We have identified a novel physiological aspect of vascular biology related to the GIP receptor in humans. Treatments targeting the GIP receptors are likely to affect splanchnic blood flow.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"22 5 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Codelivery of NGFR100W and VEGFA mRNA Enhances Vascular and Neural Repair in Diabetic Peripheral Neuropathy","authors":"Wenjing Wang, Xiang Yu, Zheng Yang, Yu Zhang, Wen Yang, Yingjie Xu, Wei Xu","doi":"10.2337/db24-0989","DOIUrl":"https://doi.org/10.2337/db24-0989","url":null,"abstract":"Diabetic peripheral neuropathy (DPN) poses significant clinical challenges due to progressive nerve degeneration and vascular insufficiency. To address both neural and vascular complications simultaneously, we employed an mRNA-based protein replacement therapy. In this study, leveraging mRNA template design, structure-based screening identified NGFR100W as a variant dissociating neuroprotective and nociceptive functions, demonstrating enhanced neuritogenic activity without pain sensitization. Additionally, transcriptome analysis of NGF mutants versus wild type further reveals the potential mechanism by which NGFR100W uncouples neuroprotective and nociceptive pathways. We cotransfected chemically modified NGFR100W mRNA and vascular endothelial growth factor A (VEGFA) mRNA, and the conditioned media collected from this transfection promoted endothelial cell migration, tubulogenesis, and neurite outgrowth. In a diabetic mouse model, combination therapy with lipid nanoparticle codelivery of NGFR100W and VEGFA mRNA significantly improved blood flow in the plantar region and mitigated nerve function decline compared with monotherapy. Histological analysis showed increased microvessel formation and higher intraepidermal nerve fiber density in treated mice. Our findings highlight the therapeutic potential of NGFR100W and VEGFA mRNA coadministration for DPN, suggesting that protein supplementation via mRNA could offer a novel strategy for clinical intervention in some chronic medical conditions. ARTICLE HIGHLIGHTS We aimed to develop a dual-targeted mRNA-based therapy to address both neural degeneration and vascular insufficiency in diabetic peripheral neuropathy. We identified NGFR100W as a mutation that enhances neuritogenic activity without pain sensitization and investigated its transcriptome to explore its ability to uncouple neuroprotective and nociceptive pathways. Combination therapy using lipid nanoparticles for codelivery of NGFR100W and VEGFA mRNA improved blood flow, increased microvessel formation, and preserved nerve function in a diabetic mouse model. This approach, which combines structure-based design and mRNA therapy, offers a novel strategy for decoupling protein functions and developing therapeutic molecules with specific functionalities.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"13 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144164922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting tsRNA-1797 alleviates diabetes-induced vascular dysfunction through modulating purine metabolism","authors":"Duo Li, Jingyue Zhang, Xiaoyan Han, Lingjie Kong, Ying Zhang, Mudi Yao, Ling Ren, Wan Mu, Qin Jiang, Biao Yan","doi":"10.2337/db24-1158","DOIUrl":"https://doi.org/10.2337/db24-1158","url":null,"abstract":"Diabetes is a metabolic disorder associated with an increased risk of systemic vascular complications. Notably, diabetic retinopathy (DR) represents a major microvascular complication and a leading cause of blindness and vision impairment. Despite its clinical significance, the precise molecular mechanisms underlying vascular dysfunction and the associated metabolic disturbances in DR remain incompletely understood. In this study, we identify tsRNA-1797, a tRNA-derived small RNA, as a critical regulator of retinal vascular dysfunction. tsRNA-1797 expression was markedly up-regulated under diabetic conditions. Functional studies demonstrated that silencing tsRNA-1797 ameliorated endothelial dysfunction in vitro, and inhibited retinal vascular dysfunction in vivo. Mechanistically, tsRNA-1797 was found to disrupt purine metabolism by regulating adenosine production through CD73. The tsRNA-1797-CD73-adenosine axis emerged as a key mediator of retinal vascular dysfunction in DR. These findings establish tsRNA-1797 as a novel regulatory factor that links metabolic dysregulation to vascular dysfunction in DR, highlighting its potential as a promising therapeutic target for diabetic vascular complications.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"73 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Normal 93: Linking the β-Cell and Insulin Sensitivity: Revisiting a 1993 Diabetes Classic by Kahn et al.","authors":"David D’Alessio, Steven E. Kahn","doi":"10.2337/dbi24-0049","DOIUrl":"https://doi.org/10.2337/dbi24-0049","url":null,"abstract":"In this month’s Classics in Diabetes featured article, published in Diabetes in 1993, the description by Kahn et al. of the relationship between insulin secretion and insulin sensitivity in 93 healthy adults without diabetes provided a model for the regulation of glucose tolerance that continues to be used today. In the study, data from a large sample of individuals studied with intravenous glucose tolerance tests demonstrated that in those with normal glucose tolerance, insulin secretion and sensitivity were related by a hyperbolic curve. This relationship supports adaptability between these parameters that maintains a constant amount of insulin action, and glycemia conforming to the normal range. These findings have led to the general view that type 2 diabetes mellitus is fundamentally a failure of β-cells to adequately supply tissues such as the liver, skeletal muscle, and adipose with insulin. This simple conception remains useful for explaining diabetes pathogenesis and interpreting experimental data some 30 years after publication, with impact meriting recognition as a Diabetes classic.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"119 1","pages":"668-671"},"PeriodicalIF":7.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-coupled receptor 35 suppresses oxidative stress response 1 in diabetic wound healing","authors":"Hainan Li, Liping Xu, Sai Pranathi Meda Venkata, Morgan Minjares, Hassan Melhem, Anjaneyulu Kowluru, Jan Hendrik Niess, Graeme Milligan, Jie-Mei Wang","doi":"10.2337/db24-0737","DOIUrl":"https://doi.org/10.2337/db24-0737","url":null,"abstract":"G protein-coupled receptor 35 (GPR35) is a poorly characterized receptor with unclear intracellular mechanisms in endothelial cells (ECs). Oxidative stress responsive 1 (OXSR1) is a serine/ threonine protein kinase that modulates cell morphology and has recently been found to promote angiogenesis. We hypothesized that GPR35 inhibition promotes EC angiogenesis via augmenting OXSR1 activity and accelerating wound healing in diabetes. Here, we show that active GPR35 contributed to the impaired migration and tube formation of human dermal microvascular endothelial cells (ECs) from type 2 diabetic (T2D) patients or ECs exposed to high glucose. Proximity labeling and coimmunoprecipitation identified OXSR1 as an interacting partner of GPR35 in ECs. GPR35 suppressed OXSR1 from translocating to nuclei to activate SMAD1/5, thereby inhibiting the transcription of angiogenic factors. Furthermore, enhanced wound angiogenic response and accelerated wound closures were observed in induced T2D mice with topical application of GPR35 siRNA, or in T2D models of transgenic mice with either global or endothelial-selective GPR35 deletion. Our data suggest that GPR35 suppresses OXSR1-dependent angiogenic activity in ECs, contributing to poor angiogenesis and delayed wound healing in T2D animals. This study provides both in vitro and in vivo evidence for GPR35 as a potential therapeutic target in tissue repair in patients with diabetes.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"3 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A functional and mechanistic explanation for the unique clinical success of the glucokinase activator dorzagliatin for treatment of type 2 diabetes","authors":"Jeff Roman, Yue Yuan, Yue Xu, Qiusha Zhu, Shaowen Wu, Fang Zhao, Xue Zhou, Shi Meng, Dongna Han, Kim Sharp, Li Chen, Changhong Li, Nicolai M Doliba","doi":"10.2337/db25-0066","DOIUrl":"https://doi.org/10.2337/db25-0066","url":null,"abstract":"Glucokinase activators (GKA) are a long-sought therapeutic modality for the treatment of Type 2 Diabetes (T2D). However, all GKAs failed clinical trials, with the recent exception of dorzagliatin (Hua Medicine). A comprehensive approach using human islet perfusions, enzyme kinetics, x-ray crystallography, and modeling studies was applied to compare the effects of dorzagliatin with the failed GKA MK-0941 (Merck Pharmaceuticals), which is well-characterized both clinically and mechanistically. Dorzagliatin improves glucose stimulation of insulin secretion (GSIS) in a dose- and glucose-dependent manner, in contrast to MK-0941 which induces maximal insulin secretion at low doses and glucose concentrations. To understand these functional differences, the atomic resolution structure of the dorzagliatin-glucokinase (GK) complex was determined and compared with the GK/MK-0941 structure. MK-0941 binds to a pocket accessible in both open and closed conformations, has a strong interaction with Y214, mutation of which produces the most clinically severe activating mutation, and produces a high energy barrier for the open-to-close transition. In contrast, dorzagliatin only binds favorably to the closed form of glucokinase, interacting primarily with R63, and causing a low energy barrier for the open-to-close transition. This provides the molecular rationale for the clinical success of dorzagliatin which can guide the future development of next-generation allosteric activators of GK.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"25 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Closing the Gap Between Vision and Victory in Type 1 Diabetes: The NIDDK Human Islet Research Network (HIRN) Initiative","authors":"Audrey V. Parent, Ashutosh Agarwal, Juan Rene Alvarez-Dominguez, Rafael Arrojo e Drigo, Mark A. Atkinson, Michael A. Brehm, Leonardo M.R. Ferreira, Klaus H. Kaestner, Vira Kravets, Joyce C. Niland, Denis O’Meally, Layla Rouse, Holger A. Russ, Cherie L. Stabler, John S. Kaddis","doi":"10.2337/db25-0097","DOIUrl":"https://doi.org/10.2337/db25-0097","url":null,"abstract":"The identification of a “rundlichen Häuflein” by Paul Langerhans more than 150 years ago marked the initiation of a global effort to unravel the mysteries of pancreatic islets, an intricate system of nutrient-sensing, hormone-secreting, and signaling cells. In type 1 diabetes, this interconnected network is vulnerable to malfunction and immune attack, with strategies to prevent or repair islet damage still in their infancy. In 2014, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) established the Human Islet Research Network (HIRN) to accelerate our understanding of the molecular and cellular basis of type 1 diabetes development. In this article, investigators from the HIRN detail pioneering advances, technologies, and systems that contextualize insulin-producing β-cells and other related cells within their physiological environment. Disease models, devices, and therapies are evaluated by the HIRN in light of promising functional and mechanistic data. Collaborative relationships and opportunities within this network are emphasized as a means of enhancing the quality of innovative research and talent in science. Topics are developed through a series of questions, achievements, and milestones, with the 75th anniversary of the NIDDK as an opportunity to reflect on the past, present, and future of type 1 diabetes research. Article Highlights The Human Islet Research Network (HIRN) was created by the National Institute of Diabetes and Digestive and Kidney Diseases to accelerate pioneering basic and translational research on the prevention, development, and progression of type 1 diabetes. There are critical knowledge gaps in research on the processes underlying human β-cell protection, loss, and replacement in type 1 diabetes. A multidisciplinary and collaborative research community focused on outstanding biological questions propels the development of innovative models, tools, and technologies and helps contextualize the complexity of this disease. Discoveries arising from the HIRN will profoundly improve our understanding of type 1 diabetes pathogenesis and expedite the development of disease avoidance, diagnosis, and treatment strategies.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"10 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Celebrating the Past, Present, and Future of NIDDK-Supported Research Centers Focused on Diabetes, Endocrinology, and Metabolic Diseases","authors":"Corinne M. Silva, Pamela L. Thornton, Shavon Artis Dickerson, Thomas L. Eggerman, Maren R. Laughlin, Julie A. Wallace, Mary C. Hanlon-Tilghman, William T. Cefalu","doi":"10.2337/db25-0039","DOIUrl":"https://doi.org/10.2337/db25-0039","url":null,"abstract":"This year marks the 75th anniversary of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health. NIDDK’s long history of research and innovation includes support of four types of collaborative research centers focused on diabetes, endocrinology, and metabolic diseases. The Diabetes Research Centers promote basic and clinical diabetes research, while the Centers for Diabetes Translation Research conduct diabetes research across the translation science spectrum. The Mouse Metabolic Phenotyping Center (MMPC)-Live program provides the research community with standardized phenotyping services for mouse models of diabetes and obesity, and the Cystic Fibrosis Research and Translation Centers advance basic, preclinical, and clinical research for cystic fibrosis. These centers have evolved over time in response to new scientific opportunities and to expand their reach to be an asset to the larger scientific community. Looking to the future, NIDDK will continue to ensure that these centers enhance the research community, foster novel and synergistic scientific collaborations, and promote career development of scientists in the early stages of their careers. We will also ensure that our centers align with NIDDK’s goal of improving health outcomes for all people with and at risk for diseases, within our mission. Article Highlights NIDDK’s research centers focused on diabetes, endocrinology, and metabolism serve broad communities of investigators and address existing research gaps to propel scientific progress. The Diabetes Research Centers support basic and clinical research, and the Centers for Diabetes Translation Research support research across the translation science spectrum. The MMPC-Live program provides phenotyping services for mouse models of diabetes and obesity, and the Cystic Fibrosis Research and Translation Centers advance basic, preclinical, and clinical research for cystic fibrosis. Future goals for the centers include fostering novel and synergistic scientific collaborations, as well as continuing to promote career development.","PeriodicalId":11376,"journal":{"name":"Diabetes","volume":"37 1","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}