Diabetologia最新文献

{"title":"A GLP-1 receptor agonist enhances islet microvascular flow through nitric oxide-dependent mechanisms in a diabetic mouse model: investigation using intravital two-photon imaging.","authors":"Tomohiko Kimura, Kengo Kidokoro, Yuichiro Iwamoto, Hideyuki Iwamoto, Toshitomo Sugisaki, Takashi Itoh, Yoshiro Fushimi, Junpei Sanada, Masashi Shimoda, Shuhei Nakanishi, Kohei Kaku, Naoki Kashihara, Hideaki Kaneto","doi":"10.1007/s00125-026-06825-z","DOIUrl":"10.1007/s00125-026-06825-z","url":null,"abstract":"<p><strong>Aims/hypothesis: </strong>Impaired regulation of islet microvascular blood flow has been implicated in beta cell dysfunction in diabetes; this dysregulation is linked to endothelial dysfunction with reduced nitric oxide bioavailability. However, dynamic regulation of islet microvascular flow has not been directly examined in vivo. We hypothesised that acute pharmacological activation of the glucagon-like peptide-1 receptor (GLP-1R) rapidly enhances islet microvascular flow through NO-dependent mechanisms under diabetic conditions.</p><p><strong>Methods: </strong>Islet microvascular dynamics were visualised in vivo using intravital two-photon microscopy in mice with hyperglycaemia induced by multiple low doses of streptozocin (STZ), which represents a model of beta cell dysfunction, and in normoglycaemic controls. Acute vascular responses to the GLP-1R agonist liraglutide were quantified by measuring peri-islet vascular volume fraction and erythrocyte velocity, with or without inhibition of nitric oxide synthase using Nω-nitro-L-arginine methyl ester (L-NAME). To assess the physiological relevance of the results, a subset of diabetic mice received chronic liraglutide treatment, followed by analyses of islet hypoxia and beta cell function.</p><p><strong>Results: </strong>Acute liraglutide administration in the diabetic mice rapidly increased peri-islet vascular volume fraction (p=0.010) and erythrocyte velocity (p=0.003). These vascular responses were completely abolished by treatment with L-NAME, and were absent in normoglycaemic mice, indicating a diabetes-specific, NO-dependent microvascular response. Chronic liraglutide treatment was associated with reduced islet hypoxia and improved glucose-stimulated insulin secretion (p=0.042), supporting the physiological relevance of acute microvascular enhancement.</p><p><strong>Conclusions/interpretation: </strong>Acute pharmacological activation of the GLP-1R rapidly enhances NO-dependent islet microvascular flow specifically under diabetic conditions. This previously unrecognised in vivo vascular response indicates dynamic regulation of the islet microenvironment by GLP-1R signalling, and suggests that rapid microvascular adaptation may contribute to preservation of beta cell function during metabolic stress.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"3273-3287"},"PeriodicalIF":10.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683654","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":"Is MASLD an independent risk factor for micro- and macrovascular complications of diabetes? A critical reappraisal and future directions.","authors":"Sabine Kahl, Cyrielle Caussy, Kenneth Cusi","doi":"10.1007/s00125-026-06817-z","DOIUrl":"10.1007/s00125-026-06817-z","url":null,"abstract":"<p><p>Recent awareness that metabolic dysfunction-associated steatotic liver disease (MASLD) is a common liver condition in individuals with type 2 diabetes and carries a significant risk of cirrhosis and extrahepatic disease has called for an examination of its relationship with diabetes-related complications. MASLD, especially at-risk steatohepatitis (metabolic dysfunction-associated steatohepatitis [MASH]) with significant fibrosis ≥F2, shares many metabolic abnormalities with type 2 diabetes, including insulin resistance, gluco- and lipotoxicity, chronic subclinical inflammation and mitochondrial impairment. In addition, many cross-sectional and longitudinal observational studies suggest an association between MASLD and micro- and macrovascular complications of type 1 and type 2 diabetes. However, a causal pathogenic relationship has been difficult to confirm given the overlap of cardiometabolic risk factors (CMRFs) in MASLD and type 2 diabetes. Complicating matters further, most of the available evidence has significant limitations. These include shortcomings in participant selection, heterogeneity in study design, use of diagnostic tools with low sensitivity for liver disease and diabetes-related complications, inadequate control for alcohol consumption or CMRFs, and lack of repeat measurements during longitudinal studies. Nevertheless, current evidence suggests that MASLD is a 'risk enhancer' for both micro- and macrovascular disease in diabetes, rather than an independent risk factor. Here, we review the underlying mechanistic pathways and clinical evidence that appear to link both conditions and identify knowledge gaps in need of future research. Until more robust evidence emerges, we hope that a greater awareness about the link between MASLD and diabetes-related micro- and macrovascular complications will prompt clinicians to educate their patients and peers on the potentially heightened health risks of MASLD and encourage clinicians to take a more proactive approach to risk stratification and intervention.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"3175-3195"},"PeriodicalIF":10.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148653205","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":"Pharmacological treatment of MASH.","authors":"Norbert Stefan, Giovanni Targher","doi":"10.1007/s00125-026-06796-1","DOIUrl":"10.1007/s00125-026-06796-1","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) includes a spectrum of progressive liver conditions ranging from isolated steatosis to metabolic dysfunction-associated steatohepatitis (MASH), advanced fibrosis and cirrhosis. Currently, MASLD is the leading cause of chronic liver disease worldwide. MASLD is strongly associated with type 2 diabetes, cardiovascular disease, chronic kidney disease and certain extrahepatic cancers. MASLD shares a common pathogenesis with cardiometabolic diseases, especially type 2 diabetes, primarily driven by unhealthy dietary habits, dysfunctional adipose tissue, insulin resistance and low-grade inflammation. Substantial heterogeneity in the pathophysiology of MASLD may influence its rate of progression, its relationship with cardiometabolic diseases and its treatment response. In addition to lifestyle interventions, including a healthy low-energy diet and increased physical activity levels, pharmacological treatment of MASLD/MASH is recommended. For individuals with type 2 diabetes and MASLD/MASH, treatment should preferably include glucagon-like peptide-1 (GLP-1) receptor agonist-based therapies and sodium-glucose cotransporter 2 (SGLT2) inhibitors, which have been shown to improve MASLD/MASH and provide established cardiorenal benefits. In this narrative review, we assess the efficacy of these pharmacotherapies and discuss other treatment approaches for MASLD/MASH, with a focus on their metabolic benefits.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"3148-3161"},"PeriodicalIF":10.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13627253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Screening and diagnosis of liver disease in diabetes: a guide and evidence-based assessment.","authors":"Sami F Qadri","doi":"10.1007/s00125-026-06816-0","DOIUrl":"10.1007/s00125-026-06816-0","url":null,"abstract":"<p><p>Most people with type 2 diabetes have metabolic dysfunction-associated steatotic liver disease (MASLD), yet fewer than 2% experience major adverse liver outcomes within 10 years. Because progression to end-stage liver disease is uncommon, identifying the small subset of individuals at highest risk remains a central clinical challenge. Liver fibrosis is the strongest prognostic determinant in MASLD, and a range of blood-based and imaging tests are used to assess the likelihood of advanced fibrosis (AF) in the clinic. Since 2023, major medical societies have recommended systematic screening for MASLD-related AF in individuals with type 2 diabetes, driven by reports suggesting a high prevalence of up to 20-40%. This review critically examines the evidence underlying these recommendations while providing a clinically oriented guide to diagnosing MASLD in type 2 diabetes. Re-analysis of data from prevalence studies suggests that the burden of AF in type 2 diabetes has been substantially overestimated and may be below 5-10%, which has profound implications for both the rationale for screening and its expected yield. Simulations and emerging real-world evidence suggest that current non-invasive tests may refer 30-50% of patients for costly second-line testing and 15% for specialist evaluation, while generating high false-positive rates and missing more than a third of all AF cases. Moreover, it remains uncertain whether diagnosing AF in type 2 diabetes currently leads to meaningful changes in management or outcomes. Existing cost-effectiveness analyses rely on assumptions about disease burden and therapeutic benefit that are not supported by available data. Together, these considerations call for a more rigorous, evidence-based approach to evaluating liver disease risk in type 2 diabetes and other populations.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"3048-3072"},"PeriodicalIF":10.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13627240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCKBR signalling controls human definitive endoderm specification and pancreatic lineage differentiation","authors":"Lama Saber, Kei Kozawa, Christos Karampelias, Changying Jing, Jessica Jaki, Melis Akgün Canan, Michael Sterr, Osvaldo Rodrigues Pereira, Oliver Czarnecki, Gregory S. Korbutt, Andrew R. Pepper, Noel Moya, Ingo Burtscher, Heiko Lickert, Mostafa Bakhti","doi":"10.1007/s00125-026-06905-0","DOIUrl":"https://doi.org/10.1007/s00125-026-06905-0","url":null,"abstract":"Aims/hypothesis Paracrine signalling by hormone-producing endocrine cells potentially influences pancreatic development, but this feedback regulation remains poorly understood. Here, we investigated the roles of gastrin (GAST), cholecystokinin (CCK) and their receptor cholecystokinin B receptor (CCKBR) during human pancreatic development. Methods Human iPSCs were differentiated stepwise into definitive endoderm and then the pancreatic endocrine lineage. To assess CCKBR function, CRISPR/Cas9 was used to generate CCKBR-knockout iPSC lines. We profiled transcriptional states by bulk and single-cell RNA-seq with computational analyses, and complemented these with biochemical assays, flow cytometry (FACS) and confocal microscopy. Results <jats:italic>CCKBR</jats:italic> expression peaked during definitive endoderm formation and progressively declined during differentiation, remaining detectable in pancreatic progenitors but largely absent from the endocrine lineage. By contrast, GAST and CCK were expressed only transiently during pancreatic progenitor and endocrine lineage formation. Pharmacological activation/inhibition and genetic knockout implicated CCKBR signalling during definitive endoderm formation. Consistently, bulk RNA-seq indicated that CCKBR deletion triggered ectodermal- and mesodermal-associated transcriptional programs and diminished pancreatic lineage specification. During pancreatic induction and lineage formation, sustained CCKBR activation with GAST or CCK attenuated endocrinogenesis and promoted epithelial structure formation. Further analysis revealed the emergence of a pancreatic ductal-like cell formation under prolonged CCKBR stimulation. Conclusions/interpretation This study provides mechanistic evidence that the GAST/CCK–CCKBR axis is functionally important during human endoderm and pancreas development. This pathway is repeatedly required during in vitro pluripotent stem cell differentiation, regulating germ-layer formation as well as ductal vs endocrine fate decisions. These findings support the optimisation of pancreatic differentiation protocols and inform future studies on whether this axis contributes to human pancreas development and disease.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"75 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149226036","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":"Renal tubule-specific Nrf2 deletion ameliorates diabetic kidney disease by attenuating glomerular hypertension and kidney injury in a mouse model of diabetes","authors":"Ke Su,Jing Zhou,Yuchao Pang,Shiao-Ying Chang,Min-Chun Liao,Wen-Xia Yang,Shuiling Zhao,Junzheng Peng,Daniel N. Leal,Michifumi Yamashita,Kana N. Miyata,Janos G. Filep,Julie R. Ingelfinger,Shao-Ling Zhang,John S. D. Chan","doi":"10.1007/s00125-026-06897-x","DOIUrl":"https://doi.org/10.1007/s00125-026-06897-x","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"22 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149208752","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":"Prediabetes subtype-based stratification reveals distinct long-term risks for type 2 diabetes","authors":"Hun Jee Choe,Wonsuk Choi,Howard H. Chang,Dimple Kondal,K. M. Venkat Narayan,Joon Ho Moon,Nam H. Cho","doi":"10.1007/s00125-026-06866-4","DOIUrl":"https://doi.org/10.1007/s00125-026-06866-4","url":null,"abstract":"Abstract Aims/hypothesis Prediabetes is heterogeneous, with subtypes defined by impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or HbA 1c , each with different risks of progression to type 2 diabetes. We compared progression across these subtypes, and evaluated the benefit of adding insulin secretion and sensitivity to risk stratification. Methods We analysed 7186 Korean adults aged 40–69 years from the community-based Korean Genome and Epidemiology Study, who were followed for up to 20 years with biennial (every 2 years) oral glucose tolerance tests and HbA 1c . Prediabetes was classified as IFG, IGT or HbA 1c -defined, and further stratified by insulinogenic index (IGI) and insulin sensitivity index (ISI). Cox regression was used to estimate diabetes risk, and multistate Markov models were used to assess annual transition probabilities and time spent in each state. Results Compared with normoglycaemia, the adjusted hazard ratios (aHRs) were 5.84 (95% CI 5.03, 6.79) for IFG, 4.60 (95% CI 4.17, 5.07) for IGT, and 4.68 (95% CI 4.22, 5.19) for HbA 1c -defined prediabetes. The risk increased stepwise with the number of criteria met: the aHRs were 3.10 (95% CI 2.81, 3.41) for one criterion, 7.33 (95% CI 6.50, 8.28) for two criteria, and 15.3 (95% CI 12.2, 19.3) for all three. Markov models showed the shortest prediabetes duration (1.7 years) and lowest regression probability (5.4%) in those meeting all three criteria. Low IGI or ISI predicted higher diabetes risk, and dual impairment conferred greatest risk (aHR 4.06; 95% CI 3.37, 4.90). Even normoglycaemic individuals with low IGI or ISI had an elevated risk of diabetes compared to those with high IGI or ISI. Conclusions/interpretation Diabetes progression differs based on both glycaemic subtype and physiological subtype. Integrating IGI and ISI with conventional definitions enhances risk stratification and may help to identify high-risk individuals for earlier targeted intervention.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"50 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149208751","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":"Up Front.","authors":"","doi":"10.1007/s00125-026-06907-y","DOIUrl":"https://doi.org/10.1007/s00125-026-06907-y","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":""},"PeriodicalIF":10.4,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215353","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":"Evolving phenotype of newly diagnosed type 2 diabetes: a 15-year population-based comparison.","authors":"Dani Kirshner, Michael Hauzer","doi":"10.1007/s00125-026-06901-4","DOIUrl":"https://doi.org/10.1007/s00125-026-06901-4","url":null,"abstract":"<p><strong>Aims/hypothesis: </strong>Our aim was to describe the phenotype at diagnosis and the early therapeutic profile of newly diagnosed type 2 diabetes across two periods spanning approximately 15 years within the same integrated healthcare system.</p><p><strong>Methods: </strong>This retrospective cohort study used electronic health record data from Clalit Health Services (Haifa & Western Galilee, Israel). Adults with incident type 2 diabetes in 2005-2008 (period 1: n=80,201) were compared with those diagnosed in 2020-2023 (period 2: n=101,392). Between-period differences are presented as crude estimates, with an age-stratified sensitivity analysis, and quantified using standardised mean differences (SMDs; values ≥0.20 indicate at least a small effect) alongside non-parametric and χ² tests.</p><p><strong>Results: </strong>The median age at diagnosis increased from 63.0 to 66.7 years between the two periods; the proportion aged ≥85 years nearly doubled (from 3.5% to 6.6%). The score for the Charlson comorbidity index increased from 4 to 6 (SMD 0.48); metabolic dysfunction-associated steatotic liver disease (MASLD) increased from 4.4% to 18.6%. HbA_1c at diagnosis decreased from 56 to 53 mmol/mol (7.3% to 7.0%); pre-diagnosis LDL-cholesterol decreased from 2.90 to 2.21 mmol/l (SMD 0.65). Within 31-90 days of diagnosis, use of sodium-glucose cotransporter 2 (SGLT2) inhibitors increased from 0.07% to 15.0%, use of glucagon-like peptide-1 receptor agonists (GLP-1RAs) increased from 0% to 11.1%, and sulfonylurea use decreased more than fourfold (20.8% to 4.5%).</p><p><strong>Conclusions/interpretation: </strong>The phenotype of newly diagnosed type 2 diabetes has been fundamentally restructured since 2008: patients are older with a higher comorbidity burden but present with better glycaemic and lipid management, with the latter reflecting statin therapy already established before diagnosis. MASLD has emerged as a major but largely ascertainment-driven comorbidity. The shift to SGLT2 inhibitors and GLP-1RAs alongside declining sulfonylurea use indicates displacement of glucose-centric strategies by a cardiorenal- and weight-driven paradigm. These findings indicate a need for age-appropriate management and trials enrolling very elderly patients.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":""},"PeriodicalIF":10.4,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206628","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":"Altered glucagon and GIP responses in South Asian versus Nordic women after gestational diabetes mellitus.","authors":"Archana Sharma, Sindre Lee-Ødegård, Jens Juul Holst, Bolette Hartmann, A Anita S Kvist, Elisabeth Qvigstad, Stina T Sollid, Ingrid Nermoen, Kåre I Birkeland","doi":"10.1007/s00125-026-06898-w","DOIUrl":"https://doi.org/10.1007/s00125-026-06898-w","url":null,"abstract":"<p><strong>Aims/hypothesis: </strong>We aimed to compare ethnic differences in levels of glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) following a pregnancy complicated by gestational diabetes mellitus (GDM), and to assess whether the higher insulin levels observed in South Asian compared with Nordic women could be explained by differences in the hormone secretory responses.</p><p><strong>Methods: </strong>We measured glucagon, GIP and GLP-1 in 178 South Asian and 107 Nordic women during an OGTT, and stratified participants by glycaemic status. Glucagon and total GLP-1 and GIP responses when fasting and post-OGTT were assessed by linear mixed models. Ethnic differences in incretin and glucagon levels were evaluated by linear regression analyses. Pre-hepatic insulin levels were estimated using deconvolution of C-peptide kinetics.</p><p><strong>Results: </strong>Ethnic differences in glucagon and incretin levels varied by glycaemic status. In the normoglycaemic South Asian group, early (0-15 min) glucagon suppression post-OGTT was significantly attenuated compared with the Nordic group (p=0.002). Fasting glucagon levels did not differ (p=0.139), but total glucagon exposure (including fasting levels) was higher in South Asian women (p=0.013). No differences in GIP and GLP responses to the OGTT were observed (p=0.490 and p=0.802). In women with prediabetes or diabetes, fasting glucagon was higher in the South Asian group (p=0.010), but there were no significant differences in early glucagon suppression post-OGTT (p=0.986). GIP responses to the OGTT were lower among South Asian women (p<0.001), despite higher insulin responses compared with the Nordic women. GLP-1 responses did not differ between the ethnic groups (p=0.661). The higher pre-hepatic insulin levels in South Asian vs Nordic normoglycaemic women were not associated with differences in incretin levels, but were associated with lower insulin sensitivity in the regression analyses (p<0.001).</p><p><strong>Conclusions/interpretation: </strong>When examined 1-3 years post-GDM, normoglycaemic South Asian women had less early glucagon suppression and higher total glucagon exposure post-OGTT compared with Nordic women. The higher pre-hepatic insulin levels were not associated with higher incretin levels, but were associated with lower insulin sensitivity.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":""},"PeriodicalIF":10.4,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206647","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}