Acta Diabetologica最新文献

{"title":"Expression of long non-coding RNAs MALAT1, MEG3, and XIST in gestational diabetes mellitus: a cross-sectional study.","authors":"Bishal Kumar Dey, Sudipta Banerjee, Pieu Adhikary, Subhankar Chowdhury, Sanchita Roy, Subesha Basu Roy, Rana Bhattacharjee","doi":"10.1007/s00592-025-02581-5","DOIUrl":"https://doi.org/10.1007/s00592-025-02581-5","url":null,"abstract":"<p><strong>Background and aims: </strong>Gestational diabetes mellitus (GDM) is defined as glucose intolerance first identified during pregnancy that does not meet the criteria for overt diabetes. Its pathophysiology shares key features with type 2 diabetes mellitus (T2D), including insulin resistance and inflammation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) are implicated in T2D. This study investigates the gene expression of lncRNAs in GDM and explores their association with insulin resistance and proinflammatory cytokines.</p><p><strong>Materials and methods: </strong>This cross-sectional study included 25 GDM and 36 non-GDM (NGDM) participants from a tertiary care antenatal clinic. GDM was diagnosed using a 75 g oral glucose tolerance test (OGTT) based on the International Association of Diabetes and Pregnancy Study Groups criteria. MALAT1, MEG3, and XIST were selected for analysis due to their reported involvement in T2D. Their gene expression levels were quantified using real-time PCR, while serum concentrations of proinflammatory cytokines (TNF-α, IL-6, IL-1β) and glycemic markers (C-peptide, fasting insulin) were measured using ELISA.</p><p><strong>Results: </strong>MALAT1, MEG3, and XIST were significantly downregulated in the GDM group compared to the NGDM group (p < 0.01). In the GDM group, all three lncRNAs showed a significant negative correlation with Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) (MALAT1: r = -0.44, p = 0.03; MEG3: r = -0.46, p = 0.04; XIST: r = -0.45, p = 0.04). Additionally, MALAT1 gene expression negatively correlated with IL-6 (r = -0.49, p = 0.03) and TNF-α (r = -0.48, p = 0.04). MEG3 and XIST gene expression negatively correlated with IL-1β (r = -0.51 and - 0.50, p = 0.03 for both) and TNF-α (r = -0.47 and - 0.52, p = 0.04 and 0.03, respectively).</p><p><strong>Conclusion: </strong>MALAT1, MEG3, and XIST are downregulated in GDM, and their gene expression levels are negatively correlated with insulin resistance and select proinflammatory cytokines. These findings suggest a potential role for lncRNA downregulation in GDM pathogenesis, warranting further investigation.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incidence and causes of major amputation in patients with diabetic foot ulcers: data from a retrospective study.","authors":"Marco Meloni, Luigi Uccioli, Aikaterini Andreadi, Laura Giurato, Valeria Ruotolo, Maria Romano, Alessandro Minasi, Ermanno Bellizzi, Federico Rolando Bonanni, Martina Salvi, Alfonso Bellia, Davide Lauro","doi":"10.1007/s00592-025-02577-1","DOIUrl":"https://doi.org/10.1007/s00592-025-02577-1","url":null,"abstract":"<p><strong>Aim: </strong>The study aimed to evaluate the rate and causes of major amputation in patients with diabetic foot syndrome.</p><p><strong>Methods: </strong>The current study is a retrospective observational study including consecutive patients referred to a tertiary-level diabetic foot service from January 2020 to November 2023 due to a new diabetic foot problem requiring hospital admission. All patients had been managed by a multi-disciplinary diabetic foot team (MDFT) through a pre-set limb salvage protocol including the management of peripheral arterial disease, infection, foot offloading, and comorbidities. At 1 year of follow-up, the following outcomes measures were evaluated: rate of major amputation, clinical characteristics of amputees, and causes of major amputation.</p><p><strong>Results: </strong>Overall, 1226 patients referring for a diabetic foot problem and requiring hospitalization were screened for the study. Among them, 30 (2.4%) patients experienced major amputation. Amputees had 69.9±10.7 years, the majority were male (73.3%) with a prevalence of type 2 diabetes (93.3%) and a long diabetes duration (25.2±9.8 years). They showed several comorbidities such as ischaemic heart disease (83.3%), heart failure (46.7%), end-stage-renal-disease (26.7%), and in addition high rate of peripheral arterial disease (PAD) (86.7%), infected wounds (98.3%), and osteomyelitis (90%). Major amputation was mainly related to untreatable limb ischemia (failure of revascularization procedure) in 56.7% of cases, calcaneus osteomyelitis and necrotizing fasciitis in 16.7% of cases, and tarsal osteomyelitis in 10% of cases.</p><p><strong>Conclusions: </strong>The rate of major amputation was very low in this population managed by a MDFT. PAD was the main cause of major amputation.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144991257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of type 2 diabetes on aging: multidimensional approaches to preserve cognitive health.","authors":"Stefania Lucia, Silvia Fornaro, Massimo Federici, Raffaella Ida Rumiati","doi":"10.1007/s00592-025-02583-3","DOIUrl":"https://doi.org/10.1007/s00592-025-02583-3","url":null,"abstract":"<p><p>The growing prevalence of type 2 diabetes (T2D) among older adults represents a major public health concern, given its association with accelerated cognitive decline and increased risk of neurodegenerative diseases. Several diabetes-related mechanisms, including chronic hyperglycaemia, oxidative stress, vascular dysfunction, and insulin resistance in the brain, negatively impact key cognitive domains, including memory and executive functions. These neuropathophysiological alterations are also linked to structural brain changes, contributing to vulnerability to dementia. This narrative review examines both established and emerging strategies aimed at counteracting the cognitive impact of T2D in aging populations. Traditional interventions, especially structured physical activity programs, have consistently demonstrated benefits for global cognitive functioning. In parallel, new pharmacological treatments, such as GLP-1 receptor agonists (e.g., semaglutide), not only improve glycemic control but may also exert neuroprotective effects. Multidomain approaches integrating metabolic management, nutritional optimization, physical exercise, and social engagement, such as those tested in the J-MIND-Diabetes study, have yielded promising outcomes in preserving cognitive functions. We argue that combining pharmacological and behavioral strategies holds significant potential for supporting cognitive health in elderly individuals with T2D. Such multimodal interventions may enhance resilience to cognitive decline, improve quality of life, and promote healthy brain aging in this at-risk population.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum lipids changes following cocoa intake in type 2 diabetes patients: a graded dose-response systematic review and meta-analysis of clinical trials.","authors":"Razieh Anari, Houra Mohseni, Soudabe Motamed, Elham Anari, Reza Amani","doi":"10.1007/s00592-025-02554-8","DOIUrl":"https://doi.org/10.1007/s00592-025-02554-8","url":null,"abstract":"<p><strong>Introduction: </strong>Hyperlipidemia, a prevalent comorbidity among type 2 diabetes patients, is a potential risk factor for cardiovascular diseases. It is unclear whether cocoa has beneficial impacts on the serum lipids of patients with diabetes.</p><p><strong>Methods: </strong>PubMed, Scopus, and Embase databases were systematically reviewed for clinical trials on cocoa intake and blood lipids in type 2 diabetes until January 1, 2024, and the reference list of relevant articles was searched manually. Two reviewers extracted data and determined the risk of bias (RoB) using the Cochrane tool. The random effect model was applied to calculate standardized mean differences (SMDs). Finally, the certainty and clinical importance of the evidence were checked (PROSPERO registration code: CRD42021224931).</p><p><strong>Result: </strong>Eleven RCTs with 506 participants were included. Different forms of cocoa and various intervention durations were applied. Only two RCTs had a low RoB. Findings showed a significant reduction in serum triglyceride (SMD: - 0.57, 95% CI - 1.05, - 0.10, I²: 82.7%), but not in other blood lipids. There was a severe‎ heterogeneity in results justified with discrepancies in age, designs, durations, interventions, body mass index, baseline blood lipids, and risk of bias. The results showed low certainty and unimportant lipid changes.</p><p><strong>Conclusion: </strong>Although cocoa may slightly change serum lipids in diabetes, its recommendation for lipids control has fair clinical benefits. Due to the lack of certainty of findings and an inadequate number of studies, further well-designed trials considering possible sources of heterogeneity with low RoB are highly recommended.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum uric acid to HDL-Chol ratio (UHR) is associated with insulin resistance/sensitivity in individuals without diabetes.","authors":"Mariangela Rubino, Mattia Massimino, Elettra Mancuso, Carolina Averta, Angela Palummo, Maria Perticone, Elena Succurro, Angela Sciacqua, Gaia Chiara Mannino, Francesco Andreozzi","doi":"10.1007/s00592-025-02576-2","DOIUrl":"https://doi.org/10.1007/s00592-025-02576-2","url":null,"abstract":"<p><strong>Background: </strong>The uric acid-to-HDL cholesterol ratio (UHR) is a promising non-insulin-based marker for metabolic risk, associated with type 2 diabetes, hypertension, hepatic steatosis, and cardiovascular disease. However, its utility in individuals with altered glucose tolerance remains unclear.</p><p><strong>Methods: </strong>We investigated the relationship between UHR and insulin sensitivity in two independent cohorts. Sample 1 (n = 1555) from the CATAMERI study, was stratified based on oral glucose tolerance test (OGTT) results, and Sample 2 (n = 332) from the EUGENE2 project, with insulin sensitivity measured via euglycemic-hyperinsulinemic clamp.</p><p><strong>Results: </strong>In Sample 1, UHR showed positive correlations with BMI, triglycerides, 2-hour plasma glucose, HOMA-IR, fasting plasma insulin (p < 0.0001 for all) and with HbA1c (p < 0.001), and negative correlations with Matsuda index (p < 0.0001) and total cholesterol (p = 0.019). Multivariable linear regression identified HOMA-IR (β = 0.100), Matsuda index (β=-0.146), InsAUC30/GluAUC30 (β = 0.120), and Stumvoll 1st-phase insulin secretion (β = 0.121) as independent UHR predictors. In Sample 2, bivariate analyses, adjusted for age, sex, and BMI, confirmed positive correlations between UHR and HbA1c (p < 0.001), 2-hour post-load glucose (p = 0.001), BMI, triglycerides, and fasting insulin (p < 0.0001 for all) and a negative correlation with Clamp M (glucose disposal, p = 0.0003). Finally, multivariable regression of Clamp M variability (adjusted for age, sex, and BMI) demonstrated significant negative associations with UHR (β= -0.230) and BMI (β= -0.375).</p><p><strong>Conclusion: </strong>These findings suggest that UHR, derived easily and inexpensively from routine clinical measurements, is a promising indicator of metabolic risk in individuals without diabetes. Its accessibility positions it as a potential tool for early diabetes prevention strategies, potentially reducing reliance on the OGTT.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Educational programs and mental health outcomes in individuals with type 1 diabetes: a scoping review.","authors":"Ilaria Milani, Gani Antony Leonardo Carreno Dextre, Rolando Francesco Elisei, Paola Ripa, Stefano Romano Capatti, Arianna Magon, Silvia Cilluffo, Stefano Terzoni, Maura Lusignani, Monica Petralito, Rosario Caruso","doi":"10.1007/s00592-025-02580-6","DOIUrl":"https://doi.org/10.1007/s00592-025-02580-6","url":null,"abstract":"<p><strong>Background: </strong>Mental health is a critical yet often underemphasized dimension in the management of individuals with Type 1 Diabetes Mellitus (T1DM), who are at elevated risk for psychological disorders. Educational interventions, including traditional education, psychoeducational, and psychosocial programs, are increasingly recognized as supporting self-care and promoting psychological well-being.</p><p><strong>Aim: </strong>This scoping review aims to systematically map the existing literature on educational programs for individuals with T1DM, with a specific focus on their impact on mental health outcomes.</p><p><strong>Methods: </strong>The review was conducted according to the Joanna Briggs Institute (JBI) methodology and guided by the Population, Concept, and Context (PCC) framework. A comprehensive search was performed across six major biomedical databases (PubMed, Embase, CINAHL, Web of Science, Scopus, PsycINFO), including studies that examined educational interventions addressing mental health in individuals with T1DM.</p><p><strong>Results: </strong>A total of 18 studies were included, covering a range of educational interventions, such as digital tools, psychological therapies (e.g., ACT, CBT), and self-care interventions, most of which were delivered by multidisciplinary teams. Many interventions demonstrated positive effects on mental health, including reduced anxiety, enhanced mood, and improved self-management. Key facilitators included professional support, peer involvement, and the integration of psychological components. Barriers included high dropout rates and limited tailoring to age-specific needs.</p><p><strong>Conclusions: </strong>Educational interventions can positively influence mental health outcomes in individuals with T1DM. However, the literature remains fragmented, and program effectiveness varies. There is a pressing need for more flexible, personalized, and age-sensitive educational interventions that incorporate emotional and psychological support and address implementation challenges.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The L-type amino acid transporter inhibitor, BCH, inhibits myotube BCAA uptake and mitochondrial function without altering myotube insulin sensitivity during insulin resistance in C2C12 myotubes.","authors":"Kipton B Travis, Kayla J Ragland, Emmalie R Spry, Toheed Zaman, Pamela M Lundin, Roger A Vaughan","doi":"10.1007/s00592-025-02570-8","DOIUrl":"https://doi.org/10.1007/s00592-025-02570-8","url":null,"abstract":"<p><strong>Introduction: </strong>Branched-chain amino acids (BCAA) are essential nutrients involved in protein synthesis. BCAA are absorbed via the L-type amino acid transporter (LAT1) in skeletal muscle where the majority of BCAA are metabolized. Higher circulating BCAA levels have been shown to correlate with insulin resistance. Some speculate that enhanced BCAA metabolism/disposal or reduced BCAA uptake may limit BCAA-mediated anabolic signaling and possibly improve insulin sensitivity.</p><p><strong>Aims: </strong>This study investigated the effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), a LAT inhibitor, on metabolism and insulin sensitivity in a myotube model of insulin resistance. Because BCAA-mediated anabolic signaling has been linked with insulin resistance, we assessed if reduced BCAA uptake via LAT inhibition would improve insulin sensitivity.</p><p><strong>Methods: </strong>C2C12 myotubes were cultured in the presence and absence of insulin resistance and treated with and without BCH. Myotube metabolism was assessed via oxygen consumption, and associated gene and protein expression were assessed using qRT-PCR and Western blot, respectively. LC/MS was performed to assess the effect of each condition on extracellular BCAA accumulation.</p><p><strong>Results and conclusions: </strong>BCH treatment and insulin resistance both increased extracellular BCAA levels which was associated with reduced protein expression/activity of BCAA catabolic enzymes. Additionally, BCH and insulin resistance were both independently associated with reduced mitochondrial function which occurred without significant changes in mitochondrial biogenesis signaling. Importantly, BCH did not alter myotube viability or insulin sensitivity, suggesting reduced metabolism was not a function of reduced viability. These observations demonstrate that reduction of BCAA uptake may not improve insulin resistance and may promote mitochondrial dysfunction.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dapagliflozin sustains heart function in type 3 cardiorenal syndrome by restoring DUSP1-dependent mitochondrial quality control.","authors":"Zunyan Li, Ang Zhang, Huida Lu, Ying Jiang, Xiuling He, Hang Zhu, Hao Zhou","doi":"10.1007/s00592-025-02579-z","DOIUrl":"https://doi.org/10.1007/s00592-025-02579-z","url":null,"abstract":"<p><strong>Aims: </strong>This study tested the hypothesis that the anti-diabetes drug dapagliflozin (DAPA) alleviates heart dysfunction induced by type 3 cardiorenal syndrome (CRS-3) by normalizing mitochondrial quality control (MQC). MQC is a stress-activated mechanism, regulated by Dual specificity phosphatase 1 (DUSP1), that maintains mitochondrial homeostasis to support heart function. Due to its known renal and cardioprotective effects, DAPA was investigated as a potential treatment for CRS-3.</p><p><strong>Methods: </strong>CRS-3 was induced in mice through renal ischemia/reperfusion. The effects of DAPA pre-treatment were assessed by measuring heart function, serum levels of myocardial injury biomarkers, oxidative stress, inflammation, and cardiomyocyte apoptosis. Assays in cardiomqyocytes from CRS-3 mice were used to analyze MQC, including mitochondrial dynamics, mitophagy, and biogenesis. The role of DUSP1 was investigated using DUSP1-knockout mice, and a docking analysis was performed to assess the DAPA-DUSP1 interaction.</p><p><strong>Results: </strong>DAPA pre-treatment dose-dependently improved heart function and reduced serum markers of myocardial injury, oxidative stress, inflammation, and cardiomyocyte apoptosis in CRS-3 mice. DAPA treatment stabilized MQC in cardiomyocytes, shown by improved mitochondrial dynamics and restored mitophagy and biogenesis. Docking analysis suggested that DAPA directly interacts with DUSP1 and suppresses its nuclear translocation. Notably, in DUSP1-knockout mice, the stabilizing effect of DAPA on MQC was abolished. Furthermore, upon DUSP1 deletion, DAPA failed to prevent CRS-3-related oxidative stress, inflammation, apoptosis, and heart dysfunction.</p><p><strong>Conclusions: </strong>Defective MQC critically contributes to CRS-3-related myocardial dysfunction. The study proposes that DAPA therapy may normalize DUSP1-dependent MQC and consequently alleviate the cardiac depression associated with CRS-3.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased expression of OX40 on peripheral CD4⁺/CD8⁺ memory T lymphocytes in the pathogenesis of type 1 diabetes.","authors":"Xingxing Fang, JiaJia Chen, Ling Lin, Feng Xu, Chen Fang, Ji Hu, Yimei Shan, Cuiping Liu","doi":"10.1007/s00592-025-02574-4","DOIUrl":"https://doi.org/10.1007/s00592-025-02574-4","url":null,"abstract":"<p><strong>Aims: </strong>Autoreactive memory T cells are considered to be a primary contributor to chronic islet inflammation in individuals with type 1 diabetes (T1D). OX40-expressing T cells not only facilitate and sustain the presence of CD4⁺ memory T cells but also promote the generation of CD8⁺ memory T cells. We aimed to investigate the role of OX40⁺CD4⁺/CD8⁺ memory T lymphocytes in the pathogenesis of T1D.</p><p><strong>Methods: </strong>A total of 35 patients diagnosed with Type 1 diabetes and 40 healthy control individuals were enrolled in this study. Peripheral Blood Mononuclear Cells (PBMCs) were isolated from the study participants and analyzed by flow cytometry. Inflammatory cytokines in the plasma were quantitatively measured. The pancreatic islet autoantibodies as well as islet function were also evaluated.</p><p><strong>Results: </strong>The frequencies and the mean fluorescence intensity (MFI) of OX40 on CD4⁺  effector memory T (Tem) cells significantly increased in patients with T1D compared to healthy controls. Importantly, the expression of OX40 on CD8⁺ Tem and central memory T (Tcm) cells was also significantly higher in T1D compared with healthy controls. However, the expression of OX40 on CD4⁺ Tem cells was not significantly higher in T1D with two or more autoantibodies than control group. Furthermore, the frequencies of OX40⁺CD8⁺ Tem cells significantly increased in T1D patients with two or more autoantibodies but not in those with one autoantibody, compared with control groups. Meanwhile, the frequencies of OX40⁺CD8⁺ Tcm cells were consistently higher across all three subgroups of T1D patients (AAb^-, 1AAb, ≥2AAb) compared to the control group. Notably, both the frequencies of OX40⁺CD4⁺ and OX40⁺CD8⁺ Tem cells exhibited significant negative correlations with the serum C-peptide levels in T1D patients. Additionally, the expression levels of OX40 on peripheral CD4⁺/CD8⁺ memory T cells were positively correlated with the levels of plasma inflammatory cytokines in patients with T1D.</p><p><strong>Conclusions: </strong>The elevated expression of OX40 on CD4⁺/CD8⁺ memory T cells was associated with the autoimmune-mediated destruction of islet beta cells in T1D. Our findings indicate that the expression levels of OX40 on peripheral CD4⁺ and CD8⁺ memory T lymphocytes may serve as potential predictive biomarkers for the severity of T1D. Additionally, OX40 expression on memory T cells may serve as a potential biomarker for assessing the efficacy of immunotherapy in T1D patients.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144937995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic challenges of glucose and lipid dysregulation in psoriatic arthritis: a narrative review from pathogenesis to clinical practice.","authors":"Mauro Fatica, Sara Ferrigno, Eneida Çela, Arianna D'Antonio, Paola Conigliaro, Marina Cardellini, Susanna Longo, Massimo Federici, Maria Sole Chimenti","doi":"10.1007/s00592-025-02565-5","DOIUrl":"https://doi.org/10.1007/s00592-025-02565-5","url":null,"abstract":"<p><p>Emerging evidence highlights a complex interconnection between metabolic dysfunction and chronic inflammation in psoriatic arthritis (PsA), positioning glucose and lipid abnormalities not only as comorbidities but as active contributors to disease pathogenesis. In fact, rather than being incidental findings, conditions such as insulin resistance, atherogenic dyslipidemia, and visceral obesity interact with the immune system, amplifying inflammatory circuits and promoting joint and systemic damage. This review delves into the metabolic dimension of PsA, shedding light on how pro-inflammatory cytokines and adipokine imbalances reshape glucose and lipid homeostasis. Special attention is given to molecular pathways, such as impaired insulin signaling and altered lipid uptake, that link systemic inflammation to cardiometabolic risk. Furthermore, we examine the impact of these metabolic alterations in clinical practice and how antirheumatic therapies might improve metabolic balance and promote long-term cardiovascular protective effects. By unraveling these interactions, we aim to provide new insights into the clinical management of PsA and underscore the need for integrated therapeutic strategies that address both inflammation and metabolic health.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144854198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}