Acta Diabetologica最新文献

{"title":"7-Ketocholesterol-induced oxidative stress impairs insulin secretion in pancreatic β-cells.","authors":"Wenjing Zhang, Jiahua Wu, Yuchen Zhao, Nan Wu, Shuiya Sun, Sunyue He, Xihua Lin, Jiaqiang Zhou","doi":"10.1007/s00592-026-02781-7","DOIUrl":"https://doi.org/10.1007/s00592-026-02781-7","url":null,"abstract":"<p><strong>Aims: </strong>Glucolipotoxicity-induced β-cell dysfunction is a key factor in the pathogenesis of type 2 diabetes (T2D). While cholesterol is known to contribute to this dysfunction, the specific role of its major oxidation product, 7-ketocholesterol, remains unclear.</p><p><strong>Methods: </strong>We quantified serum 7-ketocholesterol levels using UPLC-MS in a cohort comprising individuals with T2D and normal glucose tolerance (NGT). Using INS-1 cells and primary islets, we investigated the effects of 7-ketocholesterol on β-cell function (including glucose-stimulated insulin secretion [GSIS], perfusion and calcium dynamics) and the underlying mechanisms related to oxidative stress (reactive oxygen species [ROS], mitochondrial membrane potential [MMP], ATP) and gene/protein expression. The antioxidant N-Acetyl-L-cysteine (NAC) was employed to rescue the observed dysfunction.</p><p><strong>Results: </strong>Cohort analysis showed serum 7-ketocholesterol levels were significantly elevated in T2D patients compared to NGT controls (0.070 ± 0.035 vs. 0.051 ± 0.021 µmol/L), and this elevation correlated negatively with early-phase insulin secretion. In INS-1 cells and primary islets, 7-ketocholesterol exposure impaired GSIS and disrupted intracellular calcium signaling. Furthermore, 7-ketocholesterol induced marked oxidative stress, characterized by increased ROS production, loss of MMP, and reduced ATP levels. Mechanistically, 7-ketocholesterol promoted NRF2 nuclear translocation and upregulated the expression of antioxidant genes, including Gpx4 and Sod1. Critically, co-treatment with NAC attenuated 7-ketocholesterol-induced oxidative stress and restored insulin secretion and calcium signaling.</p><p><strong>Conclusion: </strong>Our findings suggest that elevated 7-ketocholesterol is associated with β-cell dysfunction in T2D patients and appears to impair insulin secretion by inducing oxidative stress in pancreatic β-cells, positioning 7-ketocholesterol as a potential contributor to diabetes progression.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148885846","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":"Load-capacity index and cardiometabolic risk: a longitudinal meta-analysis.","authors":"Naseem Eisa, Omar Barood","doi":"10.1007/s00592-026-02780-8","DOIUrl":"https://doi.org/10.1007/s00592-026-02780-8","url":null,"abstract":"<p><strong>Aims: </strong>The load-capacity index (LCI), defined as the ratio of fat mass to fat-free mass, represents a novel composite biomarker integrating metabolic load and functional capacity. This systematic review and meta-analysis aimed to determine the longitudinal association between LCI and incident cardiometabolic disease risk.</p><p><strong>Methods: </strong>We systematically searched PubMed, Embase, Web of Science, Cochrane Central, and Scopus from inception through January 2026 for longitudinal cohort studies reporting the association between LCI and cardiometabolic outcomes. Random-effects meta-analysis was performed using the DerSimonian-Laird method. Heterogeneity was assessed using Cochran's Q, τ², and I² statistics. Study-specific log(HR) values and standard errors are reported in the Supplementary Material to enable full reproducibility.</p><p><strong>Results: </strong>Eighteen longitudinal cohort studies comprising 129,777 participants and 5647 cardiometabolic events were included (mean follow-up: 11.4 years). Higher LCI was significantly associated with increased cardiometabolic risk (pooled HR = 1.174, 95% CI: 1.145-1.204; p < 0.0001). There was low between-study heterogeneity (I² = 11.6%; Cochran's Q = 19.22, df = 17, p = 0.3159; τ² = 0.000347). The association was consistent across age groups, sex, and body composition assessment methods (p-interaction > 0.05 for all). LCI provided incremental predictive value beyond established risk factors (NRI: 0.15-0.28; ΔC-statistic: 0.025-0.041).</p><p><strong>Conclusions: </strong>Higher LCI is independently and consistently associated with increased cardiometabolic disease risk across diverse populations (HR = 1.174, corresponding to a 17.4% increased risk per unit increase). LCI provides clinically meaningful incremental predictive value and warrants consideration as a robust supplementary tool to guide preventive interventions.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148885964","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":"Effects of dapagliflozin on proteinuria, glycemic control, and treatment burden in diabetic kidney transplant recipients: a matched cohort study.","authors":"Zeynep Ural, Ulver Derici","doi":"10.1007/s00592-026-02792-4","DOIUrl":"https://doi.org/10.1007/s00592-026-02792-4","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Aims: &lt;/strong&gt;Diabetes mellitus and persistent proteinuria are major determinants of cardiovascular morbidity, graft dysfunction, and mortality after kidney transplantation. Although sodium-glucose cotransporter-2 (SGLT2) inhibitors have demonstrated substantial cardiorenal benefits in chronic kidney disease, data regarding their use in kidney transplant recipients remain limited. This study aimed to evaluate the clinical effects of dapagliflozin on proteinuria, graft function, glycemic measures, treatment burden, and observed safety events in diabetic kidney transplant recipients.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We conducted an exploratory retrospective 1:1 clinically matched cohort study of diabetic kidney transplant recipients followed between 2010 and 2022. Among 282 transplant recipients, 68 had diabetes mellitus. Eighteen patients initiated dapagliflozin 10 mg/day and were included in the all-treated tolerability cohort; three discontinued treatment before completing 3 months because of patient preference unrelated to documented adverse events, leaving 15 recipients who received dapagliflozin for at least 12 months in the efficacy cohort. Fifteen diabetic kidney transplant recipients not receiving SGLT2 inhibitor therapy were selected as 1:1 clinically matched comparable controls according to prespecified matching criteria. Primary outcomes were changes in proteinuria and eGFR. Secondary outcomes included HbA1c, fasting plasma glucose, insulin requirements, antihypertensive medication burden, and observed safety events.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Thirty diabetic kidney transplant recipients were included in the 12-month efficacy analysis (15 dapagliflozin-treated recipients and 15 1:1 clinically matched comparable controls). Baseline demographic, transplant-related, renal, and glycemic characteristics were broadly comparable between groups. Proteinuria decreased more in the dapagliflozin group than in controls (median change, - 157 [- 310 to - 52] vs. -12 [- 48 to + 25] mg/day; Hodges-Lehmann location-shift estimate, - 171 mg/day; 95% CI, - 310 to - 32; p = 0.009), while eGFR remained stable (between-group difference in ΔeGFR, + 1.6 mL/min/1.73 m²; 95% CI, - 1.8 to + 5.0; p = 0.31). HbA1c decreased from 8.10% (65 mmol/mol) to 7.10% (54 mmol/mol) in the dapagliflozin group, whereas it decreased from 8.18% (66 mmol/mol) to 7.80% (62 mmol/mol) in controls. Greater reductions were also observed in fasting plasma glucose and daily insulin dose. Two urinary tract infections requiring oral antibiotics occurred in the dapagliflozin group and one in controls. No genital infections, diabetic ketoacidosis, acute rejection, graft loss, cardiovascular events, severe infections requiring hospitalization, or deaths were observed.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;In this exploratory 1:1 clinically matched cohort of selected diabetic kidney transplant recipients, dapagliflozin use was associated with reduced proteinuria, improved glycemi","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863432","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":"Exploring the therapeutic response to sodium-glucose cotransporter-2 inhibition in INSR-related insulin resistance monogenic diabetes: case-based analysis and narrative review.","authors":"David Franklin, Jan Mahony, Chirag Patel, Jessica Triay","doi":"10.1007/s00592-026-02795-1","DOIUrl":"https://doi.org/10.1007/s00592-026-02795-1","url":null,"abstract":"<p><strong>Background: </strong>INSR-related insulin resistance is a form of monogenic diabetes caused by pathogenic variants in the INSR gene, resulting in impaired insulin receptor signalling and a spectrum of insulin resistance. Conventional diabetes management strategies relying on insulin sensitisation or augmentation are often less effective and evidence to guide treatment in those with heterozygous INSR mutations remains limited.</p><p><strong>Index case analysis: </strong>A 63-year-old male diagnosed with type 2 diabetes aged 40 presented with a relatively stable fasting glucose and disproportionate postprandial hyperglycaemia despite prandial insulin. He had bilateral asymmetric mixed hearing loss (conductive/sensorineural) and early cardiovascular disease. C-peptide was preserved at 1.3 nmol/L with serum glucose at 7.1 mmol/L. Monogenic diabetes genetic testing identified a heterozygous likely pathogenic variant (i.e. mutation) in INSR (c.3473G > A, (p.Arg1158Gln)). Treatment with a sodium-glucose cotransporter-2 inhibitor (SGLT2 inhibitor) achieved 78% time-in-range (TIR). Subsequent SGLT2 inhibitor withdrawal for four months due to pyelonephritis led to TIR deterioration to 2% despite intensified basal insulin. Berberine initiation produced modest improvement (TIR 24%). Following re-introduction of the SGLT2 inhibitor, TIR rapidly improved to 85%, with restoration of a stable overnight profile.</p><p><strong>Literature review: </strong>A narrative review identified eight cases with INSR-related insulin resistance (Donohue/Rabson-Mendenhall/type A insulin resistance) treated with a SGLT2 inhibitor. All reports documented clinically meaningful HbA1c reductions (1.4-3.6%) and, where available, improved CGM metrics.</p><p><strong>Conclusions: </strong>SGLT2 inhibitors provide insulin-independent glycaemic benefit in INSR-related insulin resistance. AMPK-activating strategies, including metformin, berberine, and exercise, may provide adjunctive benefit via cellular glucose uptake, although evidence remains limited. We propose a two-factor therapeutic framework targeting (1) insulin-independent glucosuria and (2) AMPK-mediated glucose uptake as a rational management approach for this rare form of diabetes.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872507","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":"Advanced hybrid closed-loop therapy for type 1 diabetes in a correctional facility: a real-world case series.","authors":"Valentina Anelli, Cristina Cairone, Federico Bertuzzi, Elisa Muratore, Alessandro Viadana, Angelo Vincenzo Cornaghi, Basilio Pintaudi","doi":"10.1007/s00592-026-02793-3","DOIUrl":"https://doi.org/10.1007/s00592-026-02793-3","url":null,"abstract":"<p><strong>Background: </strong>Management of type 1 diabetes (T1D) in correctional facilities is challenging due to limited autonomy, restricted access to technologies, and non-flexible daily routines.</p><p><strong>Objective: </strong>To evaluate the feasibility and short-term glycemic outcomes of advanced hybrid closed-loop (aHCL) systems in individuals with T1D in a correctional setting.</p><p><strong>Methods: </strong>We conducted a retrospective real-world case series including adults with T1D incarcerated in a correctional facility and initiated on an advanced hybrid closed-loop (aHCL) system. Glycemic metrics were assessed at baseline and after 3 months. Continuous variables are reported as median (IQR). Paired comparisons were performed using the Wilcoxon signed-rank test.</p><p><strong>Results: </strong>Six individuals were included and five completed follow-up. Median HbA1c decreased from 9.7% to 7.8% (p = 0.043). Median time in range (TIR) increased from 41% to 49%, while time below range (TBR) and time above range (TAR) decreased from 0.5% to 0% and from 57.5% to 43%, respectively, although these changes were not statistically significant. No severe hypoglycemia or diabetic ketoacidosis events occurred.</p><p><strong>Conclusions: </strong>Use of aHCL systems in a correctional setting was feasible and associated with improved HbA1c without increased hypoglycemia. These findings support the potential role of advanced diabetes technologies in restricted environments.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863268","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":"Myosteatosis is associated with adverse in-hospital outcomes and CONUT score in hospitalized internal medicine patients.","authors":"Nicoletta Miano, Maurizio Di Marco, Sabrina Scilletta, Giorgia Todaro, Giosiana Bosco, Francesco Di Giacomo Barbagallo, Roberto Scicali, Salvatore Piro, Antonino Di Pino","doi":"10.1007/s00592-026-02785-3","DOIUrl":"https://doi.org/10.1007/s00592-026-02785-3","url":null,"abstract":"<p><strong>Aims: </strong>Myosteatosis is a marker of malnutrition and of adverse clinical outcomes and diabetes is among its contributors. Currently, no single universally accepted method exists to screen for malnutrition, but COntrolling NUTritional status (CONUT) score seems to be promising. This study aimed to assess the impact of myosteatosis on in-hospital outcomes and to test its association with CONUT score in people with and without type 2 diabetes.</p><p><strong>Methods: </strong>227 patients aged > 40 years admitted to an Internal Medicine Department were consecutively recruited, recording in-hospital outcomes. Myosteatosis was assessed as multifidus muscle to subcutaneous fat (MM/F) attenuation ratio at computed-tomography scan. CONUT was calculated using albumin, lymphocyte count and total cholesterol. The population was stratified, based on sex-differentiated tertiles of MM/F, in a low myosteatosis group (n = 152) and a high myosteatosis group (n = 75; top tertile of MM/F).</p><p><strong>Results: </strong>The high myosteatosis group showed a higher prevalence of in-hospital death (12.5 vs. 26%, P < 0.001) and pneumonia. Moreover, the high myosteatosis group experienced a longer length-of-stay and was more likely to have cultures positive for multi-drug-resistant germs. In-hospital death was independently associated with MM/F ratio (OR 2.74, 95%CI 1.11-7.75, P = 0.035). Diabetes did not show significant interaction on this association (P-for-interaction = 0.43). From multiple regression model, MM/F was independently associated with CONUT (β = 0.30, P < 0.001).</p><p><strong>Conclusions: </strong>Myosteatosis was associated with adverse in-hospital outcomes. CONUT score was independently associated with the imaging-derived MM/F ratio. Further studies specifically designed to evaluate diagnostic performance are required before CONUT can be proposed as a screening tool for myosteatosis.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863443","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":"Myeloid myeloid PRDM16 restrains macrophage inflammatory remodeling and renal fibrosis in diabetic kidney disease by limiting PI3K/AKT activation.","authors":"Shanshan Wang, Tao Zhang, Miao He","doi":"10.1007/s00592-026-02779-1","DOIUrl":"https://doi.org/10.1007/s00592-026-02779-1","url":null,"abstract":"<p><strong>Background: </strong>Diabetic kidney disease (DKD) is driven by persistent metabolic stress, immune dysregulation and progressive renal fibrosis. PRDM16 is a metabolic transcriptional regulator involved in adipose remodeling, mitochondrial activity and tissue homeostasis, but whether myeloid PRDM16 links diabetic metabolic stress to macrophage polarization and renal fibrosis remains unclear.</p><p><strong>Methods: </strong>Public DKD transcriptomic datasets were analyzed to identify PRDM16-associated immune and macrophage signatures. Myeloid PRDM16-deficient mice and littermate controls were used to establish experimental DKD. Renal injury, fibrotic remodeling, macrophage polarization and PI3K/AKT signaling were evaluated by histological staining, immunostaining, ELISA, qRT-PCR and western blotting. High glucose-stimulated BMDMs and THP-1-derived macrophages were used for mechanistic validation, and LY294002 was applied to inhibit PI3K/AKT signaling.</p><p><strong>Results: </strong>Bioinformatic analysis linked PRDM16 expression with macrophage-related immune features in DKD. In vivo, myeloid PRDM16 deficiency aggravated renal matrix accumulation, collagen deposition and α-SMA/Collagen-I expression. PRDM16 loss promoted a shift from M2-like macrophages toward M1-like inflammatory macrophages, characterized by increased CD80, CD86, NOS2, TNF-α and IL-1β, together with reduced CD206, Arg1, Fizz1, IL-10 and IL-4. Mechanistically, PRDM16 deficiency enhanced PI3K/AKT phosphorylation in macrophages, whereas LY294002 partially reversed M1-like polarization and attenuated renal inflammation and fibrosis.</p><p><strong>Conclusion: </strong>Myeloid PRDM16 acts as a metabolic-immune regulator that restrains M2-to-M1 macrophage polarization and limits renal fibrotic progression in DKD. Loss of PRDM16 aggravates macrophage-driven inflammation and fibrosis partly through PI3K/AKT activation, suggesting that the PRDM16-PI3K/AKT axis may represent a potential target for macrophage-directed intervention in diabetic kidney disease.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849447","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":"Predictors of first-ever major adverse cardiovascular events in newly diagnosed type 2 diabetes: a 5-year prospective cohort study.","authors":"Carmine Gazzaruso, Pietro Gallotti, Colomba Falcone, Livio Luzi, Adriana Coppola","doi":"10.1007/s00592-026-02786-2","DOIUrl":"https://doi.org/10.1007/s00592-026-02786-2","url":null,"abstract":"<p><strong>Aims: </strong>Cardiovascular risk stratification at the time of type 2 diabetes diagnosis remains challenging. We evaluated the incidence and baseline predictors of first-ever major adverse cardiovascular events (MACE) in patients with newly diagnosed type 2 diabetes without overt complications.</p><p><strong>Methods: </strong>We conducted a prospective cohort study of 937 consecutive adults with newly diagnosed type 2 diabetes, free of overt diabetic complications and pre-existing cardiovascular disease at baseline, followed for a mean of 62.7 ± 21.5 months. Baseline assessment included fasting C-peptide, transcutaneous oxygen tension (TcPO2), structured therapeutic patient education (TPE), and conventional metabolic and cardiovascular variables. Incident MACE was analyzed using Cox proportional hazards regression, and receiver operating characteristic analysis was used to derive an exploratory C-peptide cut-off.</p><p><strong>Results: </strong>During follow-up, 42 participants (4.5%) experienced a first MACE (0.86 per 100 person-years). In multivariable Cox analysis, higher fasting C-peptide (HR:4.70, 95%CI: 2.47-8.93, p < 0.001), lower TcPO2 (HR:15.15, 95%CI: 7.00-32.80, p < 0.001) were independently associated with MACE; non-participation in structured TPE was also associated with MACE (HR:0.26, 95%CI: 0.14-0.49, p < 0.001), but this finding should be interpreted cautiously given the observational design. The optimal C-peptide cut-off was 3.1 ng/mL (AUC 0.73). As a secondary endpoint, all-cause mortality occurred in 99 of 937 participants (10.6%; 2.02 per 100 person-years) and was independently associated with older age and lower TcPO2.</p><p><strong>Conclusions: </strong>In newly diagnosed type 2 diabetes without overt complications, higher fasting C-peptide and lower TcPO2 were associated with increased cardiovascular risk. These findings are hypothesis-generating and warrant external validation.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849452","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":"Effects of diabetes complications on body composition, dietary intake, and metabolic parameters.","authors":"Tuba Tekin, Başak İkra Yıldız, Şaziye Yoldaş, Mustafa Asım Gedikli","doi":"10.1007/s00592-026-02783-5","DOIUrl":"https://doi.org/10.1007/s00592-026-02783-5","url":null,"abstract":"<p><strong>Aim: </strong>Diabetes is a metabolic disease characterized by hyperglycemia resulting from deficiencies in the effect or secretion of insulin. Diabetes leads to various acute and chronic complications. This study investigated the impact of complications on body composition, dietary habits, and biochemical parameters in individuals with type 2 diabetes.</p><p><strong>Methods: </strong>The study included 42 diabetes patients with complications and 45 diabetic individuals without complications. A 24-hour dietary recall was conducted to assess nutritional status. The results of routine blood tests were analyzed to measure metabolic control. Measurements of participants' body weight, height, body composition, and waist and hip circumferences were recorded. Body composition was assessed utilizing a portable bioelectrical impedance analyzer. Body composition was examined using body fat percentage, body water percentage, visceral fat percentage, muscle mass, and basal metabolic rate.</p><p><strong>Results: </strong>Individuals with complications of diabetes had elevated body mass index (BMI), body fat percentage, visceral fat percentage, and waist and hip circumference (p > 0.05). They exhibited increased consumption of carbohydrates, dietary cholesterol, and saturated fats (p > 0.05). Additionally, HbA1c concentrations were higher and albumin concentrations were lower in individuals with diabetic complications (p < 0.05). CONCLUSıON: The study findings indicate that complications in individuals with type 2 diabetes negatively impact metabolic parameters, body composition, and nutritional consumption. To mitigate the risk of complications in individuals with type 2 diabetes, dietary treatments should be implemented to enhance metabolic parameters and body composition.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838916","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":"Mitochondrial structural and functional aberrations in diabetic bladder dysfunction: underlying mechanisms and therapeutic landscapes.","authors":"Junchao Wu, Huitao Wang, Rui Xu, Fei Song, Chunlei Dai, Yuanzhi Li, Wu Tang, Tao Yang, Kewei Fang","doi":"10.1007/s00592-026-02782-6","DOIUrl":"https://doi.org/10.1007/s00592-026-02782-6","url":null,"abstract":"<p><p>Diabetic bladder dysfunction (DBD) is a prevalent complication of diabetes mellitus (DM), characterized by heterogeneous urological impairments including altered bladder sensation, decreased compliance, and voiding difficulties. Emerging evidence highlights mitochondrial structural and functional aberrations as pivotal drivers of DBD pathogenesis. Chronic hyperglycemia induces excessive mitochondrial reactive oxygen species (ROS) generation, cristae disruption, impaired fission-fusion dynamics, defective mitochondrial quality control, and calcium dysregulation, collectively impairing bladder smooth muscle cell (BSMCs) bioenergetics and promoting apoptosis, inflammation, and fibrotic remodeling. These processes culminate in progressive bladder dysfunction, transitioning from compensatory hyperactivity to decompensated underactivity. Mitochondria-targeted therapeutic architectures fall into two complementary categories: repurposed guideline-based pharmacological agents and conceptual prospective interventions, the latter encompassing molecular reprogramming, cell-based therapies, and cell-free regenerative platforms. This review synthesizes current mechanistic insights into mitochondrial involvement in DBD and explores potential therapeutic landscapes, emphasizing the need for integrated, mechanism-driven interventions to advance clinical management of this condition.</p>","PeriodicalId":6921,"journal":{"name":"Acta Diabetologica","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838971","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}