Diabetes/Metabolism Research and Reviews最新文献

{"title":"Skeletal Muscle Function in Type 1 Diabetes: A Complementary Outcome for Clinical Care and Research","authors":"Antonio García-Hermoso, Jacinto Muñoz-Pardeza, Ignacio Hormazábal-Aguayo, Yasmin Ezzatvar","doi":"10.1002/dmrr.70218","DOIUrl":"https://doi.org/10.1002/dmrr.70218","url":null,"abstract":"<p>Type 1 diabetes has traditionally been conceptualised as a disorder defined by autoimmune β-cell destruction, insulin deficiency and chronic dysglycaemia [<span>1</span>]. This framework has shaped clinical management and research priorities for decades, with understandable emphasis on insulin therapy, glucose monitoring, and prevention of acute and chronic complications [<span>1</span>]. Yet a purely glucose-centred view may be limiting. Type 1 diabetes also affects skeletal muscle, a key tissue for insulin action, metabolic regulation and physical function. Increasing evidence suggests that diabetic myopathy represents an important but underrecognized component of the type 1 diabetes phenotype and a potential therapeutic target [<span>2</span>].</p><p>This commentary does not aim to provide a systematic review, nor to claim that skeletal muscle function is an established surrogate endpoint for long-term diabetes outcomes. Rather, we argue that skeletal muscle strength, physical function and exercise capacity are clinically meaningful, undermeasured outcomes that should complement, not replace, glycaemic metrics in type 1 diabetes care. The novelty of this commentary lies in explicitly positioning these dimensions as formal clinical and research outcomes, rather than simply reiterating the established role of exercise in type 1 diabetes.</p><p>This measurement gap is clinically relevant. Human studies suggest that people with type 1 diabetes may exhibit structural, metabolic and functional alterations in skeletal muscle, including reduced muscle strength, altered muscle morphology, impaired mitochondrial function, and lower exercise capacity [<span>3-6</span>]. Among the most informative studies, Dial et al. [<span>3</span>] reported impaired muscle function and altered skeletal muscle morphology across the adult lifespan in people with type 1 diabetes, with findings consistent with accelerated neuromuscular ageing even in the absence of major overt diabetic complications. These observations support the view that skeletal muscle involvement is not merely peripheral but may represent an undermeasured component of the type 1 diabetes phenotype.</p><p>The most clinically relevant phenotype is unlikely to be muscle mass alone. Muscle strength, physical function and exercise capacity may better capture what matters clinically: the ability to exercise, tolerate daily activities, maintain independence, and sustain long-term physical activity. These structural characteristics remain important, but should not be interpreted as sufficient markers of muscle health. The emerging literature on sarcopenia and dynapenia in type 1 diabetes reinforces the need to assess muscle health as a multidimensional construct combining muscle strength, muscle quantity or quality, and physical performance [<span>7</span>].</p><p>Figure 1 illustrates the conceptual shift from a traditional glucose-centred model of type 1 diabetes towards an expanded cardiometabolic model ","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70218","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing Type 1 Diabetes Treatment: 3 PM-Oriented Innovations in Islet Transplantation and Biomaterial Engineering","authors":"Fatemeh Sabet Sarvestani,&nbsp;Ramin Yaghobi,&nbsp;Mohsen Khosravi Maharlooei,&nbsp;Mehdi Golshan,&nbsp;Mohammad Hossein Karimi","doi":"10.1002/dmrr.70215","DOIUrl":"10.1002/dmrr.70215","url":null,"abstract":"<p>Type 1 Diabetes (<i>T1D</i>) is an autoimmune disorder marked by the immune-mediated destruction of pancreatic β-cells, resulting in insulin deficiency and dysregulated glucose control. Current therapies—such as insulin replacement and artificial pancreas systems—manage symptoms but fail to restore endogenous β-cell function or halt disease progression. Transplantation strategies, including islet allo- and xenotransplantation, offer potential cures but remain limited by immune rejection, donor scarcity, and the adverse effects of systemic immunosuppression. Within the framework of predictive, preventive, and personalised medicine (3 PM), <i>T1D</i> management requires a paradigm shift towards early detection, targeted prevention, and individualised therapy. Predictive biomarkers and molecular phenotyping can identify high-risk individuals and forecast graft outcomes, while preventive strategies—such as localised immunomodulation, bioenergetic support, and control of systemic inflammation—improve tolerance and graft longevity. Personalised interventions, including patient-specific biomaterials, immunoprotective encapsulation, and regulatory T cell–based or stem-cell–derived β-cell replacement, address immune and metabolic heterogeneity. Recent progress in biomaterials, encapsulation, and 3D bioprinting enables the practical implementation of this 3 PM approach by enhancing oxygenation, vascular integration, and specific scaffold design. Integration of AI-driven analytics, digital health monitoring, and multi-modal diagnostics further supports predictive control of transplant outcomes. This review highlights advances in islet transplantation and regenerative biomaterial engineering as key enablers of the transition from reactive treatment to 3 PM-guided, patient-tailored therapy for <i>T1D</i>.</p>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13453144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148698164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Bone-, Muscle- and Fat- Derived Factors Sclerostin, Irisin and Leptin Show Different Correlations With Body Composition and Bone Mineral Density in Chinese Men With Obesity: A Cross-Sectional Study","authors":"Xiang Chen,&nbsp;Sumin Shen,&nbsp;Mingxi Zou,&nbsp;Zhenlin Zhang,&nbsp;Nanwei Tong,&nbsp;Juan Li","doi":"10.1002/dmrr.70208","DOIUrl":"10.1002/dmrr.70208","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This study aimed to explore the interactions among sclerostin, irisin and leptin, as well as their associations with body composition and bone metabolism in Chinese men with obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>This study included 26 men with normal weight and 78 men with obesity. Body composition was measured using dual-emission X-ray absorptiometry. Subcutaneous fat, visceral fat and fat content in the liver and pancreas were determined by magnetic resonance. Serum sclerostin, irisin and leptin were detected using the Elisa assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with men with normal weight, serum sclerostin, irisin and leptin levels as well as whole-body and spinal bone mineral density were increased, whereas pelvic bone mineral density was not different in men with obesity. Partial analysis showed that in men with obesity, serum sclerostin was positively correlated with bone mineral density but not with body composition; serum irisin was positively correlated with fat mass percent, negatively correlated with muscle mass percent, but not with bone mineral density; serum leptin was positively correlated with fat mass, while negatively associated with muscle mass and bone mineral density. Furthermore, body weight showed beneficial effects on whole-body and spinal bone, whereas central fat distribution exerted adverse effects on pelvic bone. Stepwise linear regression revealed that serum sclerostin and whole-body muscle mass were independent predictors of bone mineral density in the over-all cohort.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Serum sclerostin, irisin and leptin show distinct correlations with body composition and bone mineral density in men with obesity, which may partly reflect the complex effects of obesity on bone metabolism.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13443498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148680678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Weight Loss-Dependent Changes in Body Composition and Bone Health in People With Obesity and Type 1 Diabetes Treated With Liraglutide, Semaglutide, or Tirzepatide","authors":"Ebaa Al Ozairi,&nbsp;Mohammad Irshad,&nbsp;Jumana Alkandri,&nbsp;Anant Mashankar,&nbsp;Stuart R. Gray,&nbsp;Carel W. le Roux","doi":"10.1002/dmrr.70213","DOIUrl":"10.1002/dmrr.70213","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This study examined changes in body composition and bone mineral density (BMD) over 12 months in people with obesity and type 1 diabetes (T1D) treated with a GLP-1 receptor agonist alone (GLP-1RA) or a dual glucose-dependent insulinotropic polypeptide (GIP/GLP-1RA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>This real-world observational study included 70 people with obesity and T1D treated with GLP-1RA alone or dual GIP/GLP-1RA. Dual-energy X-ray absorptiometry (DEXA) was used to quantify regional and total fat mass, lean mass, bone mineral content (BMC) and BMD at baseline and after 12 months of treatment. Overall changes were quantified, and changes stratified by percentage weight loss using repeated measures analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Over 12 months body weight (−6.33%; 95% CI: −7.92, −4.73; <i>p</i> &lt; 0.001), HbA1c (−0.48%; 95% CI: −0.74, −0.22; <i>p</i> &lt; 0.001), total tissue fat (−1.42%; 95% CI: −2.47, −0.36; <i>p</i> = 0.009), fat mass (−5.90%; 95% CI: −10.50, −1.57; <i>p</i> = 0.001), and lean mass (−1.75%; 95% CI: −3.50, −0.48; <i>p</i> = 0.005) decreased, while total BMC and BMD remained unchanged. Total lean mass loss was associated with body weight loss (<i>R</i>² = 0.36, <i>p</i> &lt; 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In people with obesity and T1D, 12-month GLP-1RA alone or dual GIP/GLP-1RA therapy resulted in clinically meaningful weight loss, improved glycaemic control, preferential fat mass reduction, modest lean mass loss, and preservation of total BMD. People achieving &gt; 10% weight loss derived the greatest metabolic benefit without compromising bone health, although the loss of lean mass was greater.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13440749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148680666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular–Kidney–Metabolic Syndrome Severity and Risk of Pancreatic Cancer in a Large Prospective Cohort","authors":"Munseok Choi,&nbsp;Seok-Jae Heo,&nbsp;Yu-Jin Kwon,&nbsp;Chang Moo Kang","doi":"10.1002/dmrr.70214","DOIUrl":"10.1002/dmrr.70214","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Pancreatic cancer remains one of the most lethal malignancies due to late diagnosis and limited opportunities for prevention. Cardiovascular–kidney–metabolic (CKM) syndrome reflects the cumulative burden of metabolic, renal, and cardiovascular dysfunction, but its association with pancreatic cancer risk has not been well established. We investigated this relationship in a large prospective cohort from the UK Biobank.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>Participants without pancreatic cancer at baseline (2006–2010) were followed through national cancer and mortality registries until 31 December 2022. CKM syndrome was categorised into five stages (0–4) according to American Heart Association criteria. Incident pancreatic cancer was identified using ICD-9 and ICD-10 codes. Fine–Gray subdistribution hazard models accounting for death were used to estimate subdistribution hazard ratios (SHRs) and 95% confidence intervals (CIs), with prespecified subgroup analyses performed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 326,148 participants, 1234 incident pancreatic cancer cases were identified over a mean follow-up of 13.5 years (SD 2.0). Incidence rates increased progressively from 9.0 to 48.6 per 100,000 person-years across CKM stages. Compared with CKM stage 0, multivariable-adjusted SHRs for pancreatic cancer were 1.97 (95% CI 1.28–3.02) for stage 1, 2.02 (1.42–2.87) for stage 2, and 2.08 (1.42–3.04) for stages 3–4 (<i>p</i> for trend &lt; 0.001). Associations were generally consistent across subgroup analyses according to age, sex, smoking status, and alcohol consumption, without statistically significant interaction effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Advanced CKM syndrome was independently associated with higher pancreatic cancer risk, supporting its potential role in risk stratification and early detection strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Active Free Radical Cold Atmosphere Plasma Promotes Healing of Diabetes Foot Ulcer: Mechanism and Challenge","authors":"Yiran Wang,&nbsp;Junxiao Zhang,&nbsp;Jinting Yan,&nbsp;Wenhua Bi,&nbsp;Jinlong Ma","doi":"10.1002/dmrr.70216","DOIUrl":"10.1002/dmrr.70216","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Diabetic foot ulcers (DFUs) have become an important cause of disability and death in patients with diabetes. Traditional therapies are prone to problems such as recurrence and drug resistance, which result in unsatisfactory healing effects for DFUs. Although antibiotics are not the mainstay of treatment for DFUs, antibiotic resistance poses a critical clinical challenge for DFU patients who require long-term antibiotic therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Main Text</h3>\u0000 \u0000 <p>This review summarises the mechanism by which Cold Atmosphere Plasma (CAP) kills bacteria and activates healing ability through the production of reactive oxygen/nitrogen species (RONS). RONS, as the key active species of CAP, exert antibacterial effects in a series of bacterial, cellular, and animal experiments, promote cell migration and proliferation, stimulate angiogenesis, and exert anti-inflammatory effects. However, current high-quality clinical trials are still lacking, leaving substantial room for further clinical exploration of CAP in the treatment of DFUs. Finally, the challenges and prospects of CAP in treating diabetic foot ulcers are summarised.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>As a comprehensive and innovative treatment method, the RONS produced by CAP offer a potential approach for treating DFUs and serve as a tool for promoting their healing. However, more clinical studies are needed for further verification.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetic Foot Ulcer Prevention Priorities Established by Consumers From Low Socioeconomic and Culturally Diverse Communities","authors":"Jayishni N. Maharaj,&nbsp;Jim Woodburn,&nbsp;Annette McLaren-Kennedy,&nbsp;Mohamed A. Kola,&nbsp;Daniel M. G. Winson,&nbsp;Meegan Nevin,&nbsp;Kelly Clanchy","doi":"10.1002/dmrr.70206","DOIUrl":"10.1002/dmrr.70206","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Diabetic foot ulcers (DFU) continue to occur despite established prevention guidelines, yet consumer perspectives, particularly from socioeconomically disadvantaged and culturally and linguistically diverse (CALD) communities, have been underrepresented in shaping prevention. To address this gap, we aimed to co-design a consumer-derived prevention research agenda by identifying barriers and enablers, establishing research priorities, prioritising implementation strategies, and defining meaningful outcome measures.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Four sequential workshops were conducted with 11 consumers with a history of DFU in South East Queensland, including Aboriginal and Pacific Islander participants (<i>n</i> = 4) and those from areas of socioeconomic disadvantage (<i>n</i> = 8). Rapid qualitative analysis informed iterative refinement across workshops, with priorities, implementation strategies, and outcome measures ranked by participants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Participants identified barriers across clinical, self-care, psychosocial, social, and financial domains, including feeling unsupported when trying to prevent DFU, the cognitive burden of constant vigilance, conflicting guidance, and the financial and travel costs of care. The highest-ranked research priorities were better ways to predict problems before they happen (median 2, IQR 1–4.5), formal education support (median 4, IQR 3–9), and tools to support regular foot checks (median 5, IQR 3–6). Across all three priorities, consumers consistently selected technology enabled implementation strategies, including wearable sensors, AI powered personalised learning, and smart interventions. Participants defined prevention success through quality of life, function, and confidence outcome measures rather than clinical endpoints alone.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>For socioeconomically disadvantaged and CALD populations, effective DFU prevention must be technology enabled, personalised, and developed in partnership with the consumer.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Type 5 Diabetes Mellitus: Pathophysiology, Clinical Phenotype, and Nutritional Management","authors":"İrem Nur Şahin Anılgan,&nbsp;Aslıhan Atar-Uğurlu","doi":"10.1002/dmrr.70212","DOIUrl":"https://doi.org/10.1002/dmrr.70212","url":null,"abstract":"<p>Type 5 Diabetes Mellitus (T5DM) is an emerging diabetes phenotype linked to chronic undernutrition. It predominantly affects young, lean individuals in low- and middle-income countries. After its formal recognition by the International Diabetes Federation in 2025, T5DM resurfaced as a clinically relevant insulin-deficient phenotype. It is now viewed as distinct from classical autoimmune and insulin-resistant forms of diabetes. This review synthesises recent evidence on the epidemiology, pathophysiology, clinical characteristics, and management of T5DM. Recent studies show that T5DM is influenced by early-life nutritional deprivation. This fits within the Developmental Origins of Health and Disease (DOHaD) framework. Undernutrition during key developmental periods harms pancreatic morphogenesis. It creates a permanent reduction of functional beta-cell mass through epigenetic programming. Clinically, T5DM often appears before age 30. Patients have low body mass index, sarcopenia, marked insulinopenia, absence of diabetes-associated autoantibodies, and resistance to ketosis, despite significant hyperglycemia. Diagnostic challenges remain, as patients are frequently misclassified as type 1 or type 2 diabetes. Relying only on body mass index is insufficient. Accurate diagnosis requires a multidimensional assessment including nutritional history, metabolic features, and exclusion of monogenic diabetes. T5DM is a distinct insulin-deficient phenotype caused by chronic undernutrition. Effective management requires more than glycaemic control. Nutritional rehabilitation is key, with a focus on adequate energy intake, high–biological–value protein supplementation, and correction of key micronutrient deficiencies. Given preserved insulin sensitivity, low-dose insulin should be used cautiously to avoid iatrogenic hypoglycemia. Better recognition and tailored management strategies are needed for optimal clinical outcomes.</p>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70212","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148616834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coxsackievirus B Infections Are Associated With the Risk of Islet Autoimmunity in Children With Strong Genetic Susceptibility to Type 1 Diabetes—Results From the TRIGR Divia Study","authors":"Maarit Oikarinen,&nbsp;Amirbabak Sioofy-Khojine,&nbsp;Leena Puustinen,&nbsp;David Cuthbertson,&nbsp;Jussi Lehtonen,&nbsp;Niila V. V. Jouppila,&nbsp;Johnny Ludvigsson,&nbsp;Leena Hakola,&nbsp;Sari Niinistö,&nbsp;Iris Erlund,&nbsp;Mikael Knip,&nbsp;Jeffrey P. Krischer,&nbsp;Suvi M. Virtanen,&nbsp;Heikki Hyöty,&nbsp;the TRIGR Investigators","doi":"10.1002/dmrr.70207","DOIUrl":"10.1002/dmrr.70207","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Especially, the coxsackievirus B group of enteroviruses has been linked to the development of islet autoimmunity and type 1 diabetes in genetically susceptible individuals. Our aim was to study the possible associations of 10 different microbial infections with islet autoimmunity in a large international prospective study.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>In a nested case-control study within the TRIGR study, follow-up serum samples from 240 islet autoantibody-positive case children and 436 age- and country-matched control children were analysed for IgG class antibodies against 10 different respiratory and gastrointestinal microbes using an enzyme immunoassay, and for neutralising antibodies against all six coxsackievirus B types. The samples were obtained at several time points prior to and at the time of seroconversion for multiple islet autoantibodies. All children had a first-degree relative with type 1 diabetes, and they carried risk-associated HLA-DQ alleles.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Coxsackievirus B5 was associated with an increased risk of islet autoimmunity (OR 2.22, 95% CI 1.29–3.80, <i>p</i> = 0.004, corrected <i>p</i> = 0.024), which remained after adjustment for HLA, sex, and maternal type 1 diabetes. This association was particularly seen for infections occurring more than 12 months (OR 2.02, 95% CI 1.06–3.84, <i>p</i> = 0.032) and 0–6 months (OR 2.66, 95% CI 1.11–6.35, <i>p</i> = 0.028) before the first detection of multiple islet autoantibodies. After correction for multiple comparisons, none of the other viruses showed an association with islet autoimmunity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study supports previous evidence of the risk association of coxsackievirus B infections. These results support the role of certain virus infections as possible modulating factors in the pathogenesis of type 1 diabetes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70207","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148609175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Di(2-Ethylhexyl) Phthalate Exposure and Risk of Diabetic Kidney Disease: Epidemiological Association and Mechanistic Insights","authors":"Dapeng Yin,&nbsp;Yan Li,&nbsp;Wei Wu,&nbsp;Xiaojuan Wang,&nbsp;Junhua He,&nbsp;Yikun Zhu,&nbsp;Jin Li","doi":"10.1002/dmrr.70209","DOIUrl":"10.1002/dmrr.70209","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aims to explore the association between exposure to di-(2-ethylhexyl) phthalate (DEHP) and diabetic kidney disease (DKD), and to elucidate its potential molecular mechanisms. The study findings provide scientific evidence for the prevention and control of environmental risk factors related to DKD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We utilised the United States National Health and Nutrition Examination Survey (NHANES) database to evaluate the correlations of DEHP exposure with DKD risk and renal function indices. Candidate targets were screened using network toxicology, and functional enrichment analysis was conducted. The binding ability of DEHP to the candidate mechanistic targets was verified through molecular docking. The toxicity and target effects of DEHP and its metabolites were verified using HK-2 cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The NHANES analysis demonstrated a positive correlation between DEHP exposure and the risk of DKD, with a significant dose-response relationship observed. Network toxicology identified ALB, ESR1, and MMP9 as candidate mechanistic targets in DEHP-induced DKD. In vitro experiments confirmed that DEHP and its metabolite MEHP reduced HK-2 cell viability, induced lipid deposition, and altered the expression of candidate mechanistic targets.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>DEHP is an important environmental risk factor for DKD. It may promote the development and progression of DKD by regulating key targets and interfering with lipid metabolism.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"42 6","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70209","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148609193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}