Diabetes/Metabolism Research and Reviews最新文献

{"title":"Assessing the Possibility of Recurrent Diabetic Foot Ulcer Prevention via Remote Patient Monitoring: A Feasibility Study","authors":"Caroline A. Abbott,&nbsp;Kerryn J. Franklyn,&nbsp;David E. Stuart,&nbsp;Ellen Kirwan,&nbsp;Sinead Flynn,&nbsp;Ron Scott,&nbsp;Caroline McIntosh,&nbsp;Andrew J. M. Boulton","doi":"10.1002/dmrr.70096","DOIUrl":"10.1002/dmrr.70096","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Our main aims in this study of diabetic patients at risk of foot ulcers were to evaluate: (a) adherence to the use of an at-home thermal and visual digital foot scanner, (b) the feasibility of utilising thermovisual scan data to perform remote foot assessments, thereby enabling, if indicated, remote intervention by podiatrists and (c) the validity of scanned images to identify skin lesions consistent with those found at a podiatric clinical evaluation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this single arm, open-label, 12-week pilot study in two countries, recruited patients with previous diabetic foot ulcer (DFU) (<i>n</i> = 27) were asked to stand on a digital foot scanner (OneStep), once a day at home. Plantar thermal and visual scan data were transmitted daily to a centralised monitoring service for daily review. Any abnormalities were immediately reported to the patient's podiatric healthcare provider, who determined appropriate intervention. Primary endpoints were patient adherence, device utility and data validity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>All participants with an active device (<i>n</i> = 26) took thermal and visual scans on 1547 days during 1940 active study days, averaging 5.3 ± 1.4 scans/week, with 80 ± 19% adherence (days scan recorded/days in study*100). Visual scans correctly identified all incident DFUs (<i>n</i> = 7). Podiatrists agreed that scans enabled the identification of skin integrity issues earlier than standard care (in 82% cases), finding visual scan images useful in 90% of reports and thermal data in 12%. Remote visual assessments agreed well with gold-standard podiatric examinations in identifying skin integrity risks (kappa = 0.67 [95% CI, 0.53–0.82, <i>p</i> &lt; 0.001]), also showing good sensitivity (80%) and specificity (100%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Remote foot scanning was easy to perform and was used consistently by vulnerable patients. Scans were useful for remote podiatric foot assessments and interventions, and visual images identified DFUs/skin problems to a good level. We now aim to test this monitoring system in a larger scale randomised controlled trial for DFU prevention.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70096","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145313997","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":"Tubular Injury in Diabetic Kidney Disease: Early Diagnosis and Intervention Strategies","authors":"Yi Lv,&nbsp;Chen Ye,&nbsp;Zixi Li,&nbsp;Jiajia Ye,&nbsp;Huanhuan Cao,&nbsp;Chun Zhang,&nbsp;Huajun Jiang,&nbsp;Yumei Wang","doi":"10.1002/dmrr.70098","DOIUrl":"10.1002/dmrr.70098","url":null,"abstract":"<p>Diabetic kidney disease (DKD) is the most severe complication of diabetes mellitus and has poor prognosis, often progressing to end-stage renal disease, causing substantial morbidity and mortality globally. While the pathogenesis of DKD has been extensively characterised, including glomerular hyperfiltration, podocyte injury, and tubulointerstitial fibrosis, recent findings underscore renal tubular injury as a pivotal contributor to DKD progression. High glucose levels and lipid accumulation result in tubular injury, followed by oxidative stress, endoplasmic reticulum stress, inflammation, activation of the renin–angiotensin–aldosterone system, programmed cell death, epithelial–mesenchymal transition, and intercellular crosstalk, all of which exacerbate tubular dysfunction in DKD. Notably, biomarkers of renal tubular injury, including kidney injury molecule-1, cystatin C, neutrophil gelatinase-associated lipocalin, liver fatty acid-binding protein, monocyte chemoattractant protein-1, N-acetyl-beta-glucosidase, and retinol-binding protein, along with other promising novel biomarkers, emerge earlier than microalbuminuria and serve as novel diagnostic indicators for early DKD detection. Therapeutically, we critically evaluate both established agents and emerging strategies, including hypoglycemic agents, anti-oxidative stress therapies, anti-inflammatory therapies, anti-cell death therapies, and stem cell therapy, showing promise for mitigating DKD-related tubular damage. This comprehensive review constructs a logical framework linking molecular mechanisms, novel biomarkers, and emerging therapeutic strategies for renal tubular injury in DKD. By bridging molecular mechanisms with actionable therapeutic strategies, this review highlights the pivotal role of tubulopathy in DKD pathogenesis and its implications for early diagnosis and intervention strategies.</p>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145313906","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":"Effect of Tirzepatide on Heart Failure in Type 2 Diabetes Mellitus and Obesity: A Systematic Review and Meta-Analysis","authors":"Yi-Meng He,&nbsp;Chen Zeng,&nbsp;Yu-Fan Zhang,&nbsp;Qi Wu,&nbsp;Xiao-Yu Zhou,&nbsp;Pi-Jun Yan,&nbsp;Yong Xu,&nbsp;Man Guo,&nbsp;Fang-Yuan Teng","doi":"10.1002/dmrr.70097","DOIUrl":"10.1002/dmrr.70097","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Aims&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This systematic review and meta-analysis aimed to evaluate the effects of tirzepatide on heart failure in patients with type 2 diabetes mellitus (T2DM) and obesity.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Materials and Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;An updated systematic search of the PubMed, Embase, The Cochrane Central Register of Controlled Trials, Scopus, Web of Science, and ClinicalTrials.gov databases for relevant studies, published from database inception to February 13, 2025, was performed using tirzepatide and heart failure-related search terms.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Eleven randomized controlled trials (RCTs) (funded by Eli Lilly and Co., Indianapolis, IN, USA) comprising 13,378 participants were included. Compared with placebo or other active glucose-lowering drugs, tirzepatide had a neutral effect on the overall risk for heart failure (risk ratio [RR] 0.63 [95% confidence interval (CI) 0.35–1.13]), but the effect was neither statistically nor clinically meaningful (absolute risk reduction [ARR] 0.17%, number needed to treat [NNT] 588; Food and Drug Administration (FDA) minimal important difference [MID] 1.5%). The certainty of evidence was rated as moderate according to the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) criteria (&lt;i&gt;p&lt;/i&gt; = 0.628; &lt;i&gt;I&lt;/i&gt;&lt;sup&gt;2&lt;/sup&gt; = 0.0%). Subgroup analysis revealed different pooled estimates for heart failure outcomes in the ≤ 58 years of age subgroup (RR 0.40 [95% CI 0.17–0.96]) compared with the &gt; 58 years' subgroup (RR 0.86 [95% CI 0.39–1.90]) (&lt;i&gt;p&lt;/i&gt; for interaction = 0.201). Additionally, subgroup analysis comparing tirzepatide alone with tirzepatide in combination with other agents revealed different pooled estimates (&lt;i&gt;p&lt;/i&gt; = 0.661; &lt;i&gt;I&lt;/i&gt;&lt;sup&gt;2&lt;/sup&gt; = 0.0%), with an RR 0.43 (95% CI 0.20–0.88) and 2.25 (95% CI 0.51–9.87), respectively (&lt;i&gt;p&lt;/i&gt; for interaction = 0.05). Subgroup analyses stratified according to different doses of tirzepatide, baseline body weight, body mass index, fasting plasma glucose, glycated haemoglobin, T2DM, obesity, or overweight, and intervention time indicated no association between tirzepatide use and the risk for heart failure.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Tirzepatide had no overall effect on heart failure outcomes in patients with T2DM or obesity. However, among patients ≤ 58 years of age, tirzepatide yielded a 60% relative risk reduction (i.e., RR = 0.40), while in patients undergoing monotherapy, it yielded a 57% relative risk reduction (i.e., RR = 0.43). Results of this systematic review and meta-analysis of RCTs support the safety of tirzepatide as a t","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145309700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contributions of Clinical Obesity and Preclinical Obesity to the All-Cause Mortality Risk: Findings From the UK Biobank Cohort","authors":"Manrong Xu,&nbsp;Menghan Li,&nbsp;Yawen Zhang,&nbsp;Lianxi Li,&nbsp;Yun Shen,&nbsp;Gang Hu","doi":"10.1002/dmrr.70095","DOIUrl":"10.1002/dmrr.70095","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The definition of clinical obesity was newly announced. The aim of our study was to investigate the association of preclinical obesity and clinical obesity either at baseline or determined during follow-ups with the risk of all-cause mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data were collected from 232,721 participants in the UK Biobank. Dysfunctions caused by obesity, in combination with an excess of anthropometric parameters, were used to diagnose clinical obesity. Participants were categorised into six clusters according to their baseline and follow-up dysfunction status. Time-dependent Cox proportional hazards regression was used to compare hazard ratios (HRs) for mortality across six clusters.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In a total of 19,704 deaths over a mean follow-up of 13.4 years, participants in Cluster 6 (clinical obesity at baseline; HR = 2.30, 95% CI: 2.16–2.44) and Cluster 3 (non-obesity with baseline dysfunctions; HR = 2.02, 95% CI: 1.85–2.20) exhibited the highest multivariable-adjusted mortality risk compared with participants without obesity and dysfunction at baseline and during follow-up (Cluster 1). This was followed by participants in Cluster 2 (non-obesity without baseline but with follow-up dysfunctions; HR = 1.99, 95% CI: 1.88–2.10), Cluster 5 (preclinical obesity with follow-up dysfunctions; HR = 1.97, 95% CI: 1.87–2.07), and Cluster 4 (preclinical obesity without follow-up dysfunctions; HR = 1.15, 95% CI: 1.09–1.22). Subgroup analyses showed consistently higher mortality risks in Cluster 6 across various demographics, notably among individuals with higher educational qualifications.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Clinical obesity was significantly associated with elevated all-cause mortality risk. These findings underscore the importance of early screening and intervention for dysfunctions in patients with obesity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12530463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145309654","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":"Autoimmune Type 1 Diabetes in the Era of Disease-Modifying Immune Therapy","authors":"Aaron W. Michels,&nbsp;Peter A. Gottlieb,&nbsp;Bryce Nelson,&nbsp;Colin Dayan","doi":"10.1002/dmrr.70091","DOIUrl":"10.1002/dmrr.70091","url":null,"abstract":"<p>Disease-modifying therapies have been used to treat the underlying causes of autoimmune diseases for over half a century. However, until recently, type 1 diabetes (T1D), the autoimmune form of diabetes, had not entered this therapeutic landscape. The approval of teplizumab, an anti-CD3 monoclonal antibody and the first disease-modifying therapy for use in individuals with preclinical T1D, has caused a major shift in the way healthcare providers can treat the T1D disease course. In this review, we discuss the chronic autoimmune nature of T1D and provide an overview of disease-modifying therapies that are under investigation to target the autoimmune mechanisms in T1D to preserve residual beta-cell function and prevent disease progression. The considerations for implementing these therapies into clinical practice are also discussed.</p>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70091","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253323","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":"From Obesity to Muscle Insulin Resistance: The Mediating Roles of Intramyocellular Lipids, Inflammation, and Oxidative Stress","authors":"Omid Razi,&nbsp;Camila de Moraes,&nbsp;Nastaran Zamani,&nbsp;Ayoub Saeidi,&nbsp;Marios Hadjicharalambous,&nbsp;Anthony C. Hackney,&nbsp;Juan Del Coso,&nbsp;Ismail Laher,&nbsp;Hassane Zouhal","doi":"10.1002/dmrr.70094","DOIUrl":"10.1002/dmrr.70094","url":null,"abstract":"<p>Obesity is highly correlated to muscle insulin resistance (IR), which significantly impacts metabolic health. One of the primary mechanisms connecting obesity to muscle IR is the accumulation of intramyocellular lipids (IMCL). Excessive lipid accumulation in muscle cells, that is, muscle lipotoxicity, leads to the formation of lipid metabolites, such as diacylglycerol (DAG) and ceramides, which disrupt insulin signalling pathways. These metabolites activate protein kinase C (PKC) and other kinases that inhibit insulin receptor substrate (IRS) proteins, subsequently impairing the insulin signalling cascade and reducing glucose uptake in skeletal muscle cells. This lipid-induced IR is a critical factor in the development of metabolic disorders associated with obesity. Furthermore, inflammation and oxidative stress may play significant roles in linking obesity with muscle IR. Obesity-induced inflammation is characterised by increased levels of pro-inflammatory cytokines, which activate signalling pathways, such as NF-κB and JNK. This transcription factor and stress protein further impair insulin signalling by promoting serine phosphorylation of IRS proteins. Concurrently, oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, exacerbates insulin resistance. Elevated ROS levels associated with damaging cellular components, including proteins, lipids, and DNA, may activate stress-sensitive signalling pathways, inhibiting insulin action. The current review analyses evidence on the interplay between IMCL accumulation, inflammation, and oxidative stress, establishing this interconnected triad as a vicious cycle: lipid metabolites activate inflammatory kinases, while inflammation and ROS further promote lipid deposition and mitochondrial inefficiency. This triad of mechanisms explains why muscle IR in obesity is both a cause and consequence of metabolic disease progression. Understanding these pathways is clinically urgent, as they represent actionable targets for therapies (e.g., peroxisome proliferator-activated receptor gamma [PPARγ] agonists to reduce ceramides, anti-inflammatory strategies to preserve insulin signalling). This synthesis of current evidence highlights how obesity-induced muscle IR propagates systemic metabolic risk, offering a framework for future translational research.</p>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145245648","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":"Early Life Physical Activity May Reduce the Risk of Developing Type 1 Diabetes: The Longitudinal ABIS Study","authors":"Johnny Ludvigsson,&nbsp;Noman Sohail","doi":"10.1002/dmrr.70093","DOIUrl":"10.1002/dmrr.70093","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>The impact of early-life physical activity is significant on long-term health outcomes. This study aims to investigate the relationship between early-life physical activity and later development of type 1 diabetes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>A total of 16,415 children were included in a longitudinal prospective population-based birth cohort, of whom (<i>n</i> = 169) type 1 diabetes cases were identified until 2023 using the Swedish National Diagnosis and Drug Prescription Registers. Cox regression was used for hazard ratios (HRs) with 95% confidence interval, and adjusted for low maternal education, family type 1 diabetes history, and BMI as confounders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Results show an inverse association between high physical activity and type 1 diabetes risk from age 3–25 years. Both male/female demonstrated substantial protective effects at age 3 and 5 years but female showed weaker effects at age 8 compared to males. HR for males/females at age 3 was [0.42 (0.30–0.68, <i>p</i> = 0.021); 0.45 (0.32–0.70, <i>p</i> = 0.025)], at age 5 [0.58 (0.37–0.85, <i>p</i> = 0.038); 0.63 (0.40–0.86, <i>p</i> = 0.045)], and at 8 years [0.63 (0.40–0.93, <i>p</i> = 0.046), 0.70 (0.47–1.18, <i>p</i> &gt; 0.05)]. After confounder adjustments, the effects were still significant at age 3 and five in both males/females. aHR in males/females at age 3 was [0.48 (0.34–0.80, <i>p</i> = 0.027); 0.50 (0.32–0.82, <i>p</i> = 0.025)], and at age 5 [0.66 (0.38–0.97, <i>p</i> = 0.048); 0.72 (0.45–0.95, <i>p</i> = 0.048)]. As age increases, the protective effects became weaker (<i>p</i> &gt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Physical activity in early childhood may reduce the risk of developing type 1 diabetes, and should be facilitated and encouraged.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145245599","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":"Fibre-Enriched High-Carbohydrate (FEHC) Diet Modulates Inflammation Without Affecting Bone Health in Older Women With Obesity: A Randomised Clinical Trial","authors":"Francesca Cannata,&nbsp;Viola Viola,&nbsp;Giulia Leanza,&nbsp;Alice Laudisio,&nbsp;Malak Faraj,&nbsp;Flavia Tramontana,&nbsp;Alessandra Piccoli,&nbsp;Rocky Strollo,&nbsp;Mauro Maccarrone,&nbsp;Fabrizio Russo,&nbsp;Gianluca Vadalà,&nbsp;Veronica Sansoni,&nbsp;Giovanni Lombardi,&nbsp;Giuseppe Banfi,&nbsp;Chiara Verdelli,&nbsp;Rocco Papalia,&nbsp;Nicola Napoli","doi":"10.1002/dmrr.70089","DOIUrl":"10.1002/dmrr.70089","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>In older adults, obesity is associated with frailty, conditions worsened by age related decline in bone mineral density (BMD) and muscle mass.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To evaluate whether a 3-month Fibre-Enriched High Carbohydrate (FEHC) diet preserves bone health, reduces inflammation and modulates Wnt signalling in older adults with obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this clinical trial, 86 women aged 65–85 years with obesity (BMI ≥ 30 kg/m²) undergoing hip arthroplasty were assigned to a free control diet (FCD) or a FEHC diet (FEHC) group for 3 months before surgery. Clinical, systemic, and molecular assessments were performed, including gene expression analyses in bone and muscle tissues.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A significant reduction in waist circumference was observed over time in the FEHC group (<i>p</i> = 0.037), whereas no changes were detected in body weight, BMD or bone microarchitecture. Compared to FCD, the FEHC group showed reduced circulating IL-6 (<i>p</i> = 0.03), IL-8 (<i>p</i> = 0.022) and TNFα (<i>p</i> = 0.04) levels, along with lower IL-6 gene expression in muscle (<i>p</i> = 0.035). A strong trend of increased IGF-1 gene expression in muscle tissue of the FEHC group was also observed (<i>p</i> = 0.058). Gene expression analyses revealed a significant increase in WNT5a expression in muscle (<i>p</i> = 0.049), and an upward trend in WNT10b expression in bone (<i>p</i> = 0.055) while serum levels of DKK-1 were significantly higher in the FEHC group compared to FCD (<i>p</i> &lt; 0.0001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The FEHC diet reduces systemic and local inflammation, without affecting skeletal health in older adults with obesity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201414","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":"Proteomic and Metabolomic Interplay in the Regulation of Energy Metabolism During Obesity and Metabolic Syndrome","authors":"Carlos Vinicius F. da Silva,&nbsp;Carlos José F. da Silva,&nbsp;Thaís R. Cataldi,&nbsp;Carlos A. Labate,&nbsp;Youssef B. Sade,&nbsp;Sandra Mara N. Scapin,&nbsp;Fabiano L. Thompson,&nbsp;Cristiane Thompson,&nbsp;Carina Maciel da Silva-Boghossian,&nbsp;Eidy de Oliveira Santos","doi":"10.1002/dmrr.70090","DOIUrl":"https://doi.org/10.1002/dmrr.70090","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Explore the influence of obesity and Metabolic Syndrome disorders on the plasma proteome and metabolome, through an integrated analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>We investigated metabolic and proteomic alterations associated with obesity and MetS, through mass spectrometry, using plasma samples from 49 volunteers, categorized according to BMI, and MetS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We identified 231 proteins and 77 metabolites. A subset, including DMBT1, Vanin-1, PTPRJ, <i>β</i>-hydroxybutyrate, <i>α</i>-tocopherol, and 5-oxoproline, emerged as potential key players associated with obesity and MetS. By integrating proteomic and metabolomic data, we were able to construct an interactive network involved in metabolic dysfunction, revealing associations between these molecules and clinical parameters, such as BMI, HOMA-IR and HOMA-β.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our data suggested an interplay between anti-inflammatory (DMBT1, 3-hydroxybutyrate, 5-oxoproline) and pro-inflammatory pathways (Vanin-1, <i>α</i>-tocopherol, PTPRJ) during disorders of obesity and MetS, demonstrating the potential of an integrated multi-omics approach for a better understanding of the mechanism behind obesity-associated metabolic diseases.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 7","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70090","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172052","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":"Development of a Chinese-Specific Clinical Model to Predict Maturity-Onset Diabetes of the Young","authors":"Sandra T. F. Tsoi,&nbsp;Cadmon K. P. Lim,&nbsp;Ronald C. W. Ma,&nbsp;Eric S. H. Lau,&nbsp;Baoqi Fan,&nbsp;Chun Kwan O,&nbsp;Yingnan Fan,&nbsp;Elaine Chow,&nbsp;Alice P. S. Kong,&nbsp;Wing-Yee So,&nbsp;Juliana C. N. Chan,&nbsp;Andrea O. Y. Luk","doi":"10.1002/dmrr.70087","DOIUrl":"10.1002/dmrr.70087","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Accurate identification of individuals with maturity-onset diabetes of the young (MODY) can support precision diabetes management. However, diagnosing MODY is challenging due to overlapping clinical features with type 2 diabetes. We aimed to develop a prediction model for identifying Chinese with high likelihood of MODY for further genetic testing.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We developed a logistic regression model using clinical data from an unselected cohort of 1021 Chinese with young-onset (age at diagnosis ≤ 40) non-type 1 diabetes enrolled in the Hong Kong Diabetes Register, 1.9% (<i>n</i> = 19) of whom had MODY (<i>GCK</i>-, <i>HNF1A</i>-, <i>HNF4A</i>- and <i>HNF1B</i>-MODY) by molecular confirmation. We validated the model in an independent local cohort of 822 Chinese with young-onset non-type 1 diabetes. We compared the performance of the new Chinese-specific MODY prediction model with an existing MODY probability calculator in the validation cohort.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The prediction model comprised the following clinical variables: current age, age at diagnosis, sex, body mass index, systolic blood pressure, HDL-cholesterol, LDL-cholesterol, triglyceride and fasting C-peptide. It demonstrated acceptable discrimination of patients with MODY in the validation dataset, with an area under the curve of 0.813 (95% confidence interval 0.647–0.979). At the probability cut-off of 50%, the model achieved a sensitivity of 72.7% and a specificity of 92.4%. It allows identification of one MODY case in every nine genetic tests conducted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We developed a comprehensive Chinese-specific MODY prediction model. This model can be used in unselected Chinese with young-onset non-type 1 diabetes to identify high-risk individuals for genetic testing.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11335,"journal":{"name":"Diabetes/Metabolism Research and Reviews","volume":"41 6","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dmrr.70087","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145087925","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}