World Journal of Diabetes最新文献

{"title":"Overweight in mediating the association between depression and new-onset diabetes: A population-based research from Health and Retirement Study.","authors":"Zi-Hao Zhang, Shuo-Ying Yue, Meng Su, Hong-Lu Zhang, Qing-Cui Wu, Zhi-Lin Li, Nai-Jian Zhang, Zhi-Yi Hao, Man Li, Hui-Jie Huang, Jun Ma, Yuan-Yuan Liu, Hui Wang","doi":"10.4239/wjd.v16.i3.100245","DOIUrl":"https://doi.org/10.4239/wjd.v16.i3.100245","url":null,"abstract":"<p><strong>Background: </strong>Several studies have suggested a close link between depression, overweight, and new-onset diabetes, particularly among middle-aged and older populations; however, the causal associations remain poorly understood.</p><p><strong>Aim: </strong>To investigate the role of overweight in mediating the association between depression and new-onset diabetes in middle-aged and older populations.</p><p><strong>Methods: </strong>Data of 9426 individuals aged ≥ 50 years from the 1998-2016 Health and Retirement Study database were analyzed. Weighted logistic regression was employed to obtain odds ratios (ORs) and 95% confidence intervals (95%CIs) for depression and new-onset diabetes in the middle-aged and older populations. Mediation analysis and the Sobel test were used to test the mediating effects of overweight between depression and the risk of new-onset diabetes.</p><p><strong>Results: </strong>New-onset diabetes was identified in 23.6% of the study population. Depression was significantly associated with new-onset diabetes (OR: 1.18, 95%CI: 1.03-1.35, <i>P</i> value: 0.014). Further adjustment for overweight attenuated the effect of depression on new-onset diabetes to 1.14 (95%CI: 1.00-1.30, <i>P</i> = 0.053), with a significant mediating effect (<i>P</i> of Sobel test = 0.003). The mediation analysis demonstrated that overweight accounted for 61% in depression for the risk of new-onset diabetes, with overweight having a partially mediating role in the depression-to-diabetes pathway.</p><p><strong>Conclusion: </strong>New-onset diabetes was not necessarily a direct complication of depression; rather, depression led to behaviors that increase the risk of overweight and, consequently, new-onset diabetes.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 3","pages":"100245"},"PeriodicalIF":4.2,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of duodenal mucosal resurfacing in controlling diabetes in rats.","authors":"Li-Juan Nie, Zhe Cheng, Yi-Xian He, Qian-Hua Yan, Yao-Huan Sun, Xin-Yi Yang, Jie Tian, Peng-Fei Zhu, Jiang-Yi Yu, Hui-Ping Zhou, Xi-Qiao Zhou","doi":"10.4239/wjd.v16.i3.102277","DOIUrl":"https://doi.org/10.4239/wjd.v16.i3.102277","url":null,"abstract":"<p><strong>Background: </strong>The duodenum plays a significant role in metabolic regulation, and thickened mucous membranes are associated with insulin resistance. Duodenal mucosal resurfacing (DMR), a new-style endoscopic procedure using hydrothermal energy to ablate this thickened layer, shows promise for enhancing glucose and lipid metabolism in type 2 diabetes (T2D) patients. However, the mechanisms driving these improvements remain largely unexplored.</p><p><strong>Aim: </strong>To investigate the mechanisms by which DMR improves metabolic disorders using a rat model.</p><p><strong>Methods: </strong>Rats with T2D underwent a revised DMR procedure <i>via</i> a gastric incision using a specialized catheter to abrade the duodenal mucosa. The duodenum was evaluated using histology, immunofluorescence, and western blotting. Serum assays measured glucose, lipid profiles, lipopolysaccharide, and intestinal hormones, while the gut microbiota and metabolomics profiles were analyzed through 16S rRNA gene sequencing and ultra performance liquid chromatography-mass spectrum/mass spectrum, severally.</p><p><strong>Results: </strong>DMR significantly improved glucose and lipid metabolic disorders in T2D rats. It increased the serum levels of cholecystokinin, gastric inhibitory peptide, and glucagon-like peptide 1, and reduced the length and depth of duodenal villi and crypts. DMR also enhanced the intestinal barrier integrity and reduced lipopolysaccharide translocation. Additionally, DMR modified the gut microbiome and metabolome, particularly affecting the <i>Blautia</i> genus. Correlation analysis revealed significant links between the gut microbiota, metabolites, and T2D phenotypes.</p><p><strong>Conclusion: </strong>This study illustrates that DMR addresses metabolic dysfunctions in T2D through multifaceted mechanisms, highlighting the potential role of the <i>Blautia</i> genus on T2D pathogenesis and DMR's therapeutic impact.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 3","pages":"102277"},"PeriodicalIF":4.2,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between serum retinol-binding protein and lower limb atherosclerosis risk in type 2 diabetes mellitus.","authors":"Yu-Ling Zhang, Gui-Liang Peng, Wei-Ling Leng, Yu Lian, Li-Qing Cheng, Xing Li, Yu-Lin Wang, Ling Zhou, Min Long","doi":"10.4239/wjd.v16.i3.98590","DOIUrl":"https://doi.org/10.4239/wjd.v16.i3.98590","url":null,"abstract":"<p><strong>Background: </strong>Serum retinol-binding protein (RBP) is the primary transport protein of circulating vitamin A. RBP has a crucial role in maintaining nutrient metabolism and physiologic homeostasis. Several studies have indicated that serum RBP participates in the progression of diabetes and diabetes-related complications. However, the impact of serum RBP on lower limb atherosclerosis has not been determined in individuals with type 2 diabetes mellitus (T2DM).</p><p><strong>Aim: </strong>To determine the association between serum RBP and lower limb atherosclerosis in individuals with T2DM.</p><p><strong>Methods: </strong>This retrospective study enrolled 4428 eligible T2DM patients and divided the patients into non-lower limb atherosclerosis (<i>n</i> = 1913) and lower limb atherosclerosis groups (<i>n</i> = 2515) based on lower limb arterial ultrasonography results. At hospital admission, baseline serum RBP levels were assessed, and all subjects were categorized into three groups (Q1-Q3) based on RBP tertiles. Logistic regression, restricted cubic spline regression, subgroup analysis, and machine learning were used to assess the association between RBP levels and lower limb atherosclerosis risk.</p><p><strong>Results: </strong>Among 4428 individuals with T2DM, 2515 (56.80%) had lower limb atherosclerosis. Logistic analysis showed that lower limb atherosclerosis risk increased by 1% for every 1 unit rise in serum RBP level (odds ratio = 1.01, 95% confidence interval: 1.00-1.02, <i>P</i> = 0.004). Patients in the highest tertile group (Q3) had a higher lower limb atherosclerosis risk compared to the lowest tertile group (Q1) (odds ratio = 1.36, 95% confidence interval: 1.12-1.67, <i>P</i> = 0.002). The lower limb atherosclerosis risk gradually increased with an increase in RBP tertile (<i>P</i> for trend = 0.005). Restricted cubic spline analysis indicated a linear correlation between serum RBP levels and lower limb atherosclerosis risk (non-linear <i>P</i> < 0.05). Machine learning demonstrated the significance and diagnostic value of serum RBP in predicting lower limb atherosclerosis risk.</p><p><strong>Conclusion: </strong>Elevated serum RBP levels correlate with an increased lower limb atherosclerosis risk in individuals with T2DM.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 3","pages":"98590"},"PeriodicalIF":4.2,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SMAD specific E3 ubiquitin protein ligase 1 accelerates diabetic macular edema progression by WNT inhibitory factor 1.","authors":"Li-Fang Liang, Jia-Qi Zhao, Yi-Fei Wu, Hui-Jie Chen, Tian Huang, Xiao-He Lu","doi":"10.4239/wjd.v16.i3.101328","DOIUrl":"https://doi.org/10.4239/wjd.v16.i3.101328","url":null,"abstract":"<p><strong>Background: </strong>Diabetic macular edema (DME) is the most common cause of vision loss in people with diabetes. Tight junction disruption of the retinal pigment epithelium (RPE) cells has been reported to induce DME development. SMAD-specific E3 ubiquitin protein ligase (SMURF) 1 was associated with the tight junctions of cells. However, the mechanism of SMURF1 in the DME process remains unclear.</p><p><strong>Aim: </strong>To investigate the role of SMURF1 in RPE cell tight junction during DME.</p><p><strong>Methods: </strong>ARPE-19 cells treated with high glucose (HG) and desferrioxamine mesylate (DFX) for establishment of the DME cell model. DME mice models were constructed by streptozotocin induction. The trans-epithelial electrical resistance and permeability of RPE cells were analyzed. The expressions of tight junction-related and autophagy-related proteins were determined. The interaction between insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) and SMURF1 mRNA was verified by RNA immunoprecipitation (RIP). SMURF1 N6-methyladenosine (m6A) level was detected by methylated RIP.</p><p><strong>Results: </strong>SMURF1 and vascular endothelial growth factor (VEGF) were upregulated in DME. SMURF1 knockdown reduced HG/DFX-induced autophagy, which protected RPE cell tight junctions and ameliorated retinal damage in DME mice. SMURF1 activated the Wnt/β-catenin-VEGF signaling pathway by promoting WNT inhibitory factor (WIF) 1 ubiquitination and degradation. IGF2BP2 upregulated SMURF1 expression in an m6A modification-dependent manner.</p><p><strong>Conclusion: </strong>M6A-modified SMURF1 promoted WIF1 ubiquitination and degradation, which activated autophagy to inhibit RPE cell tight junctions, ultimately promoting DME progression.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 3","pages":"101328"},"PeriodicalIF":4.2,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-sectional study of the association between triglyceride glucose-body mass index and obstructive sleep apnea risk.","authors":"Li Gong, Ming Su, Jing-Han Xu, Zhen-Fei Peng, Lin Du, Ze-Yao Chen, Yu-Zhou Liu, Lu-Cia Chan, Yin-Luan Huang, Yu-Tian Chen, Feng-Yi Huang, Chun-Li Piao","doi":"10.4239/wjd.v16.i3.98519","DOIUrl":"https://doi.org/10.4239/wjd.v16.i3.98519","url":null,"abstract":"<p><strong>Background: </strong>The triglyceride glucose-body mass index (TyG-BMI) is a novel indicator of insulin resistance (IR). Obstructive sleep apnea (OSA) is a prevalent disorder characterized by recurrent complete or partial collapse of the pharyngeal airway during sleep; however, the relationship between these two conditions remains unexplored. We hypothesized that a higher TyG-BMI is associated with the occurrence of OSA.</p><p><strong>Aim: </strong>To assess the association between TyG-BMI and OSA in adults in the United States.</p><p><strong>Methods: </strong>A cross-sectional study was conducted utilizing data from the National Health and Nutrition Examination Surveys spanning from 2005-2008 to 2015-2018. TyG-BMI was calculated as Ln [triglyceride (mg/dL) × fasting blood glucose (mg/dL)/2] × BMI. Restricted cubic splines were used to analyze the risk of TyG-BMI and OSA occurrence. To identify potential nonlinear relationships, we combined Cox proportional hazard regression with smooth curve fitting. We also conducted sensitivity and subgroup analyses to verify the robustness of our findings.</p><p><strong>Results: </strong>We included 16794 participants in the final analysis. Multivariate regression analysis showed that participants with a higher TyG-BMI had a higher OSA incidence. After adjusting for all covariates, TyG-BMI was positively correlated with the prevalence of OSA (odds ratio: 1.28; 95% confidence interval: 1.17, 1.40; <i>P</i> < 0.001); no significant nonlinear relationship was observed. Subgroup analysis showed no strong correlation between TyG-BMI and OSA in patients with diabetes. The correlation between TyG-BMI and OSA was influenced by age, sex, smoking status, marital status, hypertensive stratification, and obesity; these subgroups played a moderating role between TyG-BMI and OSA. Even after adjusting for all covariates, there was a positive association between TYG-BMI and OSA prevalence.</p><p><strong>Conclusion: </strong>A higher TyG-BMI index is linked to higher chances of developing OSA. As TyG-BMI is an indicator of IR, managing IR may help reduce the risk of OSA.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 3","pages":"98519"},"PeriodicalIF":4.2,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the effectiveness of ultrasound-assisted wound debridement in managing diabetic foot ulcers: A systematic review and meta-analysis.","authors":"Rui Yang, Geng Chen, Qing-Yun Pan, Yao Yao, Yan-Fen Li, Hai-Ting Chen, Chang-Jiang Lei, Xia Liang","doi":"10.4239/wjd.v16.i2.97077","DOIUrl":"10.4239/wjd.v16.i2.97077","url":null,"abstract":"<p><strong>Background: </strong>Diabetic foot ulcers (DFUs) present a significant clinical challenge due to their high prevalence and profound impact on morbidity. Ultrasound-assisted wound debridement (UAWD) has emerged as a potential therapeutic modality to improve healing outcomes in DFU management.</p><p><strong>Aim: </strong>To evaluate the efficacy of UAWD in treating DFUs on wound closure rates, treatment duration, and quality of life outcomes.</p><p><strong>Methods: </strong>This systematic review and meta-analysis followed PRISMA guidelines, systematically searching PubMed, Embase, Web of Science, and the Cochrane Library with no date restrictions. Randomized controlled trials (RCTs) that evaluated the efficacy of UAWD in DFU treatment were included. Data were independently extracted by two reviewers, with discrepancies resolved through consensus or third-party consultation. The risk of bias was assessed using the Cochrane tool. <i>χ</i> ² and <i>I</i> ² statistics assessed heterogeneity, informing the use of fixed or random-effects models for meta-analysis, supplemented by sensitivity analysis and publication bias assessment through funnel plots and Egger's test.</p><p><strong>Results: </strong>From 1255 articles, seven RCTs met the inclusion criteria. The studies demonstrated that UAWD significantly reduced DFU healing time (standardized mean difference = -0.78, 95%CI: -0.97 to -0.60, <i>P</i> < 0.001) and increased healing rates (odds ratio = 9.96, 95%CI: 5.99 to 16.56, <i>P</i> < 0.001) compared to standard care. Sensitivity analysis confirmed the stability of these results, and no significant publication bias was detected.</p><p><strong>Conclusion: </strong>UAWD is a promising adjunctive treatment for DFUs, significantly reducing healing times and increasing healing rates. These findings advocate for the integration of UAWD into standard DFU care protocols.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"97077"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptome and single-cell profiling of the mechanism of diabetic kidney disease.","authors":"Ying Zhou, Xiao Fang, Lin-Jing Huang, Pei-Wen Wu","doi":"10.4239/wjd.v16.i2.101538","DOIUrl":"10.4239/wjd.v16.i2.101538","url":null,"abstract":"<p><strong>Background: </strong>The NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome may play an important role in diabetic kidney disease (DKD). However, the exact link remains unclear.</p><p><strong>Aim: </strong>To investigate the role of the NLRP3 inflammasome in DKD.</p><p><strong>Methods: </strong>Using datasets from the Gene Expression Omnibus database, 30 NLRP3 inflammasome-related genes were identified. Differentially expressed genes were selected using differential expression analysis, whereas intersecting genes were selected based on overlapping differentially expressed genes and NLRP3 inflammasome-related genes. Subsequently, three machine learning algorithms were used to screen genes, and biomarkers were identified by overlapping the genes from the three algorithms. Potential biomarkers were validated by western blotting in a db/db mouse model of diabetes.</p><p><strong>Results: </strong>Two biomarkers, sirtuin 2 (SIRT2) and caspase 1 (CASP1), involved in the Leishmania infection pathway were identified. Both biomarkers were expressed in endothelial cells. Pseudo-temporal analysis based on endothelial cells showed that DKD mostly occurs during the mid-differentiation stage. Western blotting results showed that CASP1 expression was higher in the DKD group than in the control group (<i>P</i> < 0.05), and SIRT2 content decreased (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>SIRT2 and CASP1 provide a potential theoretical basis for DKD treatment.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"101538"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 <i>SPTLC1</i> on type 2 diabetes mellitus.","authors":"Bo Yi, Yan Bao, Zhong-Yuan Wen","doi":"10.4239/wjd.v16.i2.94861","DOIUrl":"10.4239/wjd.v16.i2.94861","url":null,"abstract":"<p><strong>Background: </strong>Although numerous single nucleotide polymorphism in multiple genes involve in the risk of type 2 diabetes mellitus (T2D), the single gene defects of T2D with strong family history is not clear yet. <i>SPTLC1</i> are causative for hereditary sensory and autonomic neuropathy, which is clinical overlapping with diabetic peripheral neuropathy. Mice with adipocyte-specific deletion of <i>SPTLC1</i> had impaired glucose tolerances and insulin sensitivity. Thus, it is necessary to investigate the <i>SPTLC1</i> mutations in adult-onset T2D with strong family history.</p><p><strong>Aim: </strong>To analyze the role of <i>SPTLC1</i> mutation on adult-onset T2D with strong family history.</p><p><strong>Methods: </strong>By whole-exome sequence analysis of a patient with T2D and his family members, an uncertain variant in <i>SPTLC1</i> was identified. Bioinformation analysis was used to evaluate the influence of mutation, rare variant gene-level associations for <i>SPTLC1</i> in T2D, and the relationship between <i>SPTLC1</i> mRNA and T2D in human islets from GSE25724. The effect of G371R of <i>SPTLC1</i> on the characteristics of inflammatory cytokines and apoptosis was also tested on human embryonic kidney (HEK) 293 cells.</p><p><strong>Results: </strong>A single nucleotide variation in <i>SPTLC1</i> (c.1111G>A: p.G371R) was identified in a family with T2D. The deleterious variant was predicted by functional analysis through hidden Markov models and mendelian clinically applicable pathogenicity software. This pathogenicity might be derived from the different amino acid properties. In HEK 293T cells, p.G371R of <i>SPTLC1</i> induced the expression of tumor necrosis factor-α and the percent of apoptosis. Meanwhile, rare variant gene-level associations for <i>SPTLC1</i> also refer to the high risk of T2D (the overall odds ratio = 2.4968, <i>P</i> = 0.0164). Data from GSE25724 showed that <i>SPTLC1</i> mRNA was lower in pancreatic islets from T2D human islets (<i>P</i> = 0.046), and was associated with the decreased level of insulin mRNA expression (Spearman <i>r</i> = 0.615, <i>P</i> = 0.025).</p><p><strong>Conclusion: </strong>The study classified <i>SPTLC1</i> p.G371R mutation as the likely pathogenic mutation from an adult-onset T2D patients with strong family history T2D.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"94861"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists on proteinuria and weight in a diabetes cohort.","authors":"Di-Fei Lu, Rui Zheng, Ang Li, Jun-Qing Zhang","doi":"10.4239/wjd.v16.i2.98552","DOIUrl":"10.4239/wjd.v16.i2.98552","url":null,"abstract":"<p><strong>Background: </strong>With accumulating evidence showing a benefit in the renal and cardiovascular systems, diabetes guidelines recommend that patients with diabetes and chronic kidney disease (CKD) be treated with sodium-glucose cotransporter-2 inhibitor (SGLT2i) and/or glucagon like peptide-1 receptor agonists (GLP-1RAs) for renal protection. The real-world efficacy of the two medications on the urinary albumin-creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR) remains to be explored.</p><p><strong>Aim: </strong>To evaluate the SGLT2i and GLP-1RA application rates and UACR alterations after intervention in a real-world cohort of patients with diabetes.</p><p><strong>Methods: </strong>A cohort of 5482 patients with type 2 diabetes were enrolled and followed up at the Integrated Care Clinic for Diabetes of Peking University First Hospital for at least 6 months. Propensity score matching was performed, and patients who were not recommended for GLP-1RA or SGLT2i with comparable sex categories and ages were assigned to the control group at a 1:2 ratio. Blood glucose, body weight, UACR and eGFR were evaluated after 6 months of treatment in real-world clinical practice.</p><p><strong>Results: </strong>A total of 139 (2.54%) patients started GLP-1RA, and 387 (7.06%) received SGLT2i. After 6 months, the variations in fasting blood glucose, prandial blood glucose, and glycosylated hemoglobin between the GLP-1RA group and the SGLT2i and control groups were not significantly different. UACR showed a tendency toward a greater reduction compared with the control group, although this difference was not statistically significant (GLP-1RA <i>vs</i> control, -2.20 <i>vs</i> 30.16 mg/g, <i>P</i> = 0.812; SGLT2i <i>vs</i> control, -20.61 <i>vs</i> 12.01 mg/g, <i>P</i> = 0.327); eGFR alteration also showed no significant differences. Significant weight loss was observed in the GLP-1RA group compared with the control group (GLP-1RA <i>vs</i> control, -0.90 <i>vs</i> 0.27 kg, <i>P</i> < 0.001), as well as in the SGLT2i group (SGLT2i <i>vs</i> control, -0.59 <i>vs</i> -0.03 kg, <i>P</i> = 0.010).</p><p><strong>Conclusion: </strong>Compared with patients who received other glucose-lowering drugs, patients receiving SGLT2i or GLP-1RAs presented significant weight loss, a decreasing trend in UACR and comparable glucose-lowering effects in real-world settings.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"98552"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture alleviates diabetic peripheral neuropathy through modulating mitochondrial biogenesis and suppressing oxidative stress.","authors":"Chong-Xi Yuan, Xuan Wang, Yun Liu, Tian-Cheng Xu, Zhi Yu, Bin Xu","doi":"10.4239/wjd.v16.i2.93130","DOIUrl":"10.4239/wjd.v16.i2.93130","url":null,"abstract":"<p><strong>Background: </strong>Peripheral neuropathy caused by diabetes is closely related to the vicious cycle of oxidative stress and mitochondrial dysfunction resulting from metabolic abnormalities. The effects mediated by the silent information regulator type 2 homolog-1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) axis present new opportunities for the treatment of type 2 diabetic peripheral neuropathy (T2DPN), potentially breaking this harmful cycle.</p><p><strong>Aim: </strong>To validate the effectiveness of electroacupuncture (EA) in the treatment of T2DPN and investigate its potential mechanism based on the SIRT1/PGC-1α axis.</p><p><strong>Methods: </strong>The effects of EA were evaluated through assessments of metabolic changes, morphological observations, and functional examinations of the sciatic nerve, along with measurements of inflammation and oxidative stress. Proteins related to the SIRT1/PGC-1α axis, involved in the regulation of mitochondrial biogenesis and antioxidative stress, were detected in the sciatic nerve using Western blotting to explain the underlying mechanism. A counterevidence group was created by injecting a SIRT1 inhibitor during EA intervention to support the hypothesis.</p><p><strong>Results: </strong>In addition to diabetes-related metabolic changes, T2DPN rats showed significant reductions in pain threshold after 9 weeks, suggesting abnormal peripheral nerve function. EA treatment partially restored metabolic control and reduced nerve damage in T2DPN rats. The SIRT1/PGC-1α axis, which was downregulated in the model group, was upregulated by EA intervention. The endogenous antioxidant system related to the SIRT1/PGC-1α axis, previously inhibited in diabetic rats, was reactivated. A similar trend was observed in inflammatory markers. When SIRT1 was inhibited in diabetic rats, these beneficial effects were abolished.</p><p><strong>Conclusion: </strong>EA can alleviate the symptoms of T2DNP in experimental rats, and its effects may be related to the mitochondrial biogenesis and endogenous antioxidant system mediated by the SIRT1/PGC-1α axis.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"16 2","pages":"93130"},"PeriodicalIF":4.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11718478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}