World Journal of Diabetes最新文献

{"title":"Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease.","authors":"Yue Ji, Rui-Xin Liu, Pei-Yue He, Yi-Min Zhou, Ya-Chun Li, Jing Guo, Bo Nie, Yu-Ning Liu, Wei-Jing Liu","doi":"10.4239/wjd.v17.i2.112500","DOIUrl":"10.4239/wjd.v17.i2.112500","url":null,"abstract":"<p><strong>Background: </strong>Diabetic kidney disease (DKD) continues to pose a substantial public health challenge, in which cellular senescence is recognized as a pivotal driver of disease progression. While formononetin (FN) has been documented to exhibit anti-senescence properties, its potential as a therapeutic agent for DKD and the molecular mechanisms involved remain unexplored.</p><p><strong>Aim: </strong>To evaluate the efficacy of FN using an <i>in vitro</i> model of high glucose (HG)-induced injury in MPC-5 podocytes. Transcriptomic profiling was employed to assess the influence of FN on global gene expression and to identify key signaling pathways affected by FN treatment. Furthermore, we sought to investigate the anti-senescence effects of FN and its regulatory role in the p53 signaling pathway <i>in vitro</i>.</p><p><strong>Methods: </strong>To elucidate the functional role of MDM2 in the anti-senescence mechanism of FN, MDM2 expression was silenced in MPC-5 cells using gene-specific knockdown. Finally, a mouse model of DKD was generated by combining a high-fat diet with intraperitoneal streptozotocin injections, and the therapeutic as well as anti-senescence effects of FN were evaluated <i>in vivo</i>.</p><p><strong>Results: </strong>In the HG-induced MPC-5 cell model, FN treatment significantly enhanced cell viability and reduced the secretion of senescence-associated secretory phenotype (SASP) factors in the supernatant. Transcriptomic analysis revealed the p53 signaling pathway as a central target of FN under HG conditions. FN treatment markedly suppressed β-galactosidase (β-GAL) activity, upregulated the expression of MDM2 and CCND1, downregulated the expression of p53 and p21, and inhibited p53 transcriptional activity in MPC-5 cells. These protective effects were abrogated upon MDM2 silencing. In DKD mice, FN administration improved renal function, alleviated histopathological damage, reduced renal SASP levels and β-GAL activity, and normalized the expression of key proteins in the p53 pathway.</p><p><strong>Conclusion: </strong>Our findings demonstrate that FN confers significant therapeutic benefits against DKD in both cellular and animal models. The mechanism underlying these benefits involves the delay of cellular senescence through suppression of the p53 signaling pathway.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"112500"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146202917","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":"Pathological effects of diabetic mice with <i>Helicobacter pylori</i> infection.","authors":"Wan-Ping Yang, Jin-Hai Zeng, Biao-Liang Wu, Wen-Ting Zhou, Jia-Zi Luo, Yuan-Yuan Dai, Shi-Xian Yang, Zan-Song Huang, Yan-Qiang Huang","doi":"10.4239/wjd.v17.i2.112534","DOIUrl":"10.4239/wjd.v17.i2.112534","url":null,"abstract":"<p><strong>Background: </strong><i>Helicobacter pylori</i> (<i>H. pylori</i>) is widely present in the human gastric mucosa and is closely associated with a variety of gastric diseases. Recent studies have found that <i>H. pylori</i> infection is closely associated with diabetic patients and may adversely affect their glucose metabolism and organ function. However, the effect of <i>H. pylori</i> infection on pathological changes in the body during a diabetic state remains unclear.</p><p><strong>Aim: </strong>To investigate the effects of <i>H. pylori</i> infection on the physiology and pathological changes in the organs of diabetic mice.</p><p><strong>Methods: </strong>The diabetic mice models were established using streptozotocin (STZ). The mice were infected with <i>H. pylori</i> through oral gavage, with their fasting blood glucose (FBG) and body weight monitored dynamically over a period of 1 to 13 months after infection. Pathological changes in major organs (including the pancreas, stomach, liver, and kidneys) were assessed, along with apoptosis levels in these tissues. The expression of <i>H. pylori</i> virulence factors in the liver and alterations in the intestinal microbiota were also analyzed.</p><p><strong>Results: </strong><i>H. pylori</i> infection led to significant fluctuations in FBG in diabetic mice from the 1^st to 9^th month, with FBG levels remaining consistently elevated. Body weight increased gradually but remained significantly lower than that of both uninfected diabetic mice and non-diabetic controls. Pancreatic islet cell numbers decreased, accompanied by persistent inflammation and tissue damage for over 9 months. <i>H. pylori</i> colonized the stomach for at least 7 months, causing irreversible gastric mucosal inflammation; by the 13^th month, diffuse dense inflammatory infiltration occupying the entire submucosal layer was observed. Progressive damage was observed in liver and kidney tissues, with marked expression of <i>H. pylori</i> virulence factors in the liver by the 9^th month. Additionally, significant gut microbiota dysbiosis was observed.</p><p><strong>Conclusion: </strong>The STZ-induced diabetic mouse model with <i>H. pylori</i> infection can significantly prolong the colonization time of <i>H. pylori</i> in the stomach and exacerbate the degree of damage to the stomach, liver, and kidney organs.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"112534"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203301","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 of serum bile acid profiles with the risk of gastrointestinal autonomic neuropathy in patients with type 2 diabetes mellitus.","authors":"Ke-Ying Zhu, Si-Jing Wang, Jie Li, Pan-Pan Ma, Su-Su Feng, Lin Guo, Yi-Bing Lu, Li Dong, Da-Fa Ding","doi":"10.4239/wjd.v17.i2.112859","DOIUrl":"10.4239/wjd.v17.i2.112859","url":null,"abstract":"<p><strong>Background: </strong>Diabetic gastrointestinal autonomic neuropathy (DGAN) is a common yet underrecognized manifestation of diabetic neuropathy. However, the clinical correlations and associated alterations of serum bile acid (BA) metabolism with DGAN remain unclear.</p><p><strong>Aim: </strong>To identify potential metabolite biomarkers capable of identifying DGAN among patients with type 2 diabetes mellitus (T2DM).</p><p><strong>Methods: </strong>This cross-sectional study included 26 patients with clinically defined DGAN and 69 patients with uncomplicated T2DM. Fifteen individual BAs were quantified in fasting serum using liquid chromatography-tandem mass spectrometry. Gastrointestinal symptoms were scored using the Gastrointestinal Symptom Rating Scale. Spearman's correlation, multivariable logistic regression, receiver operating characteristic, and decision curve analyses were used to explore the associations and build a predictive nomogram.</p><p><strong>Results: </strong>Orthogonal partial least squares discriminant analysis of serum BAs revealed clear separation between the T2DM and DGAN groups, identifying taurolithocholic acid (TLCA) as the key discriminator (variable importance in projection > 1, fold change < 0.5). Univariate logistic regression identified age, body mass index, hemoglobin, fasting/2-h C-peptide, albumin, and TLCA levels as protective factors and the urinary albumin-to-creatinine ratio as a risk factor. After multivariate adjustment age, fasting C-peptide levels, and TLCA levels remained independently associated with DGAN. Receiver operating characteristic analysis yielded areas under the curve of 0.651, 0.760, and 0.678 for age, fasting C-peptide, and TLCA, respectively, and the three variables collectively had an area under the curve of 0.970 (95% confidence interval: 0.937-1.000). Decision curve analysis confirmed the clinical net benefit across threshold probabilities of 9%-68%. The derived nomogram displayed excellent calibration and net clinical benefits for the model.</p><p><strong>Conclusion: </strong>These findings highlighted the association between altered BA profiles and DGAN in patients with T2DM. Combining BA profiling with conventional clinical data could facilitate the early identification of DGAN and offer new insights into early screening and BA-targeted interventions. While these findings offer valuable insights, they should nevertheless be viewed as hypothesis-generating and require further validation in larger, multicenter cohorts.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"112859"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203402","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":"Using the triglyceride-glucose index and derived indexes to forecast progression from pre-diabetes to diabetes: A 3-year follow-up study.","authors":"Bing Wang, Ming-Chuan Liu, Xu-Han Liu, Zhu Zhu, Ying-Shu Liu, Ting-Ting Zhang, Xin-Yu Li, Zheng-Nan Gao","doi":"10.4239/wjd.v17.i2.114253","DOIUrl":"10.4239/wjd.v17.i2.114253","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Pre-diabetes is a transitional metabolic stage between health and diabetes, serving as a critical warning signal for disease progression. Early intervention targeting risk factors in prediabetic individuals prevents the progression to type 2 diabetes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Aim: &lt;/strong&gt;To investigate the predictive value of the triglyceride-glucose (TyG) index and its derived indicators for new-onset diabetes in patients with pre-diabetes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A prospective community-based cohort study was carried out based on subjects aged over 40 years with pre-diabetes in Dalian, Liaoning Province, China. A total of 1352 subjects with complete follow-up data attended the follow-up survey. Multivariable Cox regression models were performed to assess the association of the TyG index and its derived indicators with risk of diabetes in patients with pre-diabetes. The diagnostic values of the TyG index and derived indicators in predicting new-onset diabetes were analyzed, and suitable cutting points were determined using the receiver operating characteristic (ROC) curve.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;During a 3-year follow-up period, 153 cases with incident diabetes were identified, with a cumulative incidence of diabetes of 11.3%; 12.6% (43/341) in males and 10.9% (110/1011) in females (&lt;i&gt;χ&lt;/i&gt; &lt;sup&gt;2&lt;/sup&gt; = 0.760, &lt;i&gt;P&lt;/i&gt; = 0.375). After adjusting for confounding factors including age, gender, body mass index (BMI) and insulin levels, the risk of diabetes with higher TyG and derived indexes [TyG-BMI and TyG-waist circumference index (TyG-WC)] increased significantly. The TyG index [hazard ratio (HR) = 1.389, 95% confidence interval (CI): 1.011-1.908, &lt;i&gt;P&lt;/i&gt; = 0.043], TyG-BMI (HR = 1.010, 95%CI: 1.005-1.015, &lt;i&gt;P&lt;/i&gt; = 0.000) and TyG-WC (HR = 1.003, 95%CI: 1.001-1.005, &lt;i&gt;P&lt;/i&gt; = 0.001) were all strongly positively correlated with the risk of future diabetes. The ROC curve analysis showed that the area under the curve (AUCs) of the TyG, TyG-BMI and TyG-WC for predicting new diabetes were 0.578 (95%CI: 0.533-0.624), 0.622 (95%CI: 0.574-0.670) and 0.609 (95%CI: 0.562-0.657), respectively. The difference in AUC between TyG-BMI and TyG was significant (&lt;i&gt;P&lt;/i&gt; = 0.047), while the differences between TyG-BMI and TyG-WC (&lt;i&gt;P&lt;/i&gt; = 0.464) and between TyG-WC and TyG (&lt;i&gt;P&lt;/i&gt; = 0.175) were not. The TyG-BMI had a larger AUC than the TyG and TyG-WC, and its difference from TyG was significant. The best cut-off points for predicting new diabetes were TyG &gt; 8.6, TyG-BMI &gt; 247 and TyG-WC &gt; 860. Although the AUC values were modest, these indices may serve as preliminary screening tools in resource-limited settings.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;The TyG index and its derived indicators were risk factors for the pre-diabetes to diabetes outcome, and may be regarded as predictors of the outcome. The risk of conversion of pre-diabetes to diabetes increased with increases in the TyG index and its derived indicators. ","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"114253"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203470","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":"Integrated hepatic transcriptome and metabolome reveal the mechanisms of Jiangtang Tiaozhi formula on improving glycolipid metabolic disorder.","authors":"Jia-Xing Tian, Yan-Jiao Zhang, Yu-Xin Zhang, Jia-Hua Wei, Xin-Yi Fang, Run-Yu Miao, Kai-Le Ma, Hui-Fang Guan, Xin-Miao Wang, Hao-Ran Wu","doi":"10.4239/wjd.v17.i2.111453","DOIUrl":"10.4239/wjd.v17.i2.111453","url":null,"abstract":"<p><strong>Background: </strong>Glycolipid metabolic disorder includes a series of chronic diseases that are closely associated with disturbances in both glucose and lipid metabolism. Jiangtang Tiaozhi formula (JTTZF) demonstrating significant hypoglycemic, lipid-modifying, and anti-inflammatory effects. However, the specific molecular mechanisms underlying JTTZF's hepatoprotective effects and its ability to ameliorate glycolipid metabolic disorder remain largely unexplored.</p><p><strong>Aim: </strong>To investigate how JTTZF improves glycolipid metabolic disorder using hepatic transcriptome and metabolome analyses.</p><p><strong>Methods: </strong>To induce glycolipid metabolic disorder, male C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks, after which they received an 8-week administration of JTTZF. Liver tissues were analyzed using transcriptomics and metabolomics. Real-time quantitative polymerase chain reaction validated key gene expression.</p><p><strong>Results: </strong>Metabolomics data revealed that JTTZF significantly regulated HFD-induced alterations in glycolipid metabolism, with notable changes in pathways such as the pentose phosphate pathway, steroid hormone biosynthesis, and purine metabolism. Transcriptomics profiles indicated that JTTZF exerted regulatory effects on lipid and glucose metabolism, primarily through pathways including peroxisome proliferators-activated receptor signaling, drug metabolism other enzymes, and regulation of lipolysis in adipocytes. Real-time quantitative polymerase chain reaction confirmed that JTTZF modulated pivotal genes associated with fatty acid synthesis, lipolysis, insulin resistance, energy metabolism, and inflammation. These findings suggest that JTTZF may act through multiple pathways to improve glycolipid metabolic disorder.</p><p><strong>Conclusion: </strong>JTTZF can ameliorate the glycolipid metabolic disorder induced by HFD-diet by regulating lipid metabolism and improving insulin tolerance.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"111453"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203312","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":"Renal and metabolic effects of semaglutide plus canagliflozin <i>vs</i> canagliflozin alone in type 2 diabetic nephropathy.","authors":"Yan Miao, Pan He, Dan-Yu Wang, Lei Yan, Hui-Xia Cao, Feng-Min Shao","doi":"10.4239/wjd.v17.i2.112867","DOIUrl":"10.4239/wjd.v17.i2.112867","url":null,"abstract":"<p><strong>Background: </strong>Diabetic nephropathy (DN) is a major microvascular complication of type 2 diabetes and a leading cause of end-stage renal disease. Both canagliflozin and semaglutide are recommended for diabetic nephropathy, yet direct evidence comparing their combination versus monotherapy remains lacking.</p><p><strong>Aim: </strong>To investigate the efficacy of combination therapy with semaglutide and canagliflozin compared with canagliflozin alone in patients with type 2 DN.</p><p><strong>Methods: </strong>A retrospective study was conducted using data sourced from the electronic medical record system of Henan Provincial People's Hospital. The study included patients with DN treated from October 2022 to March 2024. Patients were divided into two groups on the basis of their treatment: Canagliflozin monotherapy (CM) and canagliflozin and semaglutide combination therapy (CSCT). Renal function, glucose metabolism, lipid profiles, pancreatic function, oxidative stress, and inflammatory markers were assessed at baseline and 6 months after treatment. Adverse events were monitored throughout the study period.</p><p><strong>Results: </strong>Among 211 patients (107 CM, and 104 CSCT), the CSCT group demonstrated superior outcomes. The albumin-to-creatinine ratio decreased more significantly (145.87 mg/g <i>vs</i> 158.11 mg/g, <i>P</i> = 0.002), and more improvements were found in the glycated hemoglobin A1c (7.08% <i>vs</i> 7.42%, <i>P</i> = 0.005), low-density lipoprotein (86.74 mg/dL <i>vs</i> 94.86 mg/dL, <i>P</i> = 0.032), serum free fatty acids (0.46 mmol/L <i>vs</i> 0.52 mmol/L, <i>P</i> = 0.002), and insulin resistance index (3.94 <i>vs</i> 4.08, <i>P</i> = 0.011). Meanwhile, the islet β-cell function increased (51.22 <i>vs</i> 49.36, <i>P</i> = 0.022). The total adverse event rates were comparable between the two groups, and no significant increase was observed in the gastrointestinal adverse events (<i>P</i> = 0.360).</p><p><strong>Conclusion: </strong>CSCT provided significant improvements in multiple metabolic and renal parameters without increasing adverse events, thus highlighting its potential benefits for patients with DN.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"112867"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203426","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":"Decapping scavenger enzyme as a promising biomarker in diabetic foot ulcers: A need for cautious interpretation.","authors":"Xiao-Ling Huang, Ying Wang, De-Fang Chen, Jin-Nian Duan, Ntim Michael, Rong Jiang, Yu-Song Ge, Bin Wang","doi":"10.4239/wjd.v17.i2.116056","DOIUrl":"10.4239/wjd.v17.i2.116056","url":null,"abstract":"<p><p>Diabetic foot ulcer (DFU) remains a major cause of morbidity and lower-limb amputation worldwide. Accurate risk assessment and timely intervention are critical for improving healing outcomes. A recent study identified the decapping scavenger enzyme (DCPS), an N7-methylguanosine (m7G)-related gene, as a potential diagnostic and therapeutic biomarker for DFU. Reduced DCPS expression was found to impair keratinocyte proliferation, migration, and cell-cycle progression, highlighting its possible role in m7G-mediated wound repair. Despite these promising insights, several challenges must be addressed before DCPS can be translated into clinical practice. First, DCPS expression may vary among patients with metabolic or inflammatory disorders, limiting its disease specificity. Second, standardized reference ranges for DCPS quantification have not yet been established. Moreover, whether DCPS modulation can directly enhance wound healing remains uncertain. Overall, DCPS provides a novel mechanistic link between RNA methylation and chronic wound pathology, but its clinical application as a biomarker or therapeutic target warrants careful validation.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"116056"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203444","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":"Enhancing dental implant outcomes in type 2 diabetes: Addressing inflammation and risk factors.","authors":"Li-Feng Xiao, Yi-Xuan Xing, Nian-Zhe Sun","doi":"10.4239/wjd.v17.i2.113906","DOIUrl":"10.4239/wjd.v17.i2.113906","url":null,"abstract":"<p><p>This article contextualizes the recent study by Li <i>et al</i> within the broader challenge of achieving dental implant success in patients with type 2 diabetes mellitus (T2DM). The original article by Li <i>et al</i> provides a thorough retrospective analysis of 146 T2DM patients undergoing dental implant surgery, highlighting key risk factors for peri-implantitis (PI), including elevated glycosylated hemoglobin, smoking, poor oral hygiene, and anterior implant placement. The study also identifies tooth-brushing duration ≥ 3 minutes as a protective factor. We emphasize the critical need for personalized risk assessment and evidence-based clinical protocols that integrate glycemic control, behavioral modifications, and emerging monitoring strategies to mitigate PI risk and enhance long-term outcomes in this high-risk population.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"113906"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146202728","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 protects gastric Cajal cells by reducing macrophage pyroptosis in diabetic gastroparesis.","authors":"Ming-Wei Fan, Jin-Lan Tian, Shu-Hui Zhang, Zi-Jian Zhao, Xin-Ru Liu, Cheng-Xia Liu, Yan Chen","doi":"10.4239/wjd.v17.i2.114252","DOIUrl":"10.4239/wjd.v17.i2.114252","url":null,"abstract":"<p><strong>Background: </strong>This study elucidates the mechanisms through which electroacupuncture (EA) at Zusanli acupoint, applied at different frequencies, alleviates diabetic gastroparesis (DGP). The modulation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, its regulation of M2 macrophage pyroptosis, and the consequent protection of interstitial cells of Cajal (ICCs) were investigated.</p><p><strong>Aim: </strong>To investigate the mechanism by which EA alleviates DGP.</p><p><strong>Methods: </strong>A DGP rat model was induced by feeding a high-fat/high-sucrose diet combined with a single intraperitoneal injection of streptozotocin (30 mg/kg). Rats successfully modeled were randomly assigned into four groups (<i>n</i> = 6 each): Untreated DGP, sham-EA (0 Hz, 0 mA), low-frequency EA (LEA, 10 Hz, 1-3 mA), and high-frequency EA (HEA, 100 Hz, 1-3 mA). EA was delivered at Zusanli acupoint for 60 minutes daily over 8 weeks. Gastric emptying rate and whole gut transit time were evaluated. Gastric antrum tissues were examined by immunofluorescence and western blotting to assess ICC integrity, M2 macrophage distribution, pyroptosis-related markers (Gasdermin D, NOD-like receptor family pyrin domain containing 3, caspase-1), inflammatory cytokines [interleukin (IL)-1β, IL-18], and cGAS-STING signaling proteins.</p><p><strong>Results: </strong>The results of this study revealed that HEA significantly increased gastric emptying [0.69 (0.55, 0.72) <i>vs</i> DGP 0.44 (0.26, 0.48), <i>P</i> < 0.05] and reduced whole gut transit time (361.34 ± 10.51 <i>vs</i> DGP 537.33 ± 100.57, <i>P</i> < 0.01), with improved efficacy compared to LEA. In DGP rats, ICC counts were significantly reduced, transferase dUTP nick-end labeling-positive apoptotic markers were elevated, and CD206+ cells were diminished; these alterations were reversed mainly by EA, with HEA showing the greatest effect. Expression of cGAS-STING signaling components and pyroptosis-related proteins (Gasdermin D, NOD-like receptor family pyrin domain containing 3, caspase-1), along with secretion of IL-1β and IL-18, were significantly up-regulated in the DGP group. HEA significantly suppressed cGAS pathway activation, reduced pyroptosis-associated proteins and inflammatory mediators, and outperformed LEA (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>HEA ameliorates gastric dysmotility in DGP by suppressing the cGAS-STING pathway, attenuating M2 macrophage pyroptosis and inflammatory responses, and preserving ICC networks. These findings identify a novel EA/cGAS-STING/pyroptosis axis and highlight its therapeutic potential as a mechanistic target for optimizing DGP treatment strategies.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"114252"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203427","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":"Metabolic dysfunction-associated steatotic liver disease and type 2 diabetes: Pathophysiology, diagnosis, and emerging therapeutic strategies.","authors":"Mithil Gowda Suresh, Safia Mohamed, Harinivaas S Geetha, Sushmita Prabhu, Nitin Trivedi, Zhu C Ng, Priyal D Mehta, Ajit S Brar, Aalam Sohal, Manjeet K Goyal, Juniali Hatwal, Akash Batta","doi":"10.4239/wjd.v17.i2.113149","DOIUrl":"10.4239/wjd.v17.i2.113149","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD), the updated terminology for fatty liver disease linked to metabolic dysfunction, is highly prevalent among individuals with type 2 diabetes mellitus (T2DM). MASLD affects a majority of patients with T2DM and markedly increases the risk of fibrosis, cirrhosis, hepatocellular carcinoma, and cardiovascular mortality. The pathogenesis in diabetic populations reflects a convergence of insulin resistance, dyslipidemia, mitochondrial dysfunction, chronic inflammation, and genetic predisposition. Advances in non-invasive diagnostics, including elastography and serum biomarkers, enable earlier identification and staging of disease, though limitations remain in diabetic cohorts. Lifestyle modification is the cornerstone of therapy, yet emerging pharmacotherapies are reshaping the therapeutic landscape. Antidiabetic agents such as glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, and pioglitazone show hepatic benefits beyond glycemic control, while novel agents and combination regimens are under active evaluation. This narrative review synthesizes current evidence on epidemiology, mechanisms, diagnostics, and therapeutics of MASLD in T2DM, and highlights future directions in precision medicine. Integration of multidisciplinary care is essential to address this converging epidemic.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"113149"},"PeriodicalIF":4.6,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146203318","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}