World Journal of Diabetes最新文献

{"title":"Diabetic cardiomyopathy: Importance of direct evidence to support the roles of NOD-like receptor protein 3 inflammasome and pyroptosis.","authors":"Lu Cai, Yi Tan, Md Shahidul Islam, Michael Horowitz, Kupper A Wintergerst","doi":"10.4239/wjd.v15.i8.1659","DOIUrl":"10.4239/wjd.v15.i8.1659","url":null,"abstract":"<p><p>Recently, the roles of pyroptosis, a form of cell death induced by activated NOD-like receptor protein 3 (NLRP3) inflammasome, in the pathogenesis of diabetic cardiomyopathy (DCM) have been extensively investigated. However, most studies have focused mainly on whether diabetes increases the NLRP3 inflammasome and associated pyroptosis in the heart of type 1 or type 2 diabetic rodent models, and whether various medications and natural products prevent the development of DCM, associated with decreased levels of cardiac NLRP3 inflammasome and pyroptosis. The direct link of NLRP3 inflammasome and associated pyroptosis to the pathogenesis of DCM remains unclear based on the limited evidence derived from the available studies, with the approaches of <i>NLRP3</i> gene silencing or pharmaceutical application of <i>NLRP3</i> specific inhibitors. We thus emphasize the requirement for more systematic studies that are designed to provide direct evidence to support the link, given that several studies have provided both direct and indirect evidence under specific conditions. This editorial emphasizes that the current investigation should be circumspect in its conclusion, <i>i.e.</i>, not overemphasizing its role in the pathogenesis of DCM with the fact of only significantly increased expression or activation of NLRP3 inflammasome and pyroptosis in the heart of diabetic rodent models. Only clear-cut evidence-based causative roles of NLRP3 inflammasome and pyroptosis in the pathogenesis of DCM can help to develop effective and safe medications for the clinical management of DCM, targeting these biomarkers.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 8","pages":"1659-1662"},"PeriodicalIF":4.2,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11346090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082228","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":"Diabetic cardiomyopathy: Emerging therapeutic options.","authors":"Cornelius James Fernandez, Sahana Shetty, Joseph M Pappachan","doi":"10.4239/wjd.v15.i8.1677","DOIUrl":"10.4239/wjd.v15.i8.1677","url":null,"abstract":"<p><p>Diabetic cardiomyopathy (DbCM) is a common but underrecognized compli-cation of patients with diabetes mellitus (DM). Although the pathobiology of other cardiac complications of diabetes such as ischemic heart disease and cardiac autonomic neuropathy are mostly known with reasonable therapeutic options, the mechanisms and management options for DbCM are still not fully understood. In its early stages, DbCM presents with diastolic dysfunction followed by heart failure (HF) with preserved ejection fraction that can progress to systolic dysfunction and HF with reduced ejection fraction in its advanced stages unless appropriately managed. Apart from prompt control of DM with lifestyle changes and antidiabetic medications, disease-modifying therapy for DbCM includes prompt control of hypertension and dyslipidemia inherent to patients with DM as in other forms of heart diseases and the use of treatments with proven efficacy in HF. A basic study by Zhang <i>et al</i>, in a recent issue of the <i>World Journal of Diabetes</i> elaborates the potential pathophysiological alterations and the therapeutic role of teneligliptin in diabetic mouse models with DbCM. Although this preliminary basic study might help to improve our understanding of DbCM and offer a potential new management option for patients with the disease, the positive results from such animal models might not always translate to clinical practice as the pathobiology of DbCM in humans could be different. However, such experimental studies can encourage more scientific efforts to find a better solution to treat patients with this enigmatic disease.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 8","pages":"1677-1682"},"PeriodicalIF":4.2,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11346103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082227","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":"Safety of teplizumab in patients with high-risk for diabetes mellitus type 1: A systematic review.","authors":"Venkata Buddhavarapu, Gagandeep Dhillon, Harpreet Grewal, Pranjal Sharma, Rahul Kashyap, Salim Surani","doi":"10.4239/wjd.v15.i8.1793","DOIUrl":"10.4239/wjd.v15.i8.1793","url":null,"abstract":"<p><strong>Background: </strong>The incidence of diabetes mellitus type 1 (DM1) has been rising worldwide because of improvements in diagnostic techniques and improved access to care in countries with lower socioeconomic status. A new anti-CD4 antibody, Tep-lizumab, has been shown to delay the progression of DM1 and is the only medication approved for this indication. However, more information is needed about the safety profile of this drug.</p><p><strong>Aim: </strong>To identify the odds ratios (OR) of systems-based adverse effects for Teplizumab when compared to Placebo.</p><p><strong>Methods: </strong>An extensive systematic review was conducted from the inception of the medication until December 31, 2023. All clinical trials and studies that evaluated Teplizumab <i>vs</i> placebo were included in the initial review. The study protocol was designed using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines guidelines and was registered in PROSPERO (ID: CRD42024496169). Crude OR were generated using RevMan Software version 5.4.</p><p><strong>Results: </strong>After screening and review, 5 studies were selected to determine the risk of adverse effects of teplizumab compared to placebo. A total of 561 patients were included in the study population. Total adverse effects and system-based adverse effects were studied and reported. We determined that patients receiving Teplizumab had a higher risk of developing gastrointestinal (GI) (OR = 1.60, 95%CI: 1.01-2.52, <i>P</i> = 0.04), dermatological (OR = 6.33, 95%CI: 4.05-9.88, <i>P</i> < 0.00001) and hematological adverse effects (OR = 19.03, 95%CI: 11.09-32.66, <i>P</i> < 0.00001). These patients were also significantly likely to have active Epstein-Barr Virus infection (OR = 3.16, 95%CI: 1.51-6.64, <i>P</i> < 0.002). While our data showed that patients receiving Teplizumab did have a higher incidence of total adverse effects <i>vs</i> placebo, this finding did not reach statistical significance (OR = 2.25, 95%CI: 0.80-6.29, <i>P</i> = 0.12).</p><p><strong>Conclusion: </strong>Our systematic review suggests that Teplizumab patients are at risk for significant adverse effects, primarily related to GI, dermatological, and hematological systems. The total adverse effect data is limited as study populations are small. More studies should be conducted on this medication to better inform the target population of potential adverse effects.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 8","pages":"1793-1801"},"PeriodicalIF":4.2,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11346092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082236","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":"Obstructive sleep apnea: Overlooked comorbidity in patients with diabetes.","authors":"Eric D Tenda, Joshua Henrina, Jin H Cha, Muhammad R Triono, Ersananda A Putri, Dahliana J Aristy, Dicky L Tahapary","doi":"10.4239/wjd.v15.i7.1448","DOIUrl":"10.4239/wjd.v15.i7.1448","url":null,"abstract":"<p><p>In this review article, we explore the interplay between obstructive sleep apnea (OSA) and type 2 diabetes mellitus (T2DM), highlighting a significant yet often overlooked comorbidity. We delve into the pathophysiological links between OSA and diabetes, specifically how OSA exacerbates insulin resistance and disrupts glucose metabolism. The research examines the prevalence of OSA in diabetic patients and its role in worsening diabetes-related complications. Emphasizing the importance of comprehensive management, including weight control and positive airway pressure therapy, the study advocates integrated approaches to improve outcomes for patients with T2DM and OSA. This review underscores the necessity of recognizing and addressing OSA in diabetes care to ensure more effective treatment and better patient outcomes.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 7","pages":"1448-1460"},"PeriodicalIF":4.2,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11292334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141890594","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":"Clinical characteristics and treatment compounds of obesity-related kidney injury.","authors":"Tuo-Hua Mao, Han-Qi Huang, Chuan-Hai Zhang","doi":"10.4239/wjd.v15.i6.1091","DOIUrl":"10.4239/wjd.v15.i6.1091","url":null,"abstract":"<p><p>Disorders in energy homeostasis can lead to various metabolic diseases, particularly obesity. The obesity epidemic has led to an increased incidence of obesity-related nephropathy (ORN), a distinct entity characterized by proteinuria, glomerulomegaly, progressive glomerulosclerosis, and renal function decline. Obesity and its associated renal damage are common in clinical practice, and their incidence is increasing and attracting great attention. There is a great need to identify safe and effective therapeutic modalities, and therapeutics using chemical compounds and natural products are receiving increasing attention. However, the summary is lacking about the specific effects and mechanisms of action of compounds in the treatment of ORN. In this review, we summarize the important clinical features and compound treatment strategies for obesity and obesity-induced kidney injury. We also summarize the pathologic and clinical features of ORN as well as its pathogenesis and potential therapeutics targeting renal inflammation, oxidative stress, insulin resistance, fibrosis, kidney lipid accumulation, and dysregulated autophagy. In addition, detailed information on natural and synthetic compounds used for the treatment of obesity-related kidney disease is summarized. The synthesis of detailed information aims to contribute to a deeper understanding of the clinical treatment modalities for obesity-related kidney diseases, fostering the anticipation of novel insights in this domain.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 6","pages":"1091-1110"},"PeriodicalIF":4.2,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141564850","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":"Rising tide: The global surge of type 2 diabetes in children and adolescents demands action now.","authors":"Joseph M Pappachan, Cornelius James Fernandez, Ambika P Ashraf","doi":"10.4239/wjd.v15.i5.797","DOIUrl":"10.4239/wjd.v15.i5.797","url":null,"abstract":"<p><p>Childhood-onset obesity has emerged as a major public healthcare challenge across the globe, fueled by an obesogenic environment and influenced by both genetic and epigenetic predispositions. This has led to an exponential rise in the incidence of type 2 diabetes mellitus in children and adolescents. The looming wave of diabetes-related complications in early adulthood is anticipated to strain the healthcare budgets in most countries. Unless there is a collective global effort to curb the devastation caused by the situation, the impact is poised to be pro-found. A multifaceted research effort, governmental legislation, and effective social action are crucial in attaining this goal. This article delves into the current epidemiological landscape, explores evidence concerning potential risks and consequences, delves into the pathobiology of childhood obesity, and discusses the latest evidence-based management strategies for diabesity.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 5","pages":"797-809"},"PeriodicalIF":4.2,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141064758","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":"Insulin therapy in type 2 diabetes: Insights into clinical efficacy, patient-reported outcomes, and adherence challenges.","authors":"Mahmoud Emad-Eldin, Gehan F Balata, Eman A Elshorbagy, Mona S Hamed, Mohamed S Attia","doi":"10.4239/wjd.v15.i5.828","DOIUrl":"10.4239/wjd.v15.i5.828","url":null,"abstract":"<p><p>Insulin therapy plays a crucial role in the management of type 2 diabetes as the disease progresses. Over the past century, insulin formulations have undergone significant modifications and bioengineering, resulting in a diverse range of available insulin products. These products show distinct pharmacokinetic and pharmacodynamic profiles. Consequently, various insulin regimens have em-erged for the management of type 2 diabetes, including premixed formulations and combinations of basal and bolus insulins. The utilization of different insulin regimens yields disparate clinical outcomes, adverse events, and, notably, patient-reported outcomes (PROs). PROs provide valuable insights from the patient's perspective, serving as a valuable mine of information for enhancing healthcare and informing clinical decisions. Adherence to insulin therapy, a critical patient-reported outcome, significantly affects clinical outcomes and is influenced by multiple factors. This review provides insights into the clinical effectiveness of various insulin preparations, PROs, and factors impacting insulin therapy adherence, with the aim of enhancing healthcare practices and informing clinical decisions for individuals with type 2 diabetes.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 5","pages":"828-852"},"PeriodicalIF":4.2,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141064698","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":"Synaptotagmins family affect glucose transport in retinal pigment epithelial cells through their ubiquitination-mediated degradation and glucose transporter-1 regulation.","authors":"Hong Xu, Li-Bo Zhang, Yi-Yi Luo, Ling Wang, Ye-Pin Zhang, Pei-Qi Chen, Xue-Ying Ba, Jian Han, Heng Luo","doi":"10.4239/wjd.v15.i5.958","DOIUrl":"10.4239/wjd.v15.i5.958","url":null,"abstract":"<p><strong>Background: </strong>Synaptotagmins (SYTs) are a family of 17 membrane transporters that function as calcium ion sensors during the release of Ca²⁺-dependent neurotransmitters and hormones. However, few studies have reported whether members of the SYT family play a role in glucose uptake in diabetic retinopathy (DR) through Ca²⁺/glucose transporter-1 (GLUT1) and the possible regulatory mechanism of SYTs.</p><p><strong>Aim: </strong>To elucidate the role of the SYT family in the regulation of glucose transport in retinal pigment epithelial cells and explore its potential as a therapeutic target for the clinical management of DR.</p><p><strong>Methods: </strong>DR was induced by streptozotocin in C57BL/6J mice and by high glucose medium in human retinal pigment epithelial cells (ARPE-19). Bioinformatics analysis, reverse transcriptase-polymerase chain reaction, Western blot, flow cytometry, ELISA, HE staining, and TUNEL staining were used for analysis.</p><p><strong>Results: </strong>Six differentially expressed proteins (SYT2, SYT3, SYT4, SYT7, SYT11, and SYT13) were found between the DR and control groups, and SYT4 was highly expressed. Hyperglycemia induces SYT4 overexpression, manipulates Ca²⁺ influx to induce GLUT1 fusion with the plasma membrane, promotes abnormal expression of the glucose transporter GLUT1 and excessive glucose uptake, induces ARPE-19 cell apoptosis, and promotes DR progression. Parkin deficiency inhibits the proteasomal degradation of SYT4 in DR, resulting in SYT4 accumulation and enhanced GLUT1 fusion with the plasma membrane, and these effects were blocked by oe-Parkin treatment. Moreover, dysregulation of the myelin transcription factor 1 (Myt1)-induced transcription of SYT4 in DR further activated the SYT4-mediated stimulus-secretion coupling process, and this process was inhibited in the oe-MYT1-treated group.</p><p><strong>Conclusion: </strong>Our study reveals the key role of SYT4 in regulating glucose transport in retinal pigment epithelial cells during the pathogenesis of DR and the underlying mechanism and suggests potential therapeutic targets for clinical DR.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 5","pages":"958-976"},"PeriodicalIF":4.2,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141064964","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":"Cardioprotective effects of glucagon-like peptide 1 receptor agonists in heart failure: Myth or truth?","authors":"Lorenzo Nesti, Domenico Trico","doi":"10.4239/wjd.v15.i5.818","DOIUrl":"10.4239/wjd.v15.i5.818","url":null,"abstract":"<p><p>Therapy with glucagon-like peptide 1 (GLP1) receptor agonists has raised great interest for its beneficial cardiovascular effects in preventing atherosclerosis and heart failure-related outcomes. However, while evidence about atherosclerosis consistently suggests a cardioprotective potential with class effect, controversies remain on its impact on heart failure. GLP1 receptor agonists appear to prevent hospitalization for new-onset heart failure and reduce symptoms in heart failure with preserved ejection fraction (as demonstrated by the recent STEP-HFpEF Trial). Still, GLP1 agonism has resulted in neutral or even harmful effects in patients with established heart failure with reduced ejection fraction (the LIVE trial). GLP1 receptor agonists benefit the cardiovascular system indirectly through their marked metabolic effects (improved weight management, glycemic control, blood pressure, systemic and tissue inflammation), while direct effects on the heart have been questioned. Nonetheless, weight loss alone achieved through GLP1 receptor agonists has failed in improving left ventricular functions. Tirzepatide is a dual agonist of GLP1 and glucose-dependent insulinotropic polypeptide, representing an innovative treatment option in diabetes with a major impact on weight loss and promising cardiovascular benefits. Whether this class of therapies is going to change the history of heart failure is an ongoing debate.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 5","pages":"818-822"},"PeriodicalIF":4.2,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141066647","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":"Glucokinase regulatory protein rs780094 polymorphism is associated with type 2 diabetes mellitus, dyslipidemia, non-alcoholic fatty liver disease, and nephropathy.","authors":"Ashraf Al Madhoun","doi":"10.4239/wjd.v15.i5.814","DOIUrl":"10.4239/wjd.v15.i5.814","url":null,"abstract":"<p><p>In this editorial, we comment on the article by Liu <i>et al</i> published in the recent issue of the <i>World Journal of Diabetes</i> (Relationship between GCKR gene rs780094 polymorphism and type 2 diabetes with albuminuria). Type 2 diabetes mellitus (T2DM) is a chronic disorder characterized by dysregulated glucose homeostasis. The persistent elevated blood glucose level in T2DM significantly increases the risk of developing severe complications, including cardiovascular disease, re-tinopathy, neuropathy, and nephropathy. T2DM arises from a complex interplay between genetic, epigenetic, and environmental factors. Global genomic studies have identified numerous genetic variations associated with an increased risk of T2DM. Specifically, variations within the glucokinase regulatory protein (GCKR) gene have been linked to heightened susceptibility to T2DM and its associated complications. The clinical trial by Liu <i>et al</i> further elucidates the role of the GCKR rs780094 polymorphism in T2DM and nephropathy development. Their findings demonstrate that individuals carrying the CT or TT genotype at the GCKR rs780094 locus are at a higher risk of developing T2DM with albuminuria compared to those with the CC genotype. These findings highlight the importance of genetic testing and risk assessment in T2DM to develop effective preventive strategies and personalized treatment plans.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"15 5","pages":"814-817"},"PeriodicalIF":4.2,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141064602","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}