Wei Zheng, Xin Ji, Qiao qiao Yin, Chensi Wu, Chengan Xu, Hongying Pan, Chun Wu
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by high blood glucose levels resulting from insulin resistance and impaired insulin secretion. Immune dysregulation-mediated chronic low-grade inflammation is a critical factor that poses a significant risk to the metabolic disorders of T2DM and its related complications. Exosomes, as small extracellular vesicles secreted by various cells, have emerged as essential regulators of intercellular communication and immune regulation. In this review, we summarize the current understanding of the role of exosomes derived from immune and nonimmune cells in modulating immune responses in T2DM by regulating immune cell functions and cytokine production. More importantly, we suggest potential strategies for the clinical applications of exosomes in T2DM management, including biomarkers for disease diagnosis and monitoring, exosome-based therapies for drug delivery vehicles, and targeted therapy for exosomes.
{"title":"Exosomes as Emerging Regulators of Immune Responses in Type 2 Diabetes Mellitus","authors":"Wei Zheng, Xin Ji, Qiao qiao Yin, Chensi Wu, Chengan Xu, Hongying Pan, Chun Wu","doi":"10.1155/2024/3759339","DOIUrl":"https://doi.org/10.1155/2024/3759339","url":null,"abstract":"Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by high blood glucose levels resulting from insulin resistance and impaired insulin secretion. Immune dysregulation-mediated chronic low-grade inflammation is a critical factor that poses a significant risk to the metabolic disorders of T2DM and its related complications. Exosomes, as small extracellular vesicles secreted by various cells, have emerged as essential regulators of intercellular communication and immune regulation. In this review, we summarize the current understanding of the role of exosomes derived from immune and nonimmune cells in modulating immune responses in T2DM by regulating immune cell functions and cytokine production. More importantly, we suggest potential strategies for the clinical applications of exosomes in T2DM management, including biomarkers for disease diagnosis and monitoring, exosome-based therapies for drug delivery vehicles, and targeted therapy for exosomes.","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"171 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140002787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<i>Background</i>. Oxidative stress and inflammation are closely related pathophysiological processes, both occurring in type 2 diabetes mellitus (T2DM). In addition to the standard treatment of T2DM, a potential strategy has been focused on the use of bile acids (BAs) as an additional treatment. Ursodeoxycholic acid (UDCA), as the first BA used in humans, improves glucose and lipid metabolism and attenuates oxidative stress. The aim of this study was to evaluate the potential metabolic, anti-inflammatory, and antioxidative effects of UDCA in patients with T2DM. <i>Methods</i>. This prospective, double-blind, placebo-controlled clinical study included 60 patients with T2DM, randomly allocated to receive UDCA or placebo. Subjects were treated with 500 mg tablets of UDCA or placebo administered three times per day (total dose of 1500 mg/day) for eight weeks. Two study visits, at the beginning (F0) and at the end (F1) of the study, included the interview, anthropometric and clinical measurements, and biochemical analyses. <i>Results</i>. UDCA treatment showed a significant reduction in body mass index (<span><svg height="11.7782pt" style="vertical-align:-3.42938pt" version="1.1" viewbox="-0.0498162 -8.34882 18.973 11.7782" width="18.973pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,0,0)"></path></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"></path></g></svg><span></span><span><svg height="11.7782pt" style="vertical-align:-3.42938pt" version="1.1" viewbox="22.555183800000002 -8.34882 28.184 11.7782" width="28.184pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,22.605,0)"></path></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"></path></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"></use></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"></path></g><g transform="matrix(.013,0,0,-0.013,44.289,0)"></path></g></svg>)</span></span> and in diastolic blood pressure (<span><svg height="11.7782pt" style="vertical-align:-3.42938pt" version="1.1" viewbox="-0.0498162 -8.34882 18.973 11.7782" width="18.973pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"></use></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><use xlink:href="#g117-34"></use></g></svg><span></span><span><svg height="11.7782pt" style="vertical-align:-3.42938pt" version="1.1" viewbox="22.555183800000002 -8.34882 28.184 11.7782" width="28.184pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"></use></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"></use></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"></use></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"
{"title":"Beneficial Effects of Ursodeoxycholic Acid on Metabolic Parameters and Oxidative Stress in Patients with Type 2 Diabetes Mellitus: A Randomized Double-Blind, Placebo-Controlled Clinical Study","authors":"Biljana Lakić, Ranko Škrbić, Snežana Uletilović, Nebojša Mandić-Kovačević, Milkica Grabež, Mirna Popović Šarić, Miloš P. Stojiljković, Ivan Soldatović, Zorica Janjetović, Anastasija Stokanović, Nataša Stojaković, Momir Mikov","doi":"10.1155/2024/4187796","DOIUrl":"https://doi.org/10.1155/2024/4187796","url":null,"abstract":"<i>Background</i>. Oxidative stress and inflammation are closely related pathophysiological processes, both occurring in type 2 diabetes mellitus (T2DM). In addition to the standard treatment of T2DM, a potential strategy has been focused on the use of bile acids (BAs) as an additional treatment. Ursodeoxycholic acid (UDCA), as the first BA used in humans, improves glucose and lipid metabolism and attenuates oxidative stress. The aim of this study was to evaluate the potential metabolic, anti-inflammatory, and antioxidative effects of UDCA in patients with T2DM. <i>Methods</i>. This prospective, double-blind, placebo-controlled clinical study included 60 patients with T2DM, randomly allocated to receive UDCA or placebo. Subjects were treated with 500 mg tablets of UDCA or placebo administered three times per day (total dose of 1500 mg/day) for eight weeks. Two study visits, at the beginning (F0) and at the end (F1) of the study, included the interview, anthropometric and clinical measurements, and biochemical analyses. <i>Results</i>. UDCA treatment showed a significant reduction in body mass index (<span><svg height=\"11.7782pt\" style=\"vertical-align:-3.42938pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 18.973 11.7782\" width=\"18.973pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,11.342,0)\"></path></g></svg><span></span><span><svg height=\"11.7782pt\" style=\"vertical-align:-3.42938pt\" version=\"1.1\" viewbox=\"22.555183800000002 -8.34882 28.184 11.7782\" width=\"28.184pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,22.605,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,28.845,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,31.809,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,38.049,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,44.289,0)\"></path></g></svg>)</span></span> and in diastolic blood pressure (<span><svg height=\"11.7782pt\" style=\"vertical-align:-3.42938pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 18.973 11.7782\" width=\"18.973pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"><use xlink:href=\"#g113-113\"></use></g><g transform=\"matrix(.013,0,0,-0.013,11.342,0)\"><use xlink:href=\"#g117-34\"></use></g></svg><span></span><span><svg height=\"11.7782pt\" style=\"vertical-align:-3.42938pt\" version=\"1.1\" viewbox=\"22.555183800000002 -8.34882 28.184 11.7782\" width=\"28.184pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,22.605,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,28.845,0)\"><use xlink:href=\"#g113-47\"></use></g><g transform=\"matrix(.013,0,0,-0.013,31.809,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,38.049,0)\"","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"5 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140002863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mitchell J. Sammut, David P. McBey, Amit P. Sayal, C. W. James Melling
The etiology of insulin resistance (IR) development in type 1 diabetes mellitus (T1DM) remains unclear; however, impaired skeletal muscle metabolism may play a role. While IR development has been established in male T1DM rodents, female rodents have yet to be examined in this context. Resistance exercise training (RT) has been shown to improve IR and is associated with a lower risk of hypoglycemia onset in T1DM compared to aerobic exercise. The purpose of this study was to investigate the effects of RT on IR development in female T1DM rodents. Forty Sprague Dawley eight-week-old female rats were divided into four groups: control sedentary (CS; <span><svg height="8.55521pt" style="vertical-align:-0.2063904pt" version="1.1" viewbox="-0.0498162 -8.34882 17.789 8.55521" width="17.789pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,0,0)"></path></g><g transform="matrix(.013,0,0,-0.013,10.158,0)"></path></g></svg><span></span><span><svg height="8.55521pt" style="vertical-align:-0.2063904pt" version="1.1" viewbox="21.3711838 -8.34882 12.679 8.55521" width="12.679pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,21.421,0)"></path></g><g transform="matrix(.013,0,0,-0.013,27.661,0)"></path></g></svg>),</span></span> control trained (CT; <span><svg height="8.55521pt" style="vertical-align:-0.2063904pt" version="1.1" viewbox="-0.0498162 -8.34882 17.789 8.55521" width="17.789pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-111"></use></g><g transform="matrix(.013,0,0,-0.013,10.158,0)"><use xlink:href="#g117-34"></use></g></svg><span></span><span><svg height="8.55521pt" style="vertical-align:-0.2063904pt" version="1.1" viewbox="21.3711838 -8.34882 12.679 8.55521" width="12.679pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,21.421,0)"><use xlink:href="#g113-50"></use></g><g transform="matrix(.013,0,0,-0.013,27.661,0)"><use xlink:href="#g113-49"></use></g></svg>),</span></span> T1DM sedentary (DS; <span><svg height="8.55521pt" style="vertical-align:-0.2063904pt" version="1.1" viewbox="-0.0498162 -8.34882 17.789 8.55521" width="17.789pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-111"></use></g><g transform="matrix(.013,0,0,-0.013,10.158,0)"><use xlink:href="#g117-34"></use></g></svg><span></span><span><svg height="8.55521pt" style="vertical-align:-0.2063904pt" version="1.1" viewbox="21.3711838 -8.34882 12.679 8.55521" width="12.679pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,21.421,0)"><use xlink:href="#g113-50"></use></g><g transform="matrix(.013,0,0,-0.013,27.661,0)"><use xlink:href="#
{"title":"The Effects of Resistance Exercise Training on Skeletal Muscle Metabolism and Insulin Resistance Development in Female Rodents with Type 1 Diabetes","authors":"Mitchell J. Sammut, David P. McBey, Amit P. Sayal, C. W. James Melling","doi":"10.1155/2024/5549762","DOIUrl":"https://doi.org/10.1155/2024/5549762","url":null,"abstract":"The etiology of insulin resistance (IR) development in type 1 diabetes mellitus (T1DM) remains unclear; however, impaired skeletal muscle metabolism may play a role. While IR development has been established in male T1DM rodents, female rodents have yet to be examined in this context. Resistance exercise training (RT) has been shown to improve IR and is associated with a lower risk of hypoglycemia onset in T1DM compared to aerobic exercise. The purpose of this study was to investigate the effects of RT on IR development in female T1DM rodents. Forty Sprague Dawley eight-week-old female rats were divided into four groups: control sedentary (CS; <span><svg height=\"8.55521pt\" style=\"vertical-align:-0.2063904pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 17.789 8.55521\" width=\"17.789pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,10.158,0)\"></path></g></svg><span></span><span><svg height=\"8.55521pt\" style=\"vertical-align:-0.2063904pt\" version=\"1.1\" viewbox=\"21.3711838 -8.34882 12.679 8.55521\" width=\"12.679pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,21.421,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,27.661,0)\"></path></g></svg>),</span></span> control trained (CT; <span><svg height=\"8.55521pt\" style=\"vertical-align:-0.2063904pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 17.789 8.55521\" width=\"17.789pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"><use xlink:href=\"#g113-111\"></use></g><g transform=\"matrix(.013,0,0,-0.013,10.158,0)\"><use xlink:href=\"#g117-34\"></use></g></svg><span></span><span><svg height=\"8.55521pt\" style=\"vertical-align:-0.2063904pt\" version=\"1.1\" viewbox=\"21.3711838 -8.34882 12.679 8.55521\" width=\"12.679pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,21.421,0)\"><use xlink:href=\"#g113-50\"></use></g><g transform=\"matrix(.013,0,0,-0.013,27.661,0)\"><use xlink:href=\"#g113-49\"></use></g></svg>),</span></span> T1DM sedentary (DS; <span><svg height=\"8.55521pt\" style=\"vertical-align:-0.2063904pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 17.789 8.55521\" width=\"17.789pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"><use xlink:href=\"#g113-111\"></use></g><g transform=\"matrix(.013,0,0,-0.013,10.158,0)\"><use xlink:href=\"#g117-34\"></use></g></svg><span></span><span><svg height=\"8.55521pt\" style=\"vertical-align:-0.2063904pt\" version=\"1.1\" viewbox=\"21.3711838 -8.34882 12.679 8.55521\" width=\"12.679pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,21.421,0)\"><use xlink:href=\"#g113-50\"></use></g><g transform=\"matrix(.013,0,0,-0.013,27.661,0)\"><use xlink:href=\"#","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"42 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139919700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diabetic retinopathy (DR) is a severe microvascular complication of diabetes and is one of the primary causes of blindness in the working-age population in Europe and the United States. At present, no cure is available for DR, but early detection and timely intervention can prevent the rapid progression of the disease. Several treatments for DR are known, primarily ophthalmic treatment based on glycemia, blood pressure, and lipid control, which includes laser photocoagulation, glucocorticoids, vitrectomy, and antivascular endothelial growth factor (anti-VEGF) medications. Despite the clinical efficacy of the aforementioned therapies, none of them can entirely shorten the clinical course of DR or reverse retinopathy. MicroRNAs (miRNAs) are vital regulators of gene expression and participate in cell growth, differentiation, development, and apoptosis. MicroRNAs have been shown to play a significant role in DR, particularly in the molecular mechanisms of inflammation, oxidative stress, and neurodegeneration. The aim of this review is to systematically summarize the signaling pathways and molecular mechanisms of miRNAs involved in the occurrence and development of DR, mainly from the pathogenesis of oxidative stress, inflammation, and neovascularization. Meanwhile, this article also discusses the research progress and application of miRNA-specific therapies for DR.
糖尿病视网膜病变（DR）是糖尿病的一种严重微血管并发症，也是欧洲和美国劳动适龄人口失明的主要原因之一。目前，糖尿病视网膜病变尚无根治方法，但早期发现和及时干预可以防止病情迅速恶化。目前已知的几种 DR 治疗方法主要是基于血糖、血压和血脂控制的眼科治疗，包括激光光凝、糖皮质激素、玻璃体切除术和抗血管内皮生长因子（anti-VEGF）药物。尽管上述疗法具有临床疗效，但它们都不能完全缩短 DR 的临床病程或逆转视网膜病变。微RNA（miRNA）是基因表达的重要调节因子，参与细胞的生长、分化、发育和凋亡。研究表明，microRNA 在 DR 中发挥着重要作用，尤其是在炎症、氧化应激和神经变性的分子机制中。本综述旨在系统地总结 miRNAs 参与 DR 发生和发展的信号通路和分子机制，主要从氧化应激、炎症和新生血管的发病机理入手。同时，本文还探讨了针对DR的miRNA特异性疗法的研究进展和应用。
{"title":"Advances in Research Related to MicroRNA for Diabetic Retinopathy","authors":"Yahan Luo, Chunxia Li","doi":"10.1155/2024/8520489","DOIUrl":"https://doi.org/10.1155/2024/8520489","url":null,"abstract":"Diabetic retinopathy (DR) is a severe microvascular complication of diabetes and is one of the primary causes of blindness in the working-age population in Europe and the United States. At present, no cure is available for DR, but early detection and timely intervention can prevent the rapid progression of the disease. Several treatments for DR are known, primarily ophthalmic treatment based on glycemia, blood pressure, and lipid control, which includes laser photocoagulation, glucocorticoids, vitrectomy, and antivascular endothelial growth factor (anti-VEGF) medications. Despite the clinical efficacy of the aforementioned therapies, none of them can entirely shorten the clinical course of DR or reverse retinopathy. MicroRNAs (miRNAs) are vital regulators of gene expression and participate in cell growth, differentiation, development, and apoptosis. MicroRNAs have been shown to play a significant role in DR, particularly in the molecular mechanisms of inflammation, oxidative stress, and neurodegeneration. The aim of this review is to systematically summarize the signaling pathways and molecular mechanisms of miRNAs involved in the occurrence and development of DR, mainly from the pathogenesis of oxidative stress, inflammation, and neovascularization. Meanwhile, this article also discusses the research progress and application of miRNA-specific therapies for DR.","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"59 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139760528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-08eCollection Date: 2024-01-01DOI: 10.1155/2024/2350551
Ritesh Chimoriya, Kimberly Mitlehner, Chee L Khoo, Uchechukwu Levi Osuagwu, Russell Thomson, Lei Si, Michael Lean, David Simmons, Milan K Piya
Background: The Diabetes Remission Clinical Trial (DiRECT) study demonstrated that an intensive and structured weight management program in UK primary care resulted in high rates of diabetes remission in adults with recent onset type 2 diabetes mellitus (T2DM). This study was aimed at evaluating the translation of the DiRECT intervention into an Australian primary care setting.
Methods: All patients enrolled in the DiRECT-Australia Type 2 Diabetes Remission Service in a region of Sydney (Macarthur region, South Western Sydney, Australia) were included. Eligible participants were aged 20-70 years, noninsulin treated, with T2DM of ≤6 years' duration, and body mass index (BMI) ≥ 27 kg/m2. Total diet replacement of 825-853 kcal/day using meal replacements was implemented for 12 weeks, followed by an ongoing structured program until 52 weeks, with regular follow-up with a general practitioner, dietitian, and/or practice nurse.
Results: Of 39 recruited participants, 32 (82.1%) and 27 (69.2%) completed 12 weeks and 52 weeks of the structured program, respectively. Decrease in weight by -12.0 kg (95% CI: -9.6, -14.4; p < 0.001) and -9.1 kg (95% CI: -5.2, -12.9; p < 0.001) and decrease in glycated haemoglobin (HbA1c) by -1.1% (95% CI: -0.6, -1.6; p < 0.001) and -0.6% (95% CI: -0.1, -1.1; p = 0.013) were observed at 12 and 52 weeks, respectively. At the end of 12 and 52 weeks, 93.8% (30/32) and 55.6% (15/27) of those with follow-up data met the criteria for diabetes remission, respectively. Quality of life and wellbeing scores increased over the course of 12 weeks, remaining significantly higher at 52 weeks. Participants reported they would be willing to pay A$92.50 (95% CI: A$75.80, A$109.30) per fortnight for the low-calorie meal replacement shakes.
Conclusions: These findings support the feasibility of a structured diabetes remission service in an Australian primary care setting to achieve improvements in glycaemia, weight, and quality of life and wellbeing, and suggest a substantial willingness to pay for diet replacement products among participants.
{"title":"Translation of a Diabetes Remission Service into Australian Primary Care: Findings from the Evaluation of DiRECT-Australia.","authors":"Ritesh Chimoriya, Kimberly Mitlehner, Chee L Khoo, Uchechukwu Levi Osuagwu, Russell Thomson, Lei Si, Michael Lean, David Simmons, Milan K Piya","doi":"10.1155/2024/2350551","DOIUrl":"10.1155/2024/2350551","url":null,"abstract":"<p><strong>Background: </strong>The Diabetes Remission Clinical Trial (DiRECT) study demonstrated that an intensive and structured weight management program in UK primary care resulted in high rates of diabetes remission in adults with recent onset type 2 diabetes mellitus (T2DM). This study was aimed at evaluating the translation of the DiRECT intervention into an Australian primary care setting.</p><p><strong>Methods: </strong>All patients enrolled in the DiRECT-Australia Type 2 Diabetes Remission Service in a region of Sydney (Macarthur region, South Western Sydney, Australia) were included. Eligible participants were aged 20-70 years, noninsulin treated, with T2DM of ≤6 years' duration, and body mass index (BMI) ≥ 27 kg/m<sup>2</sup>. Total diet replacement of 825-853 kcal/day using meal replacements was implemented for 12 weeks, followed by an ongoing structured program until 52 weeks, with regular follow-up with a general practitioner, dietitian, and/or practice nurse.</p><p><strong>Results: </strong>Of 39 recruited participants, 32 (82.1%) and 27 (69.2%) completed 12 weeks and 52 weeks of the structured program, respectively. Decrease in weight by -12.0 kg (95% CI: -9.6, -14.4; <i>p</i> < 0.001) and -9.1 kg (95% CI: -5.2, -12.9; <i>p</i> < 0.001) and decrease in glycated haemoglobin (HbA1c) by -1.1% (95% CI: -0.6, -1.6; <i>p</i> < 0.001) and -0.6% (95% CI: -0.1, -1.1; <i>p</i> = 0.013) were observed at 12 and 52 weeks, respectively. At the end of 12 and 52 weeks, 93.8% (30/32) and 55.6% (15/27) of those with follow-up data met the criteria for diabetes remission, respectively. Quality of life and wellbeing scores increased over the course of 12 weeks, remaining significantly higher at 52 weeks. Participants reported they would be willing to pay A$92.50 (95% CI: A$75.80, A$109.30) per fortnight for the low-calorie meal replacement shakes.</p><p><strong>Conclusions: </strong>These findings support the feasibility of a structured diabetes remission service in an Australian primary care setting to achieve improvements in glycaemia, weight, and quality of life and wellbeing, and suggest a substantial willingness to pay for diet replacement products among participants.</p>","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"2024 ","pages":"2350551"},"PeriodicalIF":4.3,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10869186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139741153","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}
<i>Background</i>. A substantial proportion of those infected with COVID-19 are presenting with persistent symptoms, referred to as long COVID-19. Emerging evidence suggests that the presence of pre-existing chronic conditions, such as diabetes, may increase the risk of long COVID-19. <i>Objectives</i>. To investigate whether having pre-existing diabetes increases the risk of developing long COVID-19 in the population of middle-aged and older adults (≥50 years old) in Europe, while assessing if this relationship can be accounted for or is modified by the known long COVID-19 and diabetes risk factors (age, sex, hospitalization, pre-existing hypertension, and weight status). <i>Methods</i>. A population-based longitudinal prospective study involving a sample of respondents aged 50 years and older (<span><svg height="9.92533pt" style="vertical-align:-1.57651pt" version="1.1" viewbox="-0.0498162 -8.34882 17.789 9.92533" width="17.789pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,0,0)"></path></g><g transform="matrix(.013,0,0,-0.013,10.158,0)"></path></g></svg><span></span><span><svg height="9.92533pt" style="vertical-align:-1.57651pt" version="1.1" viewbox="21.3711838 -8.34882 30.36 9.92533" width="30.36pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,21.421,0)"></path></g><g transform="matrix(.013,0,0,-0.013,27.661,0)"></path></g><g transform="matrix(.013,0,0,-0.013,32.804,0)"></path></g><g transform="matrix(.013,0,0,-0.013,39.044,0)"><use xlink:href="#g113-49"></use></g><g transform="matrix(.013,0,0,-0.013,45.284,0)"><use xlink:href="#g113-53"></use></g></svg>)</span></span> with probable or confirmed COVID-19 infection from 27 countries that participated in both waves 7 and 8 of the Survey of Health, Ageing and Retirement in Europe and its 2020 and 2021 Corona Surveys. Logistic regression modeling was performed. <i>Results</i>. Overall, 66.8% of the respondents affected by COVID-19 infection reported at least one long COVID-19 symptom; 55.2% were female, and the average age was 64.6 years; 13.2% had pre-existing diabetes. Respondents with pre-existing diabetes had significantly higher odds of developing long COVID-19, compared to those without diabetes (<span><svg height="8.98583pt" style="vertical-align:-0.2324905pt" version="1.1" viewbox="-0.0498162 -8.75334 28.996 8.98583" width="28.996pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.013,0,0,-0.013,0,0)"></path></g><g transform="matrix(.013,0,0,-0.013,9.594,0)"></path></g><g transform="matrix(.013,0,0,-0.013,21.365,0)"><use xlink:href="#g117-34"></use></g></svg><span></span><span><svg height="8.98583pt" style="vertical-align:-0.2324905pt" version="1.1" viewbox="32.5781838 -8.75334 21.894 8.98583" width="21.894pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transfor
{"title":"Does Pre-existing Diabetes Correlate with Long COVID-19 in Europe? Evidence from the Analysis of the Survey of Health, Ageing and Retirement in Europe’s Corona Surveys","authors":"Sarah Cuschieri, Piotr Wilk","doi":"10.1155/2024/7459628","DOIUrl":"https://doi.org/10.1155/2024/7459628","url":null,"abstract":"<i>Background</i>. A substantial proportion of those infected with COVID-19 are presenting with persistent symptoms, referred to as long COVID-19. Emerging evidence suggests that the presence of pre-existing chronic conditions, such as diabetes, may increase the risk of long COVID-19. <i>Objectives</i>. To investigate whether having pre-existing diabetes increases the risk of developing long COVID-19 in the population of middle-aged and older adults (≥50 years old) in Europe, while assessing if this relationship can be accounted for or is modified by the known long COVID-19 and diabetes risk factors (age, sex, hospitalization, pre-existing hypertension, and weight status). <i>Methods</i>. A population-based longitudinal prospective study involving a sample of respondents aged 50 years and older (<span><svg height=\"9.92533pt\" style=\"vertical-align:-1.57651pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 17.789 9.92533\" width=\"17.789pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,10.158,0)\"></path></g></svg><span></span><span><svg height=\"9.92533pt\" style=\"vertical-align:-1.57651pt\" version=\"1.1\" viewbox=\"21.3711838 -8.34882 30.36 9.92533\" width=\"30.36pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,21.421,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,27.661,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,32.804,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,39.044,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,45.284,0)\"><use xlink:href=\"#g113-53\"></use></g></svg>)</span></span> with probable or confirmed COVID-19 infection from 27 countries that participated in both waves 7 and 8 of the Survey of Health, Ageing and Retirement in Europe and its 2020 and 2021 Corona Surveys. Logistic regression modeling was performed. <i>Results</i>. Overall, 66.8% of the respondents affected by COVID-19 infection reported at least one long COVID-19 symptom; 55.2% were female, and the average age was 64.6 years; 13.2% had pre-existing diabetes. Respondents with pre-existing diabetes had significantly higher odds of developing long COVID-19, compared to those without diabetes (<span><svg height=\"8.98583pt\" style=\"vertical-align:-0.2324905pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.75334 28.996 8.98583\" width=\"28.996pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,9.594,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,21.365,0)\"><use xlink:href=\"#g117-34\"></use></g></svg><span></span><span><svg height=\"8.98583pt\" style=\"vertical-align:-0.2324905pt\" version=\"1.1\" viewbox=\"32.5781838 -8.75334 21.894 8.98583\" width=\"21.894pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transfor","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"72 4 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139666801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li Zhang, Zhaoxiang Wang, Fengyan Tang, Menghuan Wu, Ying Pan, Song Bai, Bing Lu, Shao Zhong, Ying Xie
Background. Cellular senescence is thought to play a significant role in the onset and development of diabetic nephropathy. The goal of this study was to explore potential biomarkers associated with diabetic glomerulopathy from the perspective of senescence. Methods. Datasets about human glomerular biopsy samples related to diabetic nephropathy were systematically obtained from the Gene Expression Omnibus database. Hub senescence-associated genes were investigated by differential gene analysis and Least Absolute Shrinkage and Selection Operator analysis. Cluster analysis was employed to identify senescence molecular subtypes. A single-cell dataset was used to validate the above findings and further evaluate the senescence environment. The relationship between these genes and the glomerular filtration rate was explored based on the Nephroseq database. These gene expressions have also been explored in various kidney diseases. Results. Twelve representative senescence-associated genes (VEGFA, IQGAP2, JUN, PLAT, ETS2, ANG, MMP14, VEGFC, SERPINE2, CXCR2, PTGES, and EGF) were finally identified. Biological changes in immune inflammatory response, cell cycle regulation, metabolic regulation, and immune microenvironment have been observed across different molecular subtypes. The above results were also validated based on single-cell analysis. Additionally, we also identified several significantly altered cell communication pathways, including COLLAGEN, PTN, LAMININ, SPP1, and VEGF. Finally, almost all these genes could well predict the occurrence of diabetic glomerulopathy based on receiver operating characteristic analysis and are associated with the glomerular filtration rate. These genes are differently expressed in various kidney diseases. Conclusion. The present study identified potential senescence-associated biomarkers and further explored the heterogeneity of diabetic glomerulopathy that might provide new insights into the diagnosis, assessment, management, and personalized treatment of DN.
{"title":"Identification of Senescence-Associated Biomarkers in Diabetic Glomerulopathy Using Integrated Bioinformatics Analysis","authors":"Li Zhang, Zhaoxiang Wang, Fengyan Tang, Menghuan Wu, Ying Pan, Song Bai, Bing Lu, Shao Zhong, Ying Xie","doi":"10.1155/2024/5560922","DOIUrl":"https://doi.org/10.1155/2024/5560922","url":null,"abstract":"<i>Background</i>. Cellular senescence is thought to play a significant role in the onset and development of diabetic nephropathy. The goal of this study was to explore potential biomarkers associated with diabetic glomerulopathy from the perspective of senescence. <i>Methods</i>. Datasets about human glomerular biopsy samples related to diabetic nephropathy were systematically obtained from the Gene Expression Omnibus database. Hub senescence-associated genes were investigated by differential gene analysis and Least Absolute Shrinkage and Selection Operator analysis. Cluster analysis was employed to identify senescence molecular subtypes. A single-cell dataset was used to validate the above findings and further evaluate the senescence environment. The relationship between these genes and the glomerular filtration rate was explored based on the Nephroseq database. These gene expressions have also been explored in various kidney diseases. <i>Results</i>. Twelve representative senescence-associated genes (VEGFA, IQGAP2, JUN, PLAT, ETS2, ANG, MMP14, VEGFC, SERPINE2, CXCR2, PTGES, and EGF) were finally identified. Biological changes in immune inflammatory response, cell cycle regulation, metabolic regulation, and immune microenvironment have been observed across different molecular subtypes. The above results were also validated based on single-cell analysis. Additionally, we also identified several significantly altered cell communication pathways, including COLLAGEN, PTN, LAMININ, SPP1, and VEGF. Finally, almost all these genes could well predict the occurrence of diabetic glomerulopathy based on receiver operating characteristic analysis and are associated with the glomerular filtration rate. These genes are differently expressed in various kidney diseases. <i>Conclusion</i>. The present study identified potential senescence-associated biomarkers and further explored the heterogeneity of diabetic glomerulopathy that might provide new insights into the diagnosis, assessment, management, and personalized treatment of DN.","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"74 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139555031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Taichi Ochi, Stijn de Vos, Daan Touw, Petra Denig, Talitha Feenstra, Eelko Hak
<i>Aims</i>. To investigate the effect of serotonin transporter (5-HTT) polymorphisms on change in HbA1c levels six months after metformin initiation in type 2 diabetes patients. <i>Materials and Methods</i>. Participants of PROVALID (PROspective cohort study in patients with type 2 diabetes mellitus for VALidation of biomarkers) within the GIANTT (Groningen Initiative to ANalyse Type 2 Diabetes Treatment) cohort who initiated metformin were genotyped for combined 5-HTTLPR/rs25531 (L<svg height="10.1524pt" style="vertical-align:-0.04990005pt" version="1.1" viewbox="-0.0498162 -10.1025 6.17869 10.1524" width="6.17869pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.0091,0,0,-0.0091,0,-5.741)"></path></g></svg>L<svg height="10.1524pt" style="vertical-align:-0.04990005pt" version="1.1" viewbox="-0.0498162 -10.1025 6.17869 10.1524" width="6.17869pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.0091,0,0,-0.0091,0,-5.741)"><use xlink:href="#g50-43"></use></g></svg>, L<svg height="10.1524pt" style="vertical-align:-0.04990005pt" version="1.1" viewbox="-0.0498162 -10.1025 6.17869 10.1524" width="6.17869pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.0091,0,0,-0.0091,0,-5.741)"><use xlink:href="#g50-43"></use></g></svg>S<svg height="10.1524pt" style="vertical-align:-0.04990005pt" version="1.1" viewbox="-0.0498162 -10.1025 6.17869 10.1524" width="6.17869pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.0091,0,0,-0.0091,0,-5.741)"><use xlink:href="#g50-43"></use></g></svg>, and S<svg height="10.1524pt" style="vertical-align:-0.04990005pt" version="1.1" viewbox="-0.0498162 -10.1025 6.17869 10.1524" width="6.17869pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.0091,0,0,-0.0091,0,-5.741)"><use xlink:href="#g50-43"></use></g></svg>S<svg height="10.1524pt" style="vertical-align:-0.04990005pt" version="1.1" viewbox="-0.0498162 -10.1025 6.17869 10.1524" width="6.17869pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matrix(.0091,0,0,-0.0091,0,-5.741)"><use xlink:href="#g50-43"></use></g></svg>) and 5-HTT VNTR (STin 2.12, 12/-, and 10/-) polymorphisms, respectively. Multiple linear regression was applied to determine the change in HbA1c level from baseline date to six months across 5-HTTLPR/VNTR genotype groups, adjusted for baseline HbA1c, age, gender, triglyceride level, low-density lipoprotein level, and serum creatinine. <i>Results</i>. 157 participants were included, of which 56.2% were male. The average age was <span><svg height="8.69875pt" style="vertical-align:-0.3499298pt" version="1.1" viewbox="-0.0498162 -8.34882 32.222 8.69875" width="32.222pt" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink"><g transform="matr
{"title":"Tailoring Type II Diabetes Treatment: Investigating the Effect of 5-HTT Polymorphisms on HbA1c Levels after Metformin Initiation","authors":"Taichi Ochi, Stijn de Vos, Daan Touw, Petra Denig, Talitha Feenstra, Eelko Hak","doi":"10.1155/2024/7922486","DOIUrl":"https://doi.org/10.1155/2024/7922486","url":null,"abstract":"<i>Aims</i>. To investigate the effect of serotonin transporter (5-HTT) polymorphisms on change in HbA1c levels six months after metformin initiation in type 2 diabetes patients. <i>Materials and Methods</i>. Participants of PROVALID (PROspective cohort study in patients with type 2 diabetes mellitus for VALidation of biomarkers) within the GIANTT (Groningen Initiative to ANalyse Type 2 Diabetes Treatment) cohort who initiated metformin were genotyped for combined 5-HTTLPR/rs25531 (L<svg height=\"10.1524pt\" style=\"vertical-align:-0.04990005pt\" version=\"1.1\" viewbox=\"-0.0498162 -10.1025 6.17869 10.1524\" width=\"6.17869pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.0091,0,0,-0.0091,0,-5.741)\"></path></g></svg>L<svg height=\"10.1524pt\" style=\"vertical-align:-0.04990005pt\" version=\"1.1\" viewbox=\"-0.0498162 -10.1025 6.17869 10.1524\" width=\"6.17869pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.0091,0,0,-0.0091,0,-5.741)\"><use xlink:href=\"#g50-43\"></use></g></svg>, L<svg height=\"10.1524pt\" style=\"vertical-align:-0.04990005pt\" version=\"1.1\" viewbox=\"-0.0498162 -10.1025 6.17869 10.1524\" width=\"6.17869pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.0091,0,0,-0.0091,0,-5.741)\"><use xlink:href=\"#g50-43\"></use></g></svg>S<svg height=\"10.1524pt\" style=\"vertical-align:-0.04990005pt\" version=\"1.1\" viewbox=\"-0.0498162 -10.1025 6.17869 10.1524\" width=\"6.17869pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.0091,0,0,-0.0091,0,-5.741)\"><use xlink:href=\"#g50-43\"></use></g></svg>, and S<svg height=\"10.1524pt\" style=\"vertical-align:-0.04990005pt\" version=\"1.1\" viewbox=\"-0.0498162 -10.1025 6.17869 10.1524\" width=\"6.17869pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.0091,0,0,-0.0091,0,-5.741)\"><use xlink:href=\"#g50-43\"></use></g></svg>S<svg height=\"10.1524pt\" style=\"vertical-align:-0.04990005pt\" version=\"1.1\" viewbox=\"-0.0498162 -10.1025 6.17869 10.1524\" width=\"6.17869pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.0091,0,0,-0.0091,0,-5.741)\"><use xlink:href=\"#g50-43\"></use></g></svg>) and 5-HTT VNTR (STin 2.12, 12/-, and 10/-) polymorphisms, respectively. Multiple linear regression was applied to determine the change in HbA1c level from baseline date to six months across 5-HTTLPR/VNTR genotype groups, adjusted for baseline HbA1c, age, gender, triglyceride level, low-density lipoprotein level, and serum creatinine. <i>Results</i>. 157 participants were included, of which 56.2% were male. The average age was <span><svg height=\"8.69875pt\" style=\"vertical-align:-0.3499298pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 32.222 8.69875\" width=\"32.222pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matr","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"86 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139515897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background. The mortality rate among older persons with diabetes has been steadily increasing, resulting in significant health and economic burdens on both society and individuals. The objective of this study is to develop and validate a predictive nomogram for estimating the 5-year all-cause mortality risk in older persons with T2D (T2D). Methods. We obtained data from the National Health and Nutrition Survey (NHANES). A random 7 : 3 split was made between the training and validation sets. By linking the national mortality index up until December 31, 2019, we ensured a minimum of 5 years of follow-up to assess all-cause mortality. A nomogram was developed in the training cohort using a logistic regression model as well as a least absolute shrinkage and selection operator (LASSO) regression model for predicting the 5-year risk of all-cause mortality. Finally, the prediction performance of the nomogram is evaluated using several validation methods. Results. We constructed a comprehensive prediction model based on the results of multivariate analysis and LASSO binomial regression. These models were then validated using data from the validation cohort. The final model includes four independent predictors: age, gender, estimated glomerular filtration rate, and white blood cell count. The C-index values for the training and validation cohorts were 0.748 and 0.762, respectively. The calibration curve demonstrates satisfactory consistency between the two cohorts. Conclusions. The newly developed nomogram proves to be a valuable tool in accurately predicting the 5-year all-cause mortality risk among older persons with diabetes, providing crucial information for tailored interventions.
{"title":"Unveiling the Hidden Burden: Estimating All-Cause Mortality Risk in Older Individuals with Type 2 Diabetes","authors":"Dikang Pan, Hui Wang, Sensen Wu, Jingyu Wang, Yachan Ning, Jianming Guo, Cong Wang, Yongquan Gu","doi":"10.1155/2024/1741878","DOIUrl":"https://doi.org/10.1155/2024/1741878","url":null,"abstract":"<i>Background</i>. The mortality rate among older persons with diabetes has been steadily increasing, resulting in significant health and economic burdens on both society and individuals. The objective of this study is to develop and validate a predictive nomogram for estimating the 5-year all-cause mortality risk in older persons with T2D (T2D). <i>Methods</i>. We obtained data from the National Health and Nutrition Survey (NHANES). A random 7 : 3 split was made between the training and validation sets. By linking the national mortality index up until December 31, 2019, we ensured a minimum of 5 years of follow-up to assess all-cause mortality. A nomogram was developed in the training cohort using a logistic regression model as well as a least absolute shrinkage and selection operator (LASSO) regression model for predicting the 5-year risk of all-cause mortality. Finally, the prediction performance of the nomogram is evaluated using several validation methods. <i>Results</i>. We constructed a comprehensive prediction model based on the results of multivariate analysis and LASSO binomial regression. These models were then validated using data from the validation cohort. The final model includes four independent predictors: age, gender, estimated glomerular filtration rate, and white blood cell count. The C-index values for the training and validation cohorts were 0.748 and 0.762, respectively. The calibration curve demonstrates satisfactory consistency between the two cohorts. <i>Conclusions</i>. The newly developed nomogram proves to be a valuable tool in accurately predicting the 5-year all-cause mortality risk among older persons with diabetes, providing crucial information for tailored interventions.","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"26 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139509692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background. Better therapeutic drugs are required for treating hypertensive diabetic nephropathy. In our previous study, the Huaju Xiaoji (HJXJ) formula promoted the renal function of patients with diabetes and hypertensive nephropathy. In this study, we investigated the therapeutic effect and regulation mechanism of HJXJ in hypertensive diabetic mice with nephropathy. Methods. We constructed a mouse hypertensive diabetic nephropathy (HDN) model by treating mice with streptozotocin (STZ) and nomega-nitro-L-arginine methyl ester (LNAME). We also constructed a human glomerular mesangial cell (HGMC) model that was induced by high doses of sugar (30 mmol/mL) and TGFβ1 (5 ng/mL). Pathological changes were evaluated by hematoxylin and eosin (H&E) staining, periodic acid Schiff (PAS) staining, and Masson staining. The fibrosis-related molecules (TGFβ1, fibronectin, laminin, COL I, COL IV, α-SMA, and p-smad2/3) were detected by enzyme-linked immunosorbent assay (ELISA). The mRNA levels and protein expression of endoplasmic reticulum stress, fibrosis molecules, and their downstream molecules were assessed using qPCR and Western blotting assays. Results. Administering HJXJ promoted the renal function of HDN mice. HJXJ reduced the expression of ER stress makers (CHOP and GRP78) and lncMGC, miR379, miR494, miR495, miR377, CUGBP2, CPEB4, EDEM3, and ATF3 in HDN mice and model HGMCs. The positive control drugs (dapagliflozin and valsartan) also showed similar effects after treatment with HJXJ. Additionally, in model HGMCs, the overexpression of CHOP or lncMGC decreased the effects of HJXJ-M on the level of fibrosis molecules and downstream target molecules. Conclusion. In this study, we showed that the HJXJ formula may regulate ERS-lncMGC/miRNA to enhance renal function in hypertensive diabetic mice with nephropathy. This study may act as a reference for further investigating whether combining HJXJ with other drugs can enhance its therapeutic effect. The findings of this study might provide new insights into the clinical treatment of hypertensive diabetic nephropathy with HJXJ.
{"title":"Huaju Xiaoji Formula Regulates ERS-lncMGC/miRNA to Enhance the Renal Function of Hypertensive Diabetic Mice with Nephropathy","authors":"Zeng Zhang, Xiaodong Fu, Fengzhu Zhou, Duanchun Zhang, Yanqiu Xu, Zhaohua Fan, Shimei Wen, Yanting Shao, Zheng Yao, Yanming He","doi":"10.1155/2024/6942156","DOIUrl":"https://doi.org/10.1155/2024/6942156","url":null,"abstract":"<i>Background</i>. Better therapeutic drugs are required for treating hypertensive diabetic nephropathy. In our previous study, the Huaju Xiaoji (HJXJ) formula promoted the renal function of patients with diabetes and hypertensive nephropathy. In this study, we investigated the therapeutic effect and regulation mechanism of HJXJ in hypertensive diabetic mice with nephropathy. <i>Methods</i>. We constructed a mouse hypertensive diabetic nephropathy (HDN) model by treating mice with streptozotocin (STZ) and nomega-nitro-L-arginine methyl ester (LNAME). We also constructed a human glomerular mesangial cell (HGMC) model that was induced by high doses of sugar (30 mmol/mL) and TGF<i>β</i>1 (5 ng/mL). Pathological changes were evaluated by hematoxylin and eosin (H&E) staining, periodic acid Schiff (PAS) staining, and Masson staining. The fibrosis-related molecules (TGF<i>β</i>1, fibronectin, laminin, COL I, COL IV, <i>α</i>-SMA, and p-smad2/3) were detected by enzyme-linked immunosorbent assay (ELISA). The mRNA levels and protein expression of endoplasmic reticulum stress, fibrosis molecules, and their downstream molecules were assessed using qPCR and Western blotting assays. <i>Results</i>. Administering HJXJ promoted the renal function of HDN mice. HJXJ reduced the expression of ER stress makers (CHOP and GRP78) and lncMGC, miR379, miR494, miR495, miR377, CUGBP2, CPEB4, EDEM3, and ATF3 in HDN mice and model HGMCs. The positive control drugs (dapagliflozin and valsartan) also showed similar effects after treatment with HJXJ. Additionally, in model HGMCs, the overexpression of <i>CHOP</i> or <i>lncMGC</i> decreased the effects of HJXJ-M on the level of fibrosis molecules and downstream target molecules. <i>Conclusion</i>. In this study, we showed that the HJXJ formula may regulate ERS-lncMGC/miRNA to enhance renal function in hypertensive diabetic mice with nephropathy. This study may act as a reference for further investigating whether combining HJXJ with other drugs can enhance its therapeutic effect. The findings of this study might provide new insights into the clinical treatment of hypertensive diabetic nephropathy with HJXJ.","PeriodicalId":15576,"journal":{"name":"Journal of Diabetes Research","volume":"1 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139509793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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