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糖尿病影响循环中胰岛素样生长因子的水平和活性,不同类型的糖尿病对胰岛素样生长因子活性的影响是不同的.糖尿病患者体内胰岛素样生长因子的紊乱,可能参与糖尿病肾病、糖尿病视网膜病变的发生、发展.胰岛素样生长因子结合球蛋白-1可能对微血管病变起保护作用,胰岛素样生长因子结合球蛋白-3参与微血管病变的发病机制不明.  相似文献   

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98例糖尿病患者分为白蛋白尿阴性组47例(A组),微量白蛋白组51例(B组),测定各组患者IGF-1、PA、TRF、RBP含量。结果B组比A组,IGF-1、ALB、PA、TRF、RBP含量明显降低(P〈0.05-0.01)。营养不良患者比营养良好者亦明显降低(P〈0.05-0.01)。结论IGF-I与PA、TF、RBP是反映糖尿病肾病早期和营养不良的敏感指标。  相似文献   

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糖尿病肾病   总被引:48,自引:0,他引:48  
糖尿病肾病(DN)是糖尿病(DM)最常见的并发症之一,在西方国家其已成为导致慢性肾衰竭的最主要原因。本文就近来DN发病机制、诊断、治疗的主要进展、特别是与临床实践有关的内容进行阐述。  相似文献   

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选取2018年8月至2020年6月82例DN患者,治疗1个月后检测尿白蛋白排泄率(UAER),根据UAER将患者分为疾病进展组和未进展组,结果:治疗后病情进展18例,未进展64例;经单因素分析,DN患者疾病进展与性别、年龄无关(P >0.05);与血清IGF-1、HMGB1水平有关(P <0. 05).结论:经Logi...  相似文献   

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糖尿病影响循环中胰岛素样生长因子的水平和活性,不同类型的糖尿病对胰岛素样生长因子活性的影响是不同的。糖尿病患者体内胰岛素样生长因子的紊乱,可能参与糖尿病肾病、糖尿病视网膜病变的发生、发展。胰岛索样生长因子结合球蛋白-1可能对微血管病变起保护作用,胰岛素样生长因子结合球蛋白-3参与微血管病变的发病机制不明。  相似文献   

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67例T2DM患者根据24小时尿白蛋白排泄率(UAER)分为三组:NA组、MA组和CP组。采用双抗体夹心酶联免疫吸附法(ELISA)检测糖尿病组和20例正常对照组血清TGF-β1、CTGF水平。结果①NA组血TGF-β1、CTGF较正常对照组增高(P〈0.05)。②MA组较NA组增高(P〈0.05),CP组较MA组增高(P〈0.05)。③血TGF-β1、CTGF与UAER呈正相关(r=0.674,P〈0.01)。结论TGF-β1、CTGF可能在DN发生发展中起重要作用。可能成为更早期DN的敏感指标,对监测肾病进展有重要意义。  相似文献   

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糖尿病肾病(DN)是糖尿病(DM)的常见并发症,也是DM的临床表现之一。DN的患病率在逐年增加。一些资料认为我国DN在终末期肾衰竭中已上升至16%。有效的血糖、血压控制是DN防治的重要措施。降糖、降压药物的选择和使用是临床治疗中的关键问题。  相似文献   

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研究表明糖尿病视网膜病(DR)患者血清总胰岛素样生长因子(IGF)-1增高而游离IGF-1减少,玻璃体内IGF-1及IGF结合蛋白(IGFBP)1、3水平均增高,其他IGFBPs水平也发生改变。IGF-1及IGFBPs通过促进内皮细胞增殖、影响内皮细胞凋亡及影响周细胞功能等参与了新生血管形成过程。生长抑素类似物、生长激素受体拮抗剂、人重组IGF-1(rhIGF-1)、rhIGF-1-IGFBP-3混合制剂以及IGF-1受体拮抗剂等在对DR的治疗及预防方面的作用受到人们的关注。  相似文献   

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研究表明糖尿病视网膜病(DR)患者血清总胰岛素样生长因子(IGF)-1增高而游离IGF—1减少,玻璃体内IGF—1及IGF结合蛋白(IGFBP)1、3水平均增高,其他IGFBPs水平也发生改变。IGF—1及IGFBPs通过促进内皮细胞增殖、影响内皮细胞凋亡及影响周细胞功能等参与了新生血管形成过程。生长抑素类似物、生长激素受体拮抗剂、人重组IGF-1(rhIGF—1)、rhIGF-1-IGFBP-3混合制剂以及IGF—1受体拮抗剂等在对DR的治疗及预防方面的作用受到人们的关注。  相似文献   

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运用聚合酶链反应一限制性片段长度多态性(PCR—RFLP)技术检查T2DM患者249例(其中DN患者129例)及体检的98例健康对照者的基因型。结果:(1)DN组CC基因型及C等位基因频率显著高于T2DM组和正常对照组;结论:VEGF+936C/T基因多态性可能与DN的发生发展有关,C等位基因可能是DN的易感基因。  相似文献   

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Aims/hypothesis  

The AGE receptors 1, 2 and 3, which are encoded by DDOST, PRKCSH and LGALS3, respectively, may be involved in the pathogenesis of diabetic complications. We sought to find out whether these genes are associated with diabetic nephropathy, cardiovascular disease and type 1 diabetes or related quantitative traits.  相似文献   

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Background and aimsNew data has emerged regarding higher risk of coronavirus disease 2019 (COVID-19), and its severity and complications in patients with type 2 diabetes mellitus (T2DM). However, there is a dearth of evidence regarding type 1 diabetes mellitus (T1DM). This article explores the possibility of COVID 19 induced diabetes and highlights a potential bidirectional link between COVID 19 and T1DM.MethodsA literature search was performed with Medline (PubMed), Scopus, and Google Scholar electronic databases till October 2020, using relevant keywords (COVID-19 induced diabetes; COVID-19 and type 1 diabetes; COVID-19 induced DKA; new-onset diabetes after SARS-CoV-2 infection) to extract relevant studies describing relationship between COVID-19 and T1DM.ResultsPast lessons and new data teach us that severe acute respiratory syndrome coronaviruses (SARS-CoV and SARS-CoV-2) can enter islet cells via angiotensin converting enzyme-2 (ACE-2) receptors and cause reversible β-cell damage and transient hyperglycemia. There have been postulations regarding the potential new-onset T1DM triggered by COVID-19. This article reviews the available evidence regarding the impact and interlink between COVID-19 and Τ1DM. We also explore the mechanisms behind the viral etiology of Τ1DM.ConclusionsSARS-CoV-2 can trigger severe diabetic ketoacidosis at presentation in individuals with new-onset diabetes. However, at present, there is no hard evidence that SARS-CoV-2 induces T1DM on it’s own accord. Long term follow-up of children and adults presenting with new-onset diabetes during this pandemic is required to fully understand the type of diabetes induced by COVID-19.  相似文献   

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Retnakaran R  Zinman B 《Lancet》2008,371(9626):1790-1799
Type 1 diabetes is associated with a substantially increased risk of cardiovascular disease that might not always be appreciated in view of the fairly young age of patients with this condition. In fact, in type 1 diabetes, the heart is subject to a variety of pathological insults, including accelerated atherosclerosis, cardiac autonomic neuropathy, and possibly intrinsic cardiomyopathy. Although the relation between hyperglycaemia and microvascular complications has been well established, a direct effect of hyperglycaemia on cardiovascular disease in type 1 diabetes has long been debated. More recently, several studies, most notably the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications, have clarified this issue and provided conclusive evidence that hyperglycaemia is indeed a mediator of cardiovascular risk in type 1 diabetes and that intensive diabetes therapy can reduce cardiovascular disease outcomes. We review current concepts in type 1 diabetes and the heart, focusing on recent insights into the central role of hyperglycaemia.  相似文献   

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自80年代以来,1型糖尿病发病的自身免疫机制已经确立.由于胰岛β细胞遭受淋巴细胞介导的自身免疫性攻击而选择性被破坏,在临床诊断为1型糖尿病时已有接近70%~80%β细胞功能受损.  相似文献   

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