Experimental diabesity research最新文献_第4页

Growth factors in proliferative diabetic retinopathy. 增殖性糖尿病视网膜病变的生长因子研究。

Experimental diabesity research Pub Date : 2003-10-01 DOI: 10.1155/EDR.2003.287

Zia Ali Khan, Subrata Chakrabarti

引用次数: 63

Nerve growth factor and diabetic neuropathy. 神经生长因子与糖尿病神经病变。

Experimental diabesity research Pub Date : 2003-10-01 DOI: 10.1155/EDR.2003.271

Gary Pittenger, Aaron Vinik

{"title":"Nerve growth factor and diabetic neuropathy.","authors":"Gary Pittenger, Aaron Vinik","doi":"10.1155/EDR.2003.271","DOIUrl":"https://doi.org/10.1155/EDR.2003.271","url":null,"abstract":"Neuropathy is one of the most debilitating complications of both type 1 and type 2 diabetes, with estimates of prevalence between 50-90% depending on the means of detection. Diabetic neuropathies are heterogeneous and there is variable involvement of large myelinated fibers and small, thinly myelinated fibers. Many of the neuronal abnormalities in diabetes can be duplicated by experimental depletion of specific neurotrophic factors, their receptors or their binding proteins. In experimental models of diabetes there is a reduction in the availability of these growth factors, which may be a consequence of metabolic abnormalities, or may be independent of glycemic control. These neurotrophic factors are required for the maintenance of the neurons, the ability to resist apoptosis and regenerative capacity. The best studied of the neurotrophic factors is nerve growth factor (NGF) and the related members of the neurotrophin family of peptides. There is increasing evidence that there is a deficiency of NGF in diabetes, as well as the dependent neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) that may also contribute to the clinical symptoms resulting from small fiber dysfunction. Similarly, NT3 appears to be important for large fiber and IGFs for autonomic neuropathy. Whether the observed growth factor deficiencies are due to decreased synthesis, or functional, e.g. an inability to bind to their receptor, and/or abnormalities in nerve transport and processing, remains to be established. Although early studies in humans on the role of neurotrophic factors as a therapy for diabetic neuropathy have been unsuccessful, newer agents and the possibilities uncovered by further studies should fuel clinical trials for several generations. It seems reasonable to anticipate that neurotrophic factor therapy, specifically targeted at different nerve fiber populations, might enter the therapeutic armamentarium.","PeriodicalId":86960,"journal":{"name":"Experimental diabesity research","volume":"4 4","pages":"271-85"},"PeriodicalIF":0.0,"publicationDate":"2003-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/EDR.2003.271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24118234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 184

The role of the insulin-like growth factors and their binding proteins in glucose homeostasis. 胰岛素样生长因子及其结合蛋白在葡萄糖稳态中的作用。

Experimental diabesity research Pub Date : 2003-10-01 DOI: 10.1155/EDR.2003.213

Liam J Murphy

引用次数: 47

Trophic factors and cytokines in early diabetic glomerulopathy. 早期糖尿病肾小球病变的营养因子和细胞因子。

Experimental diabesity research Pub Date : 2003-10-01 DOI: 10.1155/EDR.2003.225

Frank C Brosius

引用次数: 12

The insulin-like growth factor system. 胰岛素样生长因子系统。

Experimental diabesity research Pub Date : 2003-10-01 DOI: 10.1155/EDR.2003.205

Derek Le Roith

引用次数: 241

The insulin-like growth factor system and neurological complications in diabetes. 胰岛素样生长因子系统与糖尿病的神经系统并发症。

Experimental diabesity research Pub Date : 2003-10-01 DOI: 10.1155/EDR.2003.235

Anders A F Sima, Zhen-Guo Li, Weixian Zhang

{"title":"The insulin-like growth factor system and neurological complications in diabetes.","authors":"Anders A F Sima, Zhen-Guo Li, Weixian Zhang","doi":"10.1155/EDR.2003.235","DOIUrl":"https://doi.org/10.1155/EDR.2003.235","url":null,"abstract":"The IGF system plays vital roles in neuronal development, metabolism, regeneration and survival. It consists of IGF-I, IGF-II, insulin, IGF-I-receptor, and those of IGF-II and insulin as well as IGF-binding proteins. In the last decades it has become clear that perturbations of the IGF system play important roles in the pathogenesis of diabetic neurological complications. In the peripheral nervous system IGF-I, insulin, and C-peptide particularly in type 1 diabetes participate in the development of axonal degenerative changes and contributes to impaired regenerative capacities. These abnormalities of the IGF system appear to be less pronounced in type 2 diabetes, which may in part account for the relatively milder neurological complications in this type of diabetes. The members of the IGF system also provide anti-apoptotic effects on both peripheral and central nervous system neurons. Furthermore, both insulin and C-peptide and probably IGF-I possess gene regulatory capacities on myelin constituents and axonal cytoskeletal proteins. Therefore, replenishment of various members of the IGF system provides a reasonable rational for prevention and treatment of diabetic neurological complications.","PeriodicalId":86960,"journal":{"name":"Experimental diabesity research","volume":"4 4","pages":"235-56"},"PeriodicalIF":0.0,"publicationDate":"2003-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/EDR.2003.235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24118229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 27

Role of neuropoietic cytokines in development and progression of diabetic polyneuropathy: from glucose metabolism to neurodegeneration. 神经生成细胞因子在糖尿病多发神经病变发生发展中的作用:从糖代谢到神经退行性变。

Experimental diabesity research Pub Date : 2003-10-01 DOI: 10.1155/EDR.2003.303

Dusanka S Skundric, Robert P Lisak

{"title":"Role of neuropoietic cytokines in development and progression of diabetic polyneuropathy: from glucose metabolism to neurodegeneration.","authors":"Dusanka S Skundric, Robert P Lisak","doi":"10.1155/EDR.2003.303","DOIUrl":"https://doi.org/10.1155/EDR.2003.303","url":null,"abstract":"Diabetic neuropathy develops as a result of hyperglycemia-induced local metabolic and microvascular changes in both type I and type II diabetes mellitus. Diabetic neuropathy shows slower impulse conduction, axonal degeneration, and impaired regeneration. Diabetic neuropathy affects peripheral, central, and visceral sensorimotor and motor nerves, causing improper locomotor and visceral organ dysfunctions. The pathogenesis of diabetic neuropathy is complex and involves multiple pathways. Lack of success in preventing neuropathy, even with successful treatment of hyperglycemia, suggests the presence of early mediators between hyperglycemia-induced metabolic and enzymatic changes and functional and structural properties of Schwann cells (SCs) and axons. It is feasible that once activated, such mediators can act independently of the initial metabolic stimulus to modulate SC-axonal communication. Neuropoietic cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), leukemia inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), tumor necrosis factor alpha (TNF-alpha), and transforming growth factor beta (TGF-beta), exhibit pleiotrophic effects on homeostasis of glia and neurons in central, peripheral, and autonomic nervous system. These cytokines are produced locally by resident and infiltrating macrophages, lymphocytes, mast cells, SCs, fibroblasts, and sensory neurons. Metabolic changes induced by hyperglycemia lead to dysregulation of cytokine control. Moreover, their regulatory roles in nerve degeneration and regeneration may potentially be utilized for the prevention and/or therapy of diabetic neuropathy.","PeriodicalId":86960,"journal":{"name":"Experimental diabesity research","volume":"4 4","pages":"303-12"},"PeriodicalIF":0.0,"publicationDate":"2003-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/EDR.2003.303","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24118709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 102

Knockout mice challenge our concepts of glucose homeostasis and the pathogenesis of diabetes. 敲除小鼠挑战了我们对葡萄糖稳态和糖尿病发病机制的概念。

Experimental diabesity research Pub Date : 2003-07-01 DOI: 10.1155/EDR.2003.169

C Ronald Kahn

{"title":"Knockout mice challenge our concepts of glucose homeostasis and the pathogenesis of diabetes.","authors":"C Ronald Kahn","doi":"10.1155/EDR.2003.169","DOIUrl":"https://doi.org/10.1155/EDR.2003.169","url":null,"abstract":"A central component of type 2 diabetes and the metabolic syndrome is insulin resistance. Insulin exerts a multifaceted and highly integrated series of actions via its intracellular signaling systems. Generation of mice carrying null mutations of the genes encoding proteins in the insulin signaling pathway provides a unique approach to determining the role of individual proteins in the molecular mechanism of insulin action and the pathogenesis of insulin resistance and diabetes. The role of the four major insulin receptor substrates (IRS1-4) in insulin and IGF-1 signaling have been examined by creating mice with targeted gene knockouts. Each produces a unique phenotype, indicating the complementary role of these signaling components. Combined heterozygous defects often produce synergistic or epistatic effects, although the final severity of the phenotype depends on the genetic background of the mice. Conditional knockouts of the insulin receptor have also been created using the Cre-lox system. These tissue specific knockouts have provide unique insights into the control of glucose homeostasis and the pathogenesis of type 2 diabetes, and have led to development of new hypotheses about the nature of the insulin action and development of diabetes.","PeriodicalId":86960,"journal":{"name":"Experimental diabesity research","volume":"4 3","pages":"169-82"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/EDR.2003.169","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24448778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 56

Effect of combination therapy with a calcium channel blocker and an angiotensin-converting enzyme inhibitor on renal hypertrophy and urinary albumin excretion in diabetic rats. 钙通道阻滞剂和血管紧张素转换酶抑制剂联合治疗对糖尿病大鼠肾肥大和尿白蛋白排泄的影响。

Experimental diabesity research Pub Date : 2003-07-01 DOI: 10.1155/EDR.2003.191

Birgitte Nielsen, Henning Grønbaek, Ruth Osterby, Allan Flyvbjerg

{"title":"Effect of combination therapy with a calcium channel blocker and an angiotensin-converting enzyme inhibitor on renal hypertrophy and urinary albumin excretion in diabetic rats.","authors":"Birgitte Nielsen, Henning Grønbaek, Ruth Osterby, Allan Flyvbjerg","doi":"10.1155/EDR.2003.191","DOIUrl":"https://doi.org/10.1155/EDR.2003.191","url":null,"abstract":"The objective of this study was to compare the effect of an angiotensin-converting enzyme (ACE) inhibitor and a calcium channel blocker on the development of renal changes in diabetic rats. Diabetes was induced by an intravenous injection of streptozotocin in normotensive Wistar rats. Treatment was commenced immediately in 1 set of rats with 4 treatment arms: nitrendipine (250 mg/kg fodder), enalapril (35 mg/L drinking water), both treatments in combination, or placebo. Treatment was continued for 9 weeks. Another set of rats was left with untreated diabetes for 3 months followed by 7 weeks treatment as above. When starting treatment right after induction of diabetes, nitrendipine significantly reduced urinary albumin excretion (UAE) to the nondiabetic level (P < .05) without reducing blood pressure (BP), whereas enalapril failed to significantly reduce UAE despite a reduction in BP. Combining the two treatments showed no further reduction in UAE compared to monotherapy with nitrendipine, despite a lower BP. When leaving diabetic rats untreated for 3 months, only the coadministration of nitrendipine and enalapril showed a significant reduction in UAE compared to monotherapy and placebo treatment, but showed no significant effect on BP.","PeriodicalId":86960,"journal":{"name":"Experimental diabesity research","volume":"4 3","pages":"191-9"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/EDR.2003.191","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24448680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Effect of Gymnema montanum leaves on serum and tissue lipids in alloxan diabetic rats. 芒藤叶对四氧嘧啶型糖尿病大鼠血清及组织脂质的影响。

Experimental diabesity research Pub Date : 2003-07-01 DOI: 10.1155/EDR.2003.183

R Ananthan, M Latha, K M Ramkumar, L Pari, C Baskar, V Narmatha Bai

引用次数: 88