Pathogenesis of diabetic neuropathy.

E L Feldman, M J Stevens, D A Greene
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Abstract

Diabetes mellitus affects over 14 million people in the United States and the number of diabetics is increasing by 5% per year. Diabetic neuropathy (DN) is a common complication of diabetes and occurs in approximately 50% of diabetic patients over time. Clinical trials have proven that hyperglycemia almost certainly conditions the development of DN. Despite this fact, we still do not understand the mechanism(s) underlying DN. Several possible etiologies have been proposed including altered metabolism of polyol, lipids, or amino acids, vascular insufficiency, increased superoxide-induced free radical formation, impaired axonal transport or reduced neurotrophism. Accumulating evidence suggests that these defects are likely interrelated and that their interaction(s) within the diabetic milieu are responsible for the development and progression of DN. In this review we will discuss these theories, their interrelationships and how, collectively, these ideas may begin to explain the etiology of DN.

糖尿病神经病变的发病机制。
在美国,糖尿病影响着超过1400万人,并且糖尿病患者的数量正以每年5%的速度增长。糖尿病性神经病变(DN)是糖尿病的一种常见并发症,随着时间的推移,约50%的糖尿病患者发生糖尿病性神经病变。临床试验已经证明,高血糖几乎肯定会影响糖尿病的发展。尽管如此,我们仍然不了解DN背后的机制。几种可能的病因包括多元醇、脂质或氨基酸代谢改变、血管功能不全、超氧化物诱导的自由基形成增加、轴突运输受损或神经营养性减少。越来越多的证据表明,这些缺陷可能是相互关联的,它们在糖尿病环境中的相互作用是DN的发生和发展的原因。在这篇综述中,我们将讨论这些理论,它们之间的相互关系,以及如何,总的来说,这些观点可能开始解释DN的病因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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