CELLULAR & BIOCHEMICAL BASIS OF DIABETIC MICROANGIOPATHY

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• 批准号: 6486781
• 负责人: JOSEPH R WILLIAMSON
• 金额: $ 15.75万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-08-01 至 2002-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6486781
• 关键词: biological products; biomedical resource; spectrometry

In vivo and in vitro observations in several different animal models of diabetes and in human erythrocytes indicate that elevated glucose levels per se, independent of the diabetic milieu, induce metabolic imbalances that cause hypoxia-like reductive stress. Several metabolic imbalances induced by the diabetic milieu may contribute to reductive stress, however the best characterized imbalance is increased oxidation of sorbitol to fructose couples to reduction of NAD+ to NADH by sorbitol dehydrogenase. Reductive stress contributes to oxidative stress via several mechanisms and impacts on the activity of numerous enzymes and biochemical imbalances implicated in the pathogenesis of diabetic complications. Metabolically-induced reductive stress appears to be a characteristic feature of poorly controlled diabetes which precedes, and contributes to, development of diabetic complications in general including ischemic retinopathy and neuropathy.

几种不同动物的体内和体外观察 糖尿病模型和人类红细胞表明，升高的 葡萄糖水平本身，与糖尿病环境无关，会诱导 代谢失衡导致缺氧样还原应激。 糖尿病环境引起的几种代谢失衡可能 有助于减轻压力，但最好的特征是 不平衡是山梨醇氧化成果糖的增加 山梨醇脱氢酶将 NAD+ 还原为 NADH。 减少压力 通过多种机制促进氧化应激并影响 涉及多种酶的活性和生化失衡 在糖尿病并发症的发病机制中。 代谢诱导 还原应激似乎是不良状态的一个特征 控制糖尿病先于并促进糖尿病的发展 一般糖尿病并发症，包括缺血性视网膜病变和 神经病。