CELLULAR & BIOCHEMICAL BASIS OF DIABETIC MICROANGIOPATHY

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• 批准号: 6665901
• 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: 2002
• 资助国家: 美国
• 起止时间: 2002-08-01 至 2003-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6665901
• 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外观察 糖尿病模型和人类红细胞中均显示 血糖水平本身，不受糖尿病环境的影响，导致 代谢失衡会导致类似缺氧的还原压力。 由糖尿病环境引起的几种代谢失衡可能 有助于减轻压力，但最具特点的是 不平衡是山梨醇氧化到果糖对的增加 山梨醇脱氢酶将NAD+还原为NADH。还原应力 通过几种机制和影响导致氧化应激 许多酶的活性和生化失衡牵涉其中 在糖尿病并发症的发病机制中起重要作用。新陈代谢诱导 减少压力似乎是不良的一个特征。 可控制的糖尿病先于并有助于糖尿病的发展 糖尿病并发症一般包括缺血性视网膜病变和 神经病。