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 糖尿病的模型和人类红细胞的模型表明升高 葡萄糖水平本身，独立于糖尿病环境，诱导 导致缺氧样还原应力的代谢失衡。 糖尿病环境引起的几种代谢失衡可能 有助于减轻压力，但是最佳的特征 不平衡是增加山梨糖醇对果糖夫妇的氧化增加 通过山梨糖醇脱氢酶将NAD+降低到NADH。 还原应力 通过多种机制促进氧化应激，并影响 涉及许多酶和生化失衡的活性 在糖尿病并发症的发病机理中。 代谢引起的 还原应力似乎是不良的特征 受控的糖尿病，并在发展之前 通常，糖尿病并发症，包括缺血性视网膜病和 神经病。