CELLULAR & BIOCHEMICAL BASIS OF DIABETIC MICROANGIOPATHY

几种不同动物的体内和体外观察结果 糖尿病模型和人红细胞中的结果表明， 葡萄糖水平本身，独立于糖尿病环境，诱导 代谢失衡导致缺氧样还原性应激。 糖尿病环境引起的几种代谢失衡可能 有助于还原压力，然而最好的特点是 不平衡是山梨糖醇氧化为果糖的增加， 山梨醇脱氢酶将NAD+还原为NADH。 还原应力 通过多种机制促进氧化应激， 许多酶的活性和生物化学的不平衡 糖尿病并发症的发病机制。 代谢诱导 还原应激似乎是一个典型的特征， 控制糖尿病之前，并有助于，发展 一般糖尿病并发症，包括缺血性视网膜病变， 神经病变

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.