Nishio Yoshihiko
Division of Endocrinology and Metabolism, Department of Medicine, Shiga University of Medical Science.
Nihon Rinsho. 2010 May;68(5):823-6.
Endothelial dysfunction is a proceeding abnormality in the development of atherosclerosis. Endothelial nitric oxide synthase (eNOS) activity has the central role in the endothelial function. Since insulin regulates the eNOS activity through the phosphorylation by AKT, insulin resistance is one of major factors associating with the endothelial dysfunction in obesity and diabetes. In addition, several lines of evidence suggests that hyperglycemia induces PKC activation, oxidative stress and increased hexosamine metabolism, and these abnormalities are reported to impair the eNOS activity. Thus, several abnormalities are suggested to be involved in the endothelial dysfunction found in diabetes. This article focuses the mechanisms how the hyperglycemia or insulin resistance causes abnormalities in endothelial function.
内皮功能障碍是动脉粥样硬化发展过程中的一种异常情况。内皮型一氧化氮合酶(eNOS)活性在内皮功能中起核心作用。由于胰岛素通过AKT磷酸化调节eNOS活性,胰岛素抵抗是肥胖和糖尿病中与内皮功能障碍相关的主要因素之一。此外,有多项证据表明高血糖会诱导蛋白激酶C(PKC)激活、氧化应激和己糖胺代谢增加,据报道这些异常会损害eNOS活性。因此,有几种异常情况被认为与糖尿病中发现的内皮功能障碍有关。本文重点探讨高血糖或胰岛素抵抗导致内皮功能异常的机制。