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胰岛素作用的分子基础。

Molecular basis of insulin action.

作者信息

González-Sánchez José Luis, Serrano-Ríos Manuel

机构信息

Department of Internal Medicine II, Hospital Clinico San Carlos, Madrid, Spain.

出版信息

Drug News Perspect. 2007 Oct;20(8):527-31. doi: 10.1358/dnp.2007.20.8.1157615.

DOI:10.1358/dnp.2007.20.8.1157615
PMID:18080040
Abstract

Insulin is the main anabolic and anticatabolic hormone in mammals. The stimulatory effect of insulin on glucose uptake in muscle and adipose tissue is a consequence of the rapid translocation of GLUT4 glucose transporters from an intracellular site to the cell surface. The actions of insulin are initiated by hormone binding to its cell surface receptors. Insulin receptors are ligand-stimulated protein tyrosine kinases and phosphorylate a number of proteins, known as insulin receptor substrate proteins. Insulin resistance has been recognized as a main pathogenic factor in the development of type 2 diabetes, and has been associated with dyslipidemia, hypertension, endothelial dysfunction, inflammation and coagulative state. The current challenge is the study of impaired insulin signaling pathways leading to beta-cell dysfunction and its progression to type 2 diabetes, as well as control of chronic inflammation processes that may improve insulin action.

摘要

胰岛素是哺乳动物体内主要的合成代谢和抗分解代谢激素。胰岛素对肌肉和脂肪组织中葡萄糖摄取的刺激作用是GLUT4葡萄糖转运蛋白从细胞内位点快速转运到细胞表面的结果。胰岛素的作用是由激素与其细胞表面受体结合引发的。胰岛素受体是配体刺激的蛋白酪氨酸激酶,可磷酸化多种蛋白质,即胰岛素受体底物蛋白。胰岛素抵抗已被认为是2型糖尿病发生发展的主要致病因素,并与血脂异常、高血压、内皮功能障碍、炎症和凝血状态有关。当前的挑战是研究导致β细胞功能障碍及其向2型糖尿病进展的胰岛素信号通路受损情况,以及控制可能改善胰岛素作用的慢性炎症过程。

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