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晚期糖基化终末产物与糖尿病。超越血管并发症。

Advanced glycation endproducts and diabetes. Beyond vascular complications.

作者信息

Puddu Alessandra, Viviani Giorgio L

机构信息

Department of Internal Medicine and Medical Specialties, University of Genova, Viale benedetto XV, 6, 16132 Genova, Italy.

出版信息

Endocr Metab Immune Disord Drug Targets. 2011 Jun;11(2):132-40. doi: 10.2174/187153011795564115.

DOI:10.2174/187153011795564115
PMID:21476962
Abstract

Advanced Glycation Endproducts (AGEs) are a group of heterogeneous compounds formed by the non enzymatic reactions between aldehydic group of reducing sugars with proteins, lipids or nucleic acids. Formation and accumulation of AGEs is related with the aging process and is accelerated in diabetes. Type 2 diabetes, the most common form of diabetes, is characterized by hyperglycaemia and insulin resistance associated to a progressive deterioration of beta cell function and mass. The pathogenic role of AGEs in vascular diabetic complications is widely recognised. Recently other aspects of the detrimental effects of AGEs in type 2 diabetes are emerged: AGEs interfere with the complex molecular pathway of insulin signaling, leading to insulin resistance; AGEs modify the insulin molecule, and, consequently, its function; AGEs decrease insulin secretion and insulin content. In this article we review the role of AGEs in type 2 diabetes, beyond their involvement in vascular complications.

摘要

晚期糖基化终末产物(AGEs)是一组由还原糖的醛基与蛋白质、脂质或核酸之间的非酶促反应形成的异质化合物。AGEs的形成和积累与衰老过程相关,并且在糖尿病中会加速。2型糖尿病是最常见的糖尿病类型,其特征是高血糖和胰岛素抵抗,伴有β细胞功能和数量的进行性恶化。AGEs在糖尿病血管并发症中的致病作用已得到广泛认可。最近,AGEs在2型糖尿病中的其他有害影响方面也逐渐显现出来:AGEs干扰胰岛素信号传导的复杂分子途径,导致胰岛素抵抗;AGEs修饰胰岛素分子,从而改变其功能;AGEs减少胰岛素分泌和胰岛素含量。在本文中,我们综述了AGEs在2型糖尿病中的作用,而不仅仅局限于它们在血管并发症中的作用。

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