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肥胖所导致的胰岛素抵抗分子机制的研究进展
引用本文:张岩,;陈晓亭,;宋惠珠,;亓志刚. 肥胖所导致的胰岛素抵抗分子机制的研究进展[J]. 检验医学, 2014, 0(7): 774-778
作者姓名:张岩,  陈晓亭,  宋惠珠,  亓志刚
作者单位:[1]无锡市妇幼保健院,江苏无锡214002; [2]南京医科大学附属无锡市人民医院,江苏无锡214023
摘    要:胰岛素抵抗(IR)可以定义为病理生理条件下,正常水平的胰岛素不足以使胰岛素作用的靶组织产生正常的生理效应。肥胖及身体脂肪组织的扩张可使IR的发生率增加。肥胖是心血管疾病和肝脏疾病发生的共同基础,常常是高脂血症和2型糖尿病发病的前奏。肥胖诱导的高游离脂肪酸(FFA)水平、炎症和氧化应激在IR的发生、发展中扮演重要角色。

关 键 词:胰岛素抵抗  肥胖  游离脂肪酸  炎症反应  氧化应激

Research progress on molecular pathogenesis of obesity-induced insulin resistance
Affiliation:ZHANG Yan, CHEN Xiaoting, SONG Huizhu, Ol Zhigang( 1. Wuxi Hospital for Maternal and Child Health Care, Jiangsu Wuxi 214002, China; 2. Wuxi People's Hospital, Nanjing Medical University, Jiangsu Wuxi 214023, China)
Abstract:Insulin resistance( IR) is defined as a pathophysiological condition in which normal insulin concentration does not adequately produce a normal insulin response in target tissues. It is well established that obesity and body fat distribution are associated with the increasing rate of IR. Obesity is a common cause of cardiovascular and hepatic diseases,and often precedes the onset of hyperglycemia and predicts the development of type 2 diabetes mellitus based on IR. Free fatty acids( FFA),inflammation and oxidative stress play key roles in the development and progression of IR induced by obesity.
Keywords:Insulin resistance  Obesity  Free fatty acid  Inflammation  Oxidative stress
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