瘦素与非酒精性脂肪性肝病:来自初步临床研究的提示

Li Zhang, G. Ji
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引用次数: 2

摘要

瘦素基因的产物于1994年首次从啮齿动物脂肪组织中鉴定和克隆。由于瘦素缺乏的ob/ob小鼠表现出典型的代谢综合征(MS)特征,它被最早认为在调节能量平衡中起作用。对瘦素反应较弱的个体产生了瘦素抵抗的概念。多种生物过程可促进瘦素抵抗,从而干扰相关疾病。非酒精性脂肪性肝病(Non-alcoholic fatty liver disease, NAFLD)是MS的肝脏表现形式,与糖尿病、肥胖等MS的其他组成部分一起成为世界性流行病,瘦素抵抗是其发病过程之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Leptin and Non-Alcoholic Fatty Liver Disease: Hints From Preliminary Clinical Studies
The product of the ob gene leptin was first identified and cloned from rodent adipose tissue in 1994. It was pioneerly considered to play a role in the regulation of the energy balance, as leptin deficient ob/ob mice showed typical features of metabolic syndrome (MS). Individuals that less responsive to the action of leptin led to the concept of leptin resistance. Multiple biological processes can promote leptin resistance and thus interfere with related diseases. Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of MS became world epidemics along with other MS components such as diabetes, obesity, and leptin resistance is indicated in the process.
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