运动对非酒精性脂肪肝脂联素受体后信号传导的影响  

Effects of Exercise on Nonalcoholic Fatty Liver Adiponectin Receptor Signal Transduction

作　　者：高珊珊[1] 黄婉婷[1] 闫旋飞 衣雪洁[2] 

机构地区：[1]沈阳体育学院研究生部,辽宁沈阳110102 [2]沈阳体育学院运动人体科学学院,辽宁沈阳110102

出　　处：《沈阳体育学院学报》2015年第3期83-88,共6页Journal of Shenyang Sport University

基　　金：辽宁省优秀人才支持计划(WR2013015);国家自然科学基金(81273096);沈阳体育学院重点学科方向(XKFX1511)

摘　　要：肥胖是包括脂肪肝在内的多种病症致病的危险因素。肝脏是调节脂代谢的重要器官,脂质在肝脏的过度沉积是非酒精性脂肪肝(NAFLD)的重要标志。脂肪组织分泌的脂联素(ADPN)是肥胖者体内唯一下调的脂肪因子,可通过与靶细胞膜上的受体(Adipo R)结合而激活腺苷酸活化激酶(AMPK)、过氧化物酶体增殖物活化受体α(PPARα)来调节肝脏的脂代谢,控制NAFLD的发生发展。上述各因子的表达水平直接影响到肝脏脂代谢的调节。运动减肥可明显减轻NAFLD程度,一旦停止运动可能会导致NAFLD的反弹,但具体机制并不清楚。因此,对肥胖、运动与ADPN及其受体后AMPKα、PPARα信号传导对脂肪肝及脂代谢的关系进行探讨,力图为肝脏脂代谢的分子作用机制、运动防治NAFLD的相关研究提供新的思路。Obesity is a risk factor for a variety of diseases, including fatty liver. Liver is an important organ in lipid metabo- lism and lipid deposition in the liver is an important symbol of nonalcoholic fatty liver disease （ NAFLD）. The level of adi- ponectin （ADPN） is descending in obesity. ADPN can activate the 5＇ -AMP-activated protein kinase（AMPK） and the per- oxisome proliferator-activated receptor alpha（PPARct） through combining with the receptor（AdipoR） in target cell mem- brane and then regulate the lipid metabolism of liver. What＇ s more, it can control the development of NAFLD. The metab- olism condition of lipid is contingent on the expression of aforementioned cytokines. Exercise can help lose weight and re- duce the degree of NAFLD, and the NAFLD will rebound if we stop exercising, but the specific mechanism is not clear. Therefore, this article will explore the relationship of obesity, ADPN, AMPKα, PPARα signaling on NAFLD or lipid me- tabolism, and provide new ideas for the research of prevention and treatment strategies for NAFLD.

关 键 词：非酒精性脂肪肝 运动 ADPN AMPK PPAR 

分 类 号：G804.21[文化科学—运动人体科学]