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Role of AMP-activated Protein Kinase and Adiponectin during Development of Hepatic Steatosis in High-fat Diet-induced Obesity in Rats

机译:AMP活化蛋白激酶和脂联素在高脂饮食诱导的肥胖大鼠肝脂肪变性发展中的作用

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摘要

Obesity, an abnormal condition of adipose tissue, has recently been recognized as a major cause of metabolic syndromes, especially non-alcoholic fatty liver disease (NAFLD). The aim of the present study was to examine the possible involvement of adipokines in the development of fatty liver. Sprague-Dawley (SD) rats fed a highfat (HF) diet for 15 weeks developed increased hepatocellular vacuolation, hepatic triglyceride (TG) content and serum TG, total cholesterol and free fatty acid levels, with increases in adipose tissue mass. The serum concentration of adiponectin decreased slightly in these animals. Western blotting analysis demonstrated a decrease in the levels of AMP-activated protein kinase (AMPK) and phosphorylated-AMPK in the livers of these rats. These results indicate similarities between the diet-induced obesity rat model of NAFLD and human NAFLD, thus making the rat a useful model for the further study of NAFLD, including the interactions between adipokines and hepatic fat metabolism
机译:肥胖是脂肪组织的异常状况,最近已被认为是代谢综合征的主要原因,尤其是非酒精性脂肪肝疾病(NAFLD)。本研究的目的是检查脂肪细胞发育中脂肪因子的可能参与。饲喂高脂(HF)饮食15周的Sprague-Dawley(SD)大鼠肝细胞空泡,肝甘油三酸酯(TG)含量和血清TG,总胆固醇和游离脂肪酸水平增加,脂肪组织质量增加。这些动物中脂联素的血清浓度略有下降。蛋白质印迹分析表明,这些大鼠肝脏中AMP激活的蛋白激酶(AMPK)和磷酸化的AMPK含量降低。这些结果表明饮食诱导的肥胖大鼠NAFLD模型与人类NAFLD模型之间的相似性,从而使该模型成为进一步研究NAFLD的有用模型,包括脂肪因子与肝脂肪代谢之间的相互作用。

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