Ha S-K, Kim J, Chae C
Department of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, San 56-1, Shillim-Dong, Gwanak-Gu, Seoul 151-742, Republic of Korea.
J Comp Pathol. 2011 Jul;145(1):88-94. doi: 10.1016/j.jcpa.2010.11.011. Epub 2011 Jan 20.
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 high-fat (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.
肥胖是一种脂肪组织的异常状况，最近已被确认为代谢综合征的主要原因，尤其是非酒精性脂肪性肝病（NAFLD）。本研究的目的是探讨脂肪因子在脂肪肝发展过程中可能发挥的作用。给予高脂（HF）饮食15周的斯普拉格-道利（SD）大鼠出现肝细胞空泡化增加、肝脏甘油三酯（TG）含量以及血清TG、总胆固醇和游离脂肪酸水平升高，同时脂肪组织质量增加。这些动物血清脂联素浓度略有下降。蛋白质免疫印迹分析表明，这些大鼠肝脏中AMP活化蛋白激酶（AMPK）和磷酸化AMPK的水平降低。这些结果表明，饮食诱导的NAFLD大鼠模型与人类NAFLD之间存在相似性，从而使该大鼠成为进一步研究NAFLD的有用模型，包括脂肪因子与肝脏脂肪代谢之间的相互作用。
