摘要
目的探讨过氧化物酶体增殖物活化受体（PPARγ）在高脂饮食所致非酒精性脂肪肝（NAFLD）大鼠肝脏的表达及其意义。方法模型组Wistar大鼠给予高脂饮食饲养，分批于实验第4、8、12周处死，设普通饮食饲养大鼠作对照。测定空腹血糖（FBG）、空腹胰岛素（FINS），计算胰岛素敏感指数（ISI）；测定血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、总胆固醇（TC）、甘油三酯（TG）；苏木素-伊红（HE）染色观察肝组织病理变化；反转录聚合酶链反应（RT-PCR）分别检测大鼠肝脏PPARγ mRNA的表达。结果模型组大鼠第4周呈现单纯性脂肪肝，第8-12周从单纯性脂肪肝进展为脂肪性肝炎，个别出现肝纤维化；RT-PCR显示，随着造模时间延长，肝脏PPARγ mRNA的表达逐渐减弱，于第12周达到最低。结论持续12周的高脂饮食可以成功复制大鼠NAFLD模型；模型大鼠肝脏PPARγmRNA表达随造模时间的延长而逐渐减弱，PPARγ可以通过对胰岛素抵抗的调控参与NAFLD的发生发展。
Objective To investigate the expression and possible roles of peroxisome proliferator-activated receptors gamma （PPAR-γ） in liver of rats with nonalconholie fatty liver disease （NAFLD） chronically fed with a fat-rich diet. Methods For inducing NAFLD model,a fat-rich diet was given to wistar rats for a period of 4, 8, 12 week,respectively. Normal group was fed with standard diet for 12 week. The level of aminotransferase （ALT, AS-F）, total cholesterol （TC）, triglyceride （TG） were detected by using automatic biochemistry analyzer; fasting blood glucose （FBG） was detected by glucose oxidase method; serum insulin was detected by radio-immunity assay, simultaneously the insulin sensitivity index （ISI） was calculated. The pathology of liver was observed by hematoxylin and eosin（HE） stain with microscopy. Expression of PPAR-γ in the liver was detected by reverse transcription-polymerase chain reaction （RT- PCR）. Results Some simple fatty liver were observed in model group at 4 week. From 8 week to 12 week, the liver gradually progressed from steatohepatitis alone to steatohepatitis with fibrosis. RT-PCR suggested the expression of PPAR gamma in the liver of rats NAFLD was weaken at the end of 12 week. Conclusion The rats NAFLD model could be successfully established under the fed with high-fat and high-cholesterol diet for 12 week. The expression of PPAR-γ was weaken in liver of NAFLD. Insulin resistance （IR） was associated with the development of NAFLD.
