胰岛素抵抗在高脂饮食大鼠非酒精性脂肪性肝炎发病中的作用

Insulin Resistance in the Pathogenesis of Non-alcoholic Steatohepatitis in Rats Induced by High Fat Diet

目的：探讨胰岛素抵抗在大鼠非酒精性脂肪性肝炎（NASH）发病中的作用。方法：19只雄性SD大鼠随机分为高脂饮食模型组（n＝10）和正常饮食对照组（n＝9），饲养12周，根据空腹血糖和胰岛素水平计算生腹胰岛素抵抗指数（FIRI）。结果：模型组大鼠均发生NASH，表现为肥胖、高脂血症伴肝细胞大泡性脂肪变性、小叶内炎症细胞浸润和肝细胞坏死。与正常对照组相比，模型组大鼠的空腹血糖（正常对照组：5.62mmol／L±1．07mmol／L；模型组：7．44mmol／L±1.58mmol／L）、胰岛素水平（正常对照组：239．03pmol／L±104.07pmol／L；模型组：344.40pmol／L±192．90pmol／L）和FIRI（正常对照组：9.77±5.99；模型组：17.74±11.60）均呈升高趋势，但无显著差异。结论：在高脂饮食所致大鼠NASH模型中未发现有高胰岛素血症和胰岛素抵抗现象。

Background/Aims: To explore the effect of insulin resistance on the pathogenesis of non-alcoholic steatohepatitis (NASH) of rat model. Methods: 19 male SD rats were randomly allocated into model group (n = 10) induced by high fat diet and control group (n = 9) fed with standard diet for 12 weeks. Fasting insulin resistance index (FIRI) was evaluated according to the levels of fasting blood glucose and fasting plasma insulin. Results: All rats of model group developed NASH that was characterized by obesity, hyperlipidemia and hepatocytic macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis. In comparison with the control group, fasting blood glucose (5.62 mmol/L± 1.07 mmol/Lvs 7.44 mmol/L ±1.58 mmol/L), fasting plasma insulin (239.03 pmol/L ±104.07 pmol/L vs 344.40 pmol/L ±192.90 pmol/L) and FIRI (9.77 ± 5.99 vs 17.74 ±11.60) in the model group tended to increase, but there were no significant differences among these aspects of both groups. Conclusions: The phenomena of hyperinsulinemia and insulin resistance have not been proved to be involved in the pathogenesis of NASH in rats induced by high fat diet.