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目的探讨非酒精性脂肪肝小鼠肝脏胰岛素受体底物-2(insulin receptor substrate-2,IRS-2)的表达。方法于2002年1月至2003年3月在中国医科大学附属盛京医院内分泌科将30只6~8周龄的雌性SPF级C57BL6J小鼠随机分为3组饲养,其中正常饮食组10只、高脂高糖饮食8周组10只(实验过程中死亡5只)及高脂高糖食16周组10只。测定其血脂、血清胰岛素及空腹血糖、肝功能、肝脏重量、腹部瘦肉及瘦肉含量,肝脏脂质含量及IRS-2蛋白表达。并做肝脏病理检查。结果高脂高糖饮食16周的小鼠腹部脂肪量、血清甘油三酯、空腹血糖、碱性磷酸酶显著高于正常饮食小鼠(P<0.05~0.01);白蛋白及白蛋白球蛋白比值较正常饮食小鼠显著降低(P<0.05)。高脂高糖饮食小鼠肝脏有明显脂肪变性,16周的小鼠较8周的小鼠严重。高脂高糖饮食小鼠的肝脏总胆固醇和甘油三酯含量显著高于正常饮食小鼠,16周时达到正常饮食小鼠的2倍以上;IRS-2表达低于正常饮食小鼠,16周的小鼠高于8周的。结论高脂高糖饮食可使C57BL6J小鼠出现非酒精性脂肪肝,肝脏的IRS-2蛋白表达量低于正常饮食小鼠
Objective To investigate the expression of hepatic insulin receptor substrate-2 (IRS-2) in non-alcoholic fatty liver mice. Methods From January 2002 to March 2003, 30 female SPF-class C57BL6J mice aged 6-8 weeks were randomly divided into three groups at the endocrinology department of Shengjing Hospital, China Medical University. Among them, 10 were normal diet group, High-fat and high-sugar diet 8 weeks group 10 (5 died during the experiment) and high-fat and high-sugar 16 weeks group 10. The blood lipids, serum insulin, fasting blood glucose, liver function, liver weight, abdominal lean meat and lean meat content, liver lipid content and IRS-2 protein expression were determined. And do liver pathology. Results The abdominal fat mass, serum triglyceride, fasting blood glucose and alkaline phosphatase of mice in the high-fat and high-sugar diet for 16 weeks were significantly higher than those in the normal diet (P <0.05-0.01). The albumin and albumin globulin ratio Compared with normal diet mice was significantly lower (P <0.05). The liver of the high-fat and high-sugar diet mice had obvious steatosis, and the 16-week-old mice were more severe than the 8-week-old mice. The content of total cholesterol and triglyceride in the liver of high-fat and high-sugar diet mice was significantly higher than that of the normal diet mice, reaching more than twice that of the normal diet mice at 16 weeks; the expression of IRS-2 was lower than that of the normal mice Of mice more than 8 weeks old. Conclusion High-fat and high-sugar diet can cause non-alcoholic fatty liver in C57BL6J mice, and the expression of IRS-2 protein in liver is lower than that in normal diet mice