高糖高脂饮食诱导的2型糖尿病大鼠肝脏TNFα的表达

目的探讨高糖高脂饮食诱导的2型糖尿病大鼠与脂肪肝的关系,以及TNFα在肝脏中的表达和意义。方法经高糖高脂饮食诱导结合小剂量链脲佐菌素的方法建立2型糖尿病大鼠模型,4周、8周、18周末测定血糖、血清胰岛素水平和相关生化指标,18周末光镜、电镜观察大鼠肝脏组织学改变和TNFα在肝脏的蛋白表达水平。结果4周末大鼠血清胰岛素水平明显升高诱导出胰岛素抵抗,8周末成功建立2型糖尿病大鼠模型。18周末肝脏病理切片结果显示糖尿病大鼠肝脏存在着严重的脂肪变性;电镜结果显示肝细胞线粒体肿胀变形,部分线粒体嵴融合消失,TNFα在肝脏的蛋白表达明显增加。结论高糖高脂饮食诱导的2型糖尿病大鼠合并脂肪肝,TNFα在脂肪肝的发生中起着一定作用。

Expression of tumor necrosis factor-alpha in liver of rats with high-carbohydrate-high-fat diet induced diabetes

Objective To investigate the relationship between fatty liver and type 2diabetes mellitus in rats with high-glucose-high-fat diet, and the expression of tumor necrosis factor-alpha in liver. Methods The model of type 2 diabetes mellitus was set up by feeding high-glucose-high-fat diet and by injecting STZ. Fasting blood glucose, fasting serum insulin and related biochemistric index at the end of 4,8 and 18 weeks were measured, respectively. At the end of 18 weeks, liver tissue was examined with light microscope and electron microscope. The protein expression of tumor necrosis factor-alpha was examined by immmunohischemistry. Results Insulin resistance was induced in rats at the end of 4 weeks as the level of serum insulin markedly increased. The rats model of type 2 diabetes mellitus with insulin resistance was set up successfully at the end of 8 weeks. Light microscope showed liver tissue steatosis. Electron microscope showed mitochondria swelling, crista fusion and disappearing at the end of 18 weeks. And, the protein expression of tumor necrosis factor-alpha in liver was increase markedly. Conclusion Tumor necrosis factor-alpha might be involved in the pathogenesis of fatty liver.