高脂饲养小鼠糖耐量异常的机理研究

目的：研究高脂饲养对小鼠骨骼肌胰岛素信号通路的影响，并对其葡萄糖耐受机制进行初步探讨。方法：C57/B6 J雄性小鼠随机分为正常对照组、高脂饲养组2组，分别进食正常饲料和高脂饲料，6周后检测小鼠空腹血糖、血脂并进行糖耐量试验。应用Western blotting 检测骨骼肌中Akt及其底物TBC1D1信号分子的表达变化。结果：高脂饲养组小鼠血脂升高（P＜0.05），空腹血糖及腹腔注射葡萄糖后在0.5、1、2 h 3个时间点的血糖也显著上升（P＜0.05），骨骼肌中Akt 和TBC1D1磷酸化的表达水平均显著下降（P＜0.01）。结论：高脂饲养小鼠存在糖耐量异常，骨骼肌中Akt和TBC1 D1的磷酸化表达下降可能是高脂诱导小鼠糖耐量异常的机制之一。

Study on the mechanism of abnormal glucose tolerance in mice fed a high-fat diet

Objective：To study the effect of high-fat diet on insulin signaling pathway in skeletal muscle of mice , and examine the mechanism of abnormal glucose tolerance .Methods：Male C57BL/6J mice were randomized into normal diet group and high-fat diet group .Blood lipid , fast blood glucose , and glucose tolerance were measured after 6 weeks.Total and phosphorylated proteins of Akt and TBC 1D1 in skeletal muscle were determined via immunoblotting .Results：Fast blood glucose and blood lipid in high-fat diet group were obviously increased （ P〈0.05）.The blood glucose also increased significantly in 0.5, 1, 2 h after intraperitoneal injection of glucose （P〈0.05）, while phosphorylated proteins of Akt and TBC1D1 in skeletal muscle significantly decreased （P〈0.01）. Conclusion：Abnormal glucose tolerance exists in high-fat diet mice .The decreased expression of phosphorylated Akt and TBC1D1 in skeletal muscle may be associated with abnormal glucose tolerance induced by high-fat diet.