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目的研究腺苷酸活化蛋白激酶(AMPK)基因在C57BL/6J小鼠糖脂代谢中的作用。方法分别取5周龄AMPK基因敲除(AMPK-KO)小鼠和C_(57)BL/6J对照小鼠各24只,分为正常饲料(ND)喂养和高脂高糖饲料(HFD)喂养两组。喂养12周,每两周测定小鼠禁食4 h血糖(FBG),实验结束前行口服糖耐量实验(OGTT),解剖取样,检测血生化指标、脂酶活性及相关蛋白的表达。结果 AMpK-KO小鼠血糖、TC、LDL-C、HbA_1c、6-磷酸葡萄糖脱氢酶(G6PD)活性、糖原合成酶激酶(GSK)活性、肝脏PPARγ蛋白表达量明显高于对照小鼠(P<0.05);其胰岛素含量、肝糖原含量、肌糖原含量、肝脂酶(HL)活性、脂蛋白酯酶(LPL)活性、总脂酶活性、葡萄糖激酶(GK)活性、肝组织P-AMPK蛋白、葡萄糖转运蛋白4(GluT-4)蛋白的表达量低于对照组(P<0.05)。结论 AMPK基因通过调节C57BL/6J小鼠糖脂代谢,在T2DM的发病中起重要作用。
Objective To study the role of AMPK gene in glucose and lipid metabolism in C57BL / 6J mice. Methods A total of 24 AMPK knockout mice (AMPK-KO) and C57BL / 6J control mice (5 weeks old) were divided into normal diet (ND) and high fat and fat diet (HFD) Two groups. The rats were fasted for 12 weeks. The fasting blood glucose (FBG) of mice was measured every two weeks. Oral glucose tolerance test (OGTT), anatomical sampling, blood biochemical parameters, lipase activity and related protein expression were performed before the end of the experiment. Results The levels of glucose, TC, LDL-C, HbA_1c, G6PD, GSK and PPARγ in AMpK-KO mice were significantly higher than those in control mice (P <0.05). The contents of insulin, hepatic glycogen, muscle glycogen, hepatic lipase (HL), lipoprotein lipase activity (LPL), total lipase activity, glucokinase (GK) The expression of P-AMPK and GluT-4 protein were lower than that of the control group (P <0.05). Conclusion AMPK gene plays an important role in the pathogenesis of T2DM by regulating glucose and lipid metabolism in C57BL / 6J mice.