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目的:观察二甲双胍对2型糖尿病模型大鼠脂肪组织中腺苷酸活化蛋白激酶α2(AMPKα2)及过氧化物酶体增值物激活受体γ(PPARγ)的表达,及其对胰岛素抵抗的影响。方法:高脂饮食伴一次性腹腔注射STZ的方法制备2型糖尿病模型,造模成功后随机分为模型组(DM-C)和治疗组(DM-T)。DM-T组给予盐酸二甲双胍灌胃治疗。测定大鼠治疗前后的体质量,实验末测定各组大鼠肾周及睾周脂肪质量,并检测各组大鼠血糖、胰岛素水平,计算大鼠脂体比,胰岛素敏感指数。同时以半定量逆转录-聚合酶链反应法(RT-PCR)检测各组大鼠脂肪组织AMPKα2及PPARγmRNA的表达。结果:与DM-C组比较,治疗组大鼠脂肪组织AMPKα2及PPARγmRNA的表达及血清胰岛素、胰岛素敏感指数显著增高(P<0.05);DM-T组大鼠血糖显著降低(P<0.05)。结论:二甲双胍可能通过上调2型糖尿病大鼠脂肪组织AMPKα2及PPARγmRNA的表达,调节机体糖代谢,改善胰岛素敏感性。
AIM: To observe the effect of metformin on the expression of AMPKα2 and PPARγ in adipose tissue of type 2 diabetic rats and its effect on insulin resistance. Methods: Type 2 diabetes mellitus was induced by high fat diet with a single intraperitoneal injection of STZ. The rats were randomly divided into model group (DM-C) and treatment group (DM-T) after successful modeling. DM-T group given metformin hydrochloride intragastric treatment. The body weight was measured before and after treatment. At the end of the experiment, the perihepatic and peritumoral fat mass of rats in each group were determined. The blood glucose and insulin levels in each group were measured. The lipid ratio and insulin sensitivity index were calculated. At the same time, the expression of AMPKα2 and PPARγmRNA in adipose tissue were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Results: Compared with DM-C group, the expression of AMPKα2 and PPARγmRNA and the serum insulin and insulin sensitivity index of adipose tissue in treatment group were significantly increased (P <0.05); the blood glucose of DM-T group was significantly decreased (P <0.05). Conclusion: Metformin may regulate glucose metabolism and improve insulin sensitivity by up-regulating the expression of AMPKα2 and PPARγmRNA in adipose tissue of type 2 diabetic rats.