芪白合剂对初发2型糖尿病KKAy小鼠胰岛素抵抗及其相关基因mRNA表达的影响

目的：观察芪白合剂对初发2型糖尿病KKAy小鼠胰岛素抵抗及相关基因磷脂酰肌醇3-激酶（phosphatidylinositol 3-kinase,PI3-K）、磷酸烯醇丙酮酸羧激酶（phosphoenolpyruvate carboxykinase,PEPCK）、过氧化物酶体增殖物激活受体γ辅激活因子1（peroxisome proliferator-activated receptor γ coactivator 1,PGC1）mRNA表达的影响,探讨该方对2型糖尿病小鼠胰岛素抵抗的基因调控机制。方法：KKAy雄性小鼠短期给予高脂高热量饮食喂养诱导2型糖尿病。将糖尿病小鼠随机分为模型组和芪白合剂组,另选9只C57BL/6J作为正常对照。芪白合剂组于模型成功的第2天开始灌胃给予830g/L的芪白合剂,模型组和正常对照组给予0.05%羧甲基纤维素钠,0.1mL/g每日1次。4周后,尾静脉取血测空腹血糖（fasting plasma glucose,FPG）水平,放射免疫法检测空腹血清胰岛素（fasting serum insulin,FINS）水平,计算胰岛素敏感指数。实时荧光定量聚合酶链反应法检测肝组织中PI3-K、PEPCK和PGC1mRNA的表达。结果：模型组、芪白合剂组小鼠FPG、FINS均高于正常对照组（P〈0.01）,ISI低于正常对照组（P〈0.01）。芪白合剂组小鼠FPG低于模型组,ISI高于模型组（P〈0.05）。模型组小鼠肝组织PI3-K、PEPCK和PGC1mRNA的表达均低于正常对照组（P〈0.01）,芪白合剂组小鼠肝组织PI3-K和PGC1 mRNA的表达均高于模型组（P〈0.05）。结论：芪白合剂具有改善2型糖尿病小鼠胰岛素抵抗的作用,其作用机制可能与提高2型糖尿病小鼠肝组织PI3-K和PGC1mRNA的表达有关。

Effects of Astragalus membranaceus and Potentilla discolor mixture on insulin resistance and its related mRNA expressions in KKAy mice with type 2 diabetes

OBJECTIVE：To investigate the effects of Astragalus membranaceus and Potentilla discolor mixture（APM） on insulin resistance（IR）and mRNA expressions of IR-related genes,including phosphatidylinositol 3-kinase （PI3-K）,phosphoenolpyruvate carboxykinase（PEPCK）and peroxisome proliferator-activated receptorγ coactivator 1（PGC1）in KKAy mice with early type 2 diabetes and to explore the gene regulation mechanisms of AMP. METHODS：After giving short-term high-fat and high-calorie diet to induce type 2 diabetes,male KKAy mice were randomly divided into model and APM groups.Nine C57BL/6J mice were used as normal control in addition.The mice in the APM group were treated with 830 g/L of the APM liquid by gastric infusion while the mice in the model group and the normal control group were given 0.05%sodium carboxymethyl cellulose at a dose of 0.1 mL/g body weight once per day.After four weeks,fasting plasma glucose（FPG）was tested using tail vein blood.Fasting serum insulin（FINS）was tested by radioimmunoassay.Insulin sensitivity index （ISI）was calculated as the natural logarithm of the product of FPG and FINS.The mRNA expressions ofPI3-K,PEPCK and PGC1in liver tissues were tested by real-time fluorescence quantitative polymerase chain reaction assay. RESULTS：Both the levels of FPG and FINS in the model group and the APM group were increased,while the ISI values were decreased when compared to those of the normal control group（P0.01）.The level of FPG in the APM group was decreased,while ISI was increased when compared to those of the model group（P 0.05）.All of the mRNA expressions of PI3-K,PEPCK,and PGC1 in liver tissue of the model group were decreased compared with the normal control group（P0.01）.The mRNA expressions of PI3-K and PGC1in the liver tissue of the APM group were higher than those in the model group（P0.05）. CONCLUSION：APM can improve the insulin resistance of mice with type 2 diabetes.The mechanism may be related to increasing the mRNA expressions of PI3-K and PGC1in the liver tissue.