复方薏荷茶对肥胖小鼠改善胰岛素抵抗的调节机制研究

Regulation mechanism of Compound Yihe Tea on improving insulin resistance in obesity mice

研究复方薏荷茶对C57BL/6J肥胖小鼠改善胰岛素抵抗的调节作用。将32只雄性C57BL/6J小鼠随机分为4组:空白组、模型组、复方薏荷茶低浓度组和高浓度组。空白组给予标准饲料,其余组给予高脂饲料造模饲养6周。6周后给药组每日分别灌胃复方薏荷茶40,20 mg/kg。第11周尾静脉取血测定血糖浓度,第12周测定血清中总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密脂蛋白胆固醇(LDL-C)的含量。取肝脏组织分别用HE和油红O染色,免疫组化法测定肝脏组织中GLUT4蛋白的表达量,Western blot法测定脂肪组织中PI3K,Akt和GLUT4蛋白的表达量。结果显示,复方薏荷茶组与模型组相比可显著降低肥胖小鼠的体质量,提高对葡萄糖的耐受量,降低血清中的TC、TG、LDL-C水平,改善肝脏组织病变,提高脂肪组织中PI3K,Akt,GLUT4和肝脏组织中GLUT4蛋白的表达量。实验结果表明,复方薏荷茶具有改善血糖和血脂的作用,可减轻肝脏组织中的脂肪堆积,从PI3K-Akt-GLUT4通路上调节组织对葡萄糖的利用,对肥胖小鼠胰岛素抵抗有较好的调节作用。

The aim of this study was to investigate the effect of Compound Yihe Tea on improving insulin resistance in obesity mice.Thirty-two male C57BL/6J mice were randomly divided into 4 groups:the normal fat diet group(NFD group),high fat diet group(HFD group),Compound Yihe Tea low dosage group[20 mg/(kg·d),YH-L group]and high dosage group[40 mg/(kg·d),YH-H group].NFD group was given standard feed,and the remaining mice were administered with high fat diet.After 6 weeks,YH-H and YH-L groups were given Compound Yihe Tea for 6 weeks.Blood glucose was measured at week 11 and serum levels of total cholesterol(TC),serum triglyceride(TG),low-density lipoprotein cholesterol(LDL-C)and high-density lipoprotein cholesterol(HDL-C)were measured at week 12.Liver tissues were prepared for oil red O and HE staining.Immunohistochemical analysis was used to test the protein expression of GLUT4 in liver.Protein expressions of PI3K,Akt and GLUT4 in epididymis white adipose tissue(WAT)were tested by Western blot.The results showed that Compound Yihe Tea could effectively reduce body weights and the serum levels of TC,TG and LDL-C.Furthermore Compound Yihe Tea could improve the histopathological changes of liver,up-regulate the protein expression of PI3K,Akt and GLUT4 in epididymis WAT and the protein expression of GLUT4 in liver.Compound Yihe Tea can reduce the fat accumulation in liver tissue,improve the indexes of blood glucose and lipid levels,and improve insulin resistance via PI3K-AKT-GLUT4 pathway.