Regulation mechanism of Compound Yihe Tea on improving insulin resistance in obesity mice
10.11665/j.issn.1000-5048.20200111
- VernacularTitle:复方薏荷茶对肥胖小鼠改善胰岛素抵抗的调节机制研究
- Author:
Congying GUO
;
Songlin YANG
;
Jun WANG
;
Weitao LIAO
;
Lingfeng MO
;
Danshui ZHOU
;
Weiju NI
;
Yu ZENG
- Publication Type:Journal Article
- Keywords:
Compound Yihe Tea;
obesity;
mice;
PI3K-AKT-GLUT4 pathway;
insulin resistance
- From:
Journal of China Pharmaceutical University
2020;51(1):68-75
- CountryChina
- Language:Chinese
-
Abstract:
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.