Effects of dihydromyricetin on insulin resistance in 3 T3-L1 adipocytes and its mechanism
10.3969/j.issn.1001-1978.2014.11.020
- VernacularTitle:二氢杨梅素对胰岛素抵抗3 T3-L1脂肪细胞的改善作用及其机制研究
- Author:
Xingyi WAN
;
Lihui GAO
;
Guohua FENG
;
Yuan ZHANG
;
Xu LIU
;
Ling LI
- Publication Type:Journal Article
- Keywords:
dihydromyricetin;
insulin resistance;
3 T3-L1 adipocytes;
GLUT4;
Akt2;
adiponectin
- From:
Chinese Pharmacological Bulletin
2014;(11):1580-1584,1585
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of dihydro-myricetin (DMY) on the insulin resistance in 3T3-L1 adipocytes and its mechanism. Methods The differ-entiated adipocytes were treated with 1 μmol · L-1 dexamethasone ( dex ) for 7 days to induce insulin re-sistance. With or without insulin, DMY (1 × 10 -6 ~ 1 × 10 -8 mol·L-1 ) was exposed to the normal and in-sulin-resistant 3 T3-L1 adipocytes for 48 hour and 72 hour, respectively. Rosiglitazone ( 1 × 10 -6 mol · L-1 ) was used as a positive control. The glucose up-take was evaluated by glucose consumption. The mR-NA expressions of glucose transporter 4 ( GLUT4 ) , protein kinase B ( PKB/Akt) and adiponectin were de-termined by RT-PCR analysis. Results DMY ( 5 × 10 -7 ~ 1 × 10 -8 mol·L-1 ) concentration-dependently increased the glucose uptake in insulin-resistant 3 T3-L1 adipocytes, similar to rosiglitazone. However, DMY did not affect the glucose consumption in normal 3T3-L1 cells. After treatment of DMY to insulin-resist-ant 3T3-L1 adipocytes for 72 hours, the expressions of GLUT4 , Akt2 and adiponectin mRNA were markedly increased, compared with the dexamethasone-treated group. Conclusion DMY could improve the insulin resistance in 3T3-L1 adipocytes, which is related to in-creasing the mRNA expression of GLUT4 , Akt2 and adiponectin.
