Dihydromyricetin promoted browning of subscapular adipose tissues in obese mice fed with high-fat diet via activating AMPK-PGC1 a-Sirtl signaling pathway / 中国药理学通报

ABSTRACT

Aim To observe the effect of dihydromyricetin (DHM) on the browning of subscapular adipose tissues in the high-fat diet fed obese mice, and clarify the mechanism. Methods C57BL/6J mice were fed with normal and high-fat diet, and were treated with or without low dose (125 mg • kg"1 • d"1) or high dose (250 mg • kg"1 • d"1) DHM for 16W. The body mass of mice was measured every four weeks during the experiment. After 16 weeks, the mice were fasted overnight. Blood samples were taken for fasting blood glucose. The mice were then sacrificed and the body length measured. The Lee' s index was calculated. The size of the subscapular adipocytes was observed by HE staining. The mRNA and protein expression of uncoupling protein 1 (UCP1) , PR domain containing 16 (Prdml6) , adenylate-activated protein kinase (AMPK) , peroxisome proliferator-activated receptor gamma-assisted activator alpha (PGCla) and silencing signal regulator 1 (Sirtl) were assessed by real time quantitative PCR and Western blot assay. Results Compared with normal control group (ND group) , the body mass of mice in high-fat diet group (HFD group) significantly increased, suggesting that the obese mice model was successfully replicated. In addition , blood glucose, Lee' s index and the fat cell diameter of the subscapular adipose tissues in HFD group all significantly increased, while the mRNA and pro-tein expression of UCP1, Prdml6, AMPK, PGCla and Sirtl significantly decreased. DHM markedly re-versed the changes of the above indexes of HFD mice, but DHM did not significantly affect the above indexes of normal mice. Conclusions Dihydromyricetin promotes the browning of subscapular adipose tissues in mice fed with high-fat diet, which might be via activating AMPK-PGC1 a-Sirtl signaling pathway.