Baicalin promotes the activation of brown and white adipose tissue through AMPK/PGC1a pathway

Obesity occurs when energy intake overtops energy expenditure. Promoting activation of brown adipose tissue (BAT) and white adipose tissue (WAT) has been proven a promising therapeutic strategy for obesity. Baicalin (BAI) has been shown to be protective for various animal models of cardiovascular diseases, such as pulmonary hypertension, atherosclerosis and myocardial hypertrophy. However, whether BAI could stimulate activation of BAT or browning of WAT remains unknown. Here we show that BAI limits weight gaining, ameliorates glucose tolerance, improves cold tolerance and promotes brown-like tissue formation in diet induced obesity mice model. BAI increases the mitochondrial copy number as judged by mtDNA detection. BAI also increases the expression of UCP1 and other classical browning-specific genes in BAT and WAT and cultured C3H10T1/2 adipocytes through a mechanism involving AMPK/PGC1 alpha pathway. Collectively, our study established a role for BAI in regulating energy metabolism, which will provide new idea and theoretical basis for the treatment of obesity.

Automated summary

The study demonstrates that baicalin (BAI) can limit weight gain, improve glucose tolerance, enhance cold tolerance, and promote brown-like tissue formation in diet-induced obesity mice. BAI increases mitochondrial copy number and activates the AMPK/PGC1 alpha pathway, leading to the upregulation of UCP1 and other browning-related genes in brown adipose tissue and white adipose tissue.