Epigallocatechin‐3‐gallate reduces visceral adiposity partly through the regulation of beclin1‐ dependent autophagy in white adipose tissues

Epigallocatechin‐3‐gallate (EGCG) is a primary bioactive phytochemical in green tea. Its therapeutic potential in metabolic diseases has been reported; however, the molecular mechanisms of the anti‐obesity effect of EGCG have not been fully elucidated. In this study, we examined the effects of EGCG on lipid metabolism and autophagy in adipose tissue. After 8 weeks of high‐fat diet feeding, mice were treated with EGCG (20 mg/kg/day) for 2 weeks to test in vivo anti‐obesity effects of EGCG. EGCG treatment improved glucose tolerance and caused body weight loss. Interestingly, reduced adipose tissue mass was more prominent in visceral compared to subcutaneous white adipose tissue. Mechanistically, EGCG treatment increased autophagic flux in white adipose tissue through the AMP‐activated protein kinase‐mediated signaling pathway. Adipocyte‐specific knockout of Beclin1 mitigated the effects of EGCG on visceral adipose tissue mass and glucose tolerance, indicating that the anti‐obesity effect of EGCG requires Beclin1‐dependent autophagy. Collectively, our data demonstrated that EGCG has anti‐obesity effects through the upregulation of Beclin1‐dependent autophagy and lipid catabolism in white adipose tissue (WAT).