Dietary Apigenin Relieves Body Weight and Glycolipid Metabolic Disturbance via Pro‐Browning of White Adipose Mediated by Autophagy Inhibition

Abstract

ScopeApigenin (AP) has many pharmacological activities, including anti‐inflammation, hyperlipidemia‐lowering, and so on. Previous studies show that AP can reduce lipid accumulation in adipocytes in vitro. However, it remains unclear whether and how AP can promote fat‐browning. Therefore, mouse obesity model and preadipocyte induction model in vitro are used to investigate the effects of AP on glycolipid metabolism, browning and autophagy as well as the possible mechanisms.Methods and resultsThe obese mice are intragastrically administrated with AP (0.1 mg g−1 d−1) for 4 weeks; meanwhile, the differentiating preadipocytes are respectively treated with the indicated concentrations of AP for 48 h. Metabolic phenotype, lipid accumulation, and fat‐browning are respectively evaluated by morphological, functional, and specific markers analysis. The results show that AP treatment alleviates the body weight, glycolipid metabolic disorder, and insulin resistance in the obese mice , which is contributed to the pro‐browning effects of AP in vivo and in vitro. Moreover, the study finds that the pro‐browning effect of AP is accomplished through autophagy inhibition mediated by the activation of PI3K‐Akt‐mTOR pathway.ConclusionsThe findings highlight that autophagy inhibition promotes the browning of white adipocytes and suggest that AP would prevent and treat obesity and the associated metabolic disorders.

The associations between dietary flavonoid intake and hyperlipidemia: data from the national health and nutrition examination survey 2007–2010 and 2017–2018

“…Total flavones include apigenin and luteolin. Apigenin lowers blood lipid levels (55), reduces lipid accumulation in adipocytes, and promotes browning of white adipocytes through autophagy inhibition, thereby ameliorating abnormalities in lipid metabolism (56). Luteolin improves lipid levels and hepatic steatosis (57,58).…”