褐变
芹菜素
自噬
PI3K/AKT/mTOR通路
脂肪组织
白色脂肪组织
内分泌学
化学
内科学
炎症
药理学
生物
生物化学
信号转导
医学
类黄酮
细胞凋亡
抗氧化剂
作者
Shaofeng Xiong,Shumin Yu,Kun Wang,Xiaowei Xiong,Min Xia,Guohua Zeng,Qiren Huang
标识
DOI:10.1002/mnfr.202200763
摘要
Scope Apigenin (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 results The 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. Conclusions The 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.
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