首页    期刊浏览 2024年11月23日 星期六
登录注册

文章基本信息

  • 标题:Resveratrol-induced brown fat-like phenotype in 3T3-L1 adipocytes partly via mTOR pathway
  • 本地全文:下载
  • 作者:Weiyao Liao ; Zihui Liu ; Xiaohan Yin
  • 期刊名称:Food & Nutrition Research
  • 印刷版ISSN:1654-661X
  • 出版年度:2020
  • 页码:1-8
  • DOI:10.29219/fnr.v64.3656
  • 出版社:Co-Action Publishing
  • 摘要:Background : Browning of white adipose tissues (WAT) is recognized as a novel way to combat obesity and its related comorbidities. Thus, a lot of dietary agents contributing to browning of WAT have been identified. Objective : In this study, we try to explore the mechanism of the browning of WAT induced by resveratrol (Res) in 3T3-L1 adipocytes. Methods : The levels of cell viability and lipid accumulation were evaluated under different concentrations of Res. Cell signaling pathway analysis was performed to investigate the possible mechanisms of the WAT browning effect of Res in 3T3-L1 cells. Results : We found that Res induced the brown fat-like phenotype by activating protein expressions of brown adipocyte-specific markers, such as peroxisome proliferator-activated receptor gamma (PPAR-γ), peroxisome proliferator- activated receptor gamma coactivator-1 alpha (PGC-1α), and uncoupling protein 1 (UCP1). Besides, Res reduced lipid accumulation, as shown by Oil Red O staining. The increased small lipid droplets implied that Res-treated 3T3-L1 adipocytes had some features of brown adipocytes. The brown fat-like phenotype in 3T3-L1 adipocytes induced by Res was possibly mediated by activation of mammalian target of rapamycin (mTOR), as brown adipocyte-specific markers were decreased by rapamycin, an inhibitor of mTOR and the MHY1485 treatment, an activator of mTOR, showed the similar effect of Res on browning markers. Conclusions : Res induced brown-like adipocyte phenotype in 3T3-L1 adipocytes partly via mTOR pathway, which provided new insights into the utilization of Res to prevent obesity and related comorbidities.
  • 关键词:resveratrol; 3T3-L1 adipocytes; Browning; mTOR
国家哲学社会科学文献中心版权所有