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  • 标题:Effects of (−)-Epigallocatechin Gallate (EGCG) on Energy Expenditure and Microglia-Mediated Hypothalamic Inflammation in Mice Fed a High-Fat Diet
  • 本地全文:下载
  • 作者:Jihong Zhou ; Limin Mao ; Ping Xu
  • 期刊名称:Nutrients
  • 电子版ISSN:2072-6643
  • 出版年度:2018
  • 卷号:10
  • 期号:11
  • 页码:1681-1693
  • DOI:10.3390/nu10111681
  • 出版社:MDPI Publishing
  • 摘要:Obesity is an escalating global epidemic caused by an imbalance between energy intake and expenditure. (−)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been reported to be conducive to preventing obesity and alleviating obesity-related chronic diseases. However, the role of EGCG in energy metabolism disorders and central nervous system dysfunction induced by a high-fat diet (HFD) remains to be elucidated. The aim of this study was to evaluate the effects of EGCG on brown adipose tissue (BAT) thermogenesis and neuroinflammation in HFD-induced obese C57BL/6J mice. Mice were randomly divided into four groups with different diets: normal chow diet (NCD), normal chow diet supplemented with 1% EGCG (NCD EGCG), high-fat diet (HFD), and high-fat diet supplemented with 1% EGCG (HFD EGCG). Investigations based on a four-week experiment were carried out including the BAT activity, energy consumption, mRNA expression of major inflammatory cytokines in the hypothalamus, nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) phosphorylation, and immunofluorescence staining of microglial marker Iba1 in hypothalamic arcuate nucleus (ARC). Experimental results demonstrated that dietary supplementation of EGCG significantly inhibited HFD-induced obesity by enhancing BAT thermogenesis, and attenuated the hypothalamic inflammation and microglia overactivation by regulating the NF-κB and STAT3 signaling pathways.
  • 关键词:obesity; brown adipose tissue; thermogenesis; central nervous system; hypothalamus; microglia; neuroinflammation obesity ; brown adipose tissue ; thermogenesis ; central nervous system ; hypothalamus ; microglia ; neuroinflammation
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