Epigallocatechin-3-gallate (EGCG) attenuates non-alcoholic fatty liver disease via modulating the interaction between gut microbiota and bile acids

DOI Web Site 3 Citations 31 References Open Access
  • Naito Yuji
    Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine Department of Endoscopy and Ultrasound Medicine, University Hospital, Kyoto Prefectural University of Medicine
  • Ushiroda Chihiro
    Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine
  • Mizushima Katsura
    Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine
  • Inoue Ryo
    Laboratory of Animal Science, Setsunan University
  • Yasukawa Zenta
    Nutrition Division, Taiyo Kagaku Co., Ltd.
  • Abe Aya
    Nutrition Division, Taiyo Kagaku Co., Ltd.
  • Takagi Tomohisa
    Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine Department for Medical Innovation and Translational Medical Science, Kyoto Prefectural University of Medicine

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Abstract

<p>The spectrum of non-alcoholic fatty liver disease (NAFLD) ranges from simple hepatic steatosis commonly associated with obesity, to non-alcoholic steatohepatitis, which can progress to fibrosis, cirrhosis and hepatocellular carcinoma. Recent reports have indicated the crucial role of gut microbiota and their metabolites in the progression of NAFLD. In the present review, we demonstrated the influence of oral administration of (−)-epigallocatechin-3-gallate (EGCG) on the gut microbiota, serum bile acid profile, and gene expression in the liver in mice fed a high-fat diet (HFD). EGCG significantly inhibited the increase in histological fatty deposit and triglyceride accumulation in the liver induced by HFD, and improved intestinal dysbiosis. One of important findings is that the abundance of Proteobacteria and Defferibacteres phylums increased markedly in the HFD group, and this increase was significantly suppressed in the EGCG group. Interestingly, taurine-conjugated cholic acid (TCA) increased in the HFD group, like the mirror image against a marked decrease in the cholic acid (CA) value, and this increase was markedly inhibited in the EGCG group. TCA is not a simple serum biomarker for liver injury but TCA may be a causal factor to disturb lipid metabolism. The distribution of correlation coefficients by Heatmap analysis showed that the abundance of Akkermansia and Parabacteroides genus showed a positive correlation with CA and a negative correlation with TCA, and significantly increased in the EGCG group as compared with the HFD group. In addition, nutrigenomics approaches demonstrated that sirtuin signaling, EIF2 pathway and circadian clock are involved in the anti-steatotic effects of EGCG. In the present paper, we summarized recent update data of EGCG function focusing on intestinal microbiota and their interaction with host cells.</p>

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