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.