Gut microbiota have profound effects on
bile acid metabolism by promoting deconjugation, dehydrogenation, and dehydroxylation of primary
bile acids in the distal small intestine and colon. High-fat diet-induced
dysbiosis of gut microbiota and
bile acid dysregulation may be involved in the pathology of steatosis in patients with
non-alcoholic fatty liver disease.
Epigallocatechin-3-gallate (EGCG), the most abundant polyphenolic
catechin in
green tea, has been widely investigated for its inhibitory or preventive effects against
fatty liver. The aim of the present study was to investigate the effects of EGCG on the abundance of gut microbiota and the composition of serum
bile acids in high-fat diet-fed mice and determine the specific bacterial genera that can improve the serum
bile acid dysregulation associated with EGCG anti-hepatic steatosis action. Male C57BL/6N mice were fed with the control diet, high-fat diet, or high-fat diet + EGCG at a concentration of 0.32% for 8 weeks. EGCG significantly inhibited the increases in weight, the area of fatty lesions, and the
triglyceride content in the liver induced by the high-fat diet. Principal coordinate analysis revealed significant differences in microbial structure among the groups. At the genus level, EGCG induced changes in the microbiota composition in high-fat diet-fed mice, showing a significantly higher abundance of Adlercreutzia, Akkermansia, Allobaculum and a significantly lower abundance of Desulfovibrionaceae. EGCG significantly reversed the decreased population of serum primary
cholic acid and β-
muricholic acid as well as the increased population of
taurine-conjugated
cholic acid, β-
muricholic acid and
deoxycholic acid in high-fat diet-fed mice. Finally, the correlation analysis between
bile acid profiles and gut microbiota demonstrated the contribution of Akkermansia and Desulfovibrionaceae in the improvement of
bile acid dysregulation in high-fat diet-fed mice by treatment with EGCG. In conclusion, the present study suggests that EGCG could alter
bile acid metabolism, especially
taurine deconjugation, and suppress
fatty liver disease by improving the intestinal
luminal environment.