FIGURE 9.

Potential mechanism for DG prevents against obesity through modulating gut microbiota in high-fat diet fed mice. Primary BAs, generated from cholesterol in liver, were secreted to intestinal tract by conjugating with taurine in mice, later, these conjugated BAs were hydrolyzed to produce unconjugated BAs by BSH enzymes generated from intestinal microbes. BSH enriched microbes was reduced by DG intervention causing increased levels of conjugated BAs, which suppressed ileal FXR-FGF15 feedback signaling, followed by repression of BA synthesis gene (CYP7A1) expression, leading to changes in BA profile, and ultimately brought a series of metabolic improvements including lower serum glucose and insulin levels, increased insulin sensitivity, few hepatic steatosis and resistance to weight gain. Moreover, DG treatment decreased LPS-producing genera resulting in decline of serum LPS level, inducing amelioration of colonic inflammation, intestinal barrier impairment and metabolic disorders like obesity and insulin resistance. Abbreviations: DG, diammonium glycyrrhizinate. BAs, bile acids. BSH, bile-salt hydrolase. FXR, farnesoid X-activated receptor. FGF15, fibroblast growth factor 15. CYP7A1, cholesterol 7α hydroxylase. LPS, lipopolysaccharide.