Figure 3.

Potential mechanisms of interaction between HFD and chronic diseases via bile acid. Cholesterol can stimulate the secretion of bile acids, which forms a secondary bile acid with the help of intestinal bacteria through a 7α‐dehydroxylation reaction. Secondary bile acids like DCA with high hydrophobicity disrupt the plasma membrane structure and destroy the intestinal barrier, while opportunistic pathogens resistant to bile rapidly multiply. As a signal molecule, bile acids bind FXR and TGR5 to further promote immune‐cell infiltration, regulate insulin resistance and regulate lipid metabolism. DCA, deoxycholic acid; FXR, farnesoid X receptor; TGR5, Takeda G protein‐coupled receptor 5; UDCA, ursodeoxycholic acid.