Bile salts and dietary phenolic compounds

Bile salts and dietary phenolic compounds represent a complex physiological and chemical interaction between endogenous steroid detergents and exogenous plant-derived bioactives rather than a single therapeutic protein or receptor. Bile salts, synthesized from cholesterol in the liver, are essential for the emulsification and absorption of dietary fats and fat-soluble vitamins in the small intestine. Dietary phenolic compounds, such as flavonoids and phenolic acids, are known to interact with these bile salts in the intestinal lumen, often forming insoluble complexes or altering micellar structures. This interaction is a primary mechanism by which certain plant-based diets lower serum cholesterol, as it inhibits the reabsorption of bile acids and dietary lipids, forcing the liver to utilize more cholesterol for de novo bile acid synthesis. Beyond physical interaction, both bile salts and specific polyphenols act as ligands for key metabolic receptors, including the Farnesoid X receptor (FXR) and the G protein-coupled bile acid receptor 1 (TGR5). Consequently, this interplay is a significant area of research for developing nutritional and pharmacological interventions for metabolic disorders, including hyperlipidemia, type 2 diabetes, and non-alcoholic fatty liver disease.

Other names

Bile acid-polyphenol interactionBile acid-phenolic complexesBile acid-phytochemical interplay

Dietary phenolic compounds interact with bile salts in the intestinal lumen to form insoluble complexes or alter micellar structures, which inhibits the absorption of dietary cholesterol and promotes the fecal excretion of bile acids. This process reduces the enterohepatic circulation of bile acids, leading to the compensatory up-regulation of hepatic cholesterol 7α-hydroxylase (CYP7A1) and the conversion of endogenous cholesterol into new bile acids. Furthermore, both bile salts and specific polyphenols act as signaling molecules that modulate the activity of the Farnesoid X receptor (FXR) and the G protein-coupled bile acid receptor 1 (TGR5) to regulate systemic lipid and glucose metabolism.