Satiety regulation via gut fiber effects

This entry refers to the *mechanism* by which dietary fiber modulates satiety, not a single molecular target. Dietary fiber, especially fermentable types, is metabolized by gut microbes to produce short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate. These SCFAs act on free fatty acid receptors (FFAR2/GPR43 and FFAR3/GPR41) on enteroendocrine L cells, stimulating the secretion of satiety hormones like glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). These hormones, as well as cholecystokinin (CCK), transmit signals to the brain either through the circulation or the vagal nerve, delaying gastric emptying, reducing hunger, and ultimately lowering food intake. Thus, \"satiety regulation via gut fiber effects\" is a broad mechanism, using multiple molecular and neural routes to promote feelings of fullness and regulate energy balance[1][2][3]. This is not considered a single therapeutic target; it is a physiological mechanism involving diverse receptors and signaling pathways. For structured database purposes, research should instead focus on specific contributing molecules such as \"Glucagon-like peptide 1 receptor,\" \"Peptide YY receptor Y2,\" or \"Free fatty acid receptor 2 (GPR43)\" when molecular-level detail is required[1][2].

Other names

fiber-induced satietydietary fiber-induced appetite regulationgut microbiota-mediated satiety

Stimulation of enteroendocrine cells to release satiety hormones (GLP-1, PYY, CCK); Fermentation by gut microbes to generate SCFAs, which activate receptors (e.g., FFAR2, FFAR3); Modulation of gut-brain neural circuits via vagal nerve activation