Satiety via dietary fiber-induced gastric distension

Satiety via dietary fiber-induced gastric distension" refers to the **physiological process** whereby consumption of high-fiber foods leads to physical expansion of the stomach. This **gastric distension** activates stretch receptors in the stomach wall that signal through vagal afferent nerves to the brainstem, promoting feelings of fullness and reducing subsequent food intake. In addition to mechanical effects, certain fibers slow gastric emptying and stimulate enteroendocrine cells in the gut to release hormones such as cholecystokinin (CCK), glucagon-like peptide 1 (GLP‑1), and peptide YY—further enhancing satiety signals. Fermentation products from some fibers also contribute by stimulating these hormonal pathways. The overall effect is reduced hunger, increased satiation during meals, lower energy intake over time, improved weight control outcomes in both animal models and humans—and potential benefits for metabolic health including glucose regulation.[1][2][3][4][5] This entry does **not represent a discrete molecular target** like a receptor or enzyme but rather describes an integrated physiological response involving multiple tissues and signaling pathways. Therefore it should not be considered a canonical therapeutic target for drug development but rather an important mechanism leveraged through dietary interventions. If you require information on specific molecules involved in this pathway—such as GLP‑1 receptor or vagal afferent mechanoreceptors—please specify so structured data can be provided at that level.

Other names

Gastric distension-mediated satietyFiber-induced fullnessDietary fiber and satiety signalingGastric stretch-induced appetite suppression

not a druggable molecular target; mechanism involves mechanical expansion of the stomach by fiber-rich foods, leading to activation of vagal afferents and gut hormone secretion