Satiety
The feeling of fullness and satisfaction after eating that suppresses further food intake. GLP-1 receptor agonists promote satiety through both central brain effects and peripheral gastrointestinal effects, contributing significantly to the weight loss observed in clinical trials.
Technical Context
Satiety is regulated by a complex neuroendocrine network: peripheral signals (GLP-1, PYY, CCK — released from gut after eating → activate vagal afferents and directly stimulate brainstem areas; ghrelin — suppressed after eating), brainstem integration (nucleus tractus solitarius/NTS receives vagal inputs and circulating hormone signals), and hypothalamic processing (arcuate nucleus POMC/CART anorexigenic neurons activated, NPY/AgRP orexigenic neurons suppressed; signals relayed to paraventricular nucleus → reduced food intake). GLP-1 RAs promote satiety through: direct activation of GLP-1Rs on NTS neurons, hypothalamic arcuate and paraventricular neurons, and vagal afferent neurons; delayed gastric emptying (prolonging gastric distension signals); and possible effects on food reward pathways (reduced preference for high-fat, high-sugar foods — demonstrated in functional MRI studies with semaglutide).