Satiety promotion

Satiety promotion refers to the complex physiological and pharmacological process of inducing a sense of fullness and suppressing the drive to eat, thereby reducing overall caloric intake. It is not a single molecular target, such as a specific receptor or enzyme, but rather a therapeutic outcome achieved by modulating various pathways within the gut-brain axis. Key molecular mediators involved in this process include the Glucagon-like peptide 1 receptor (GLP-1R), the Melanocortin 4 receptor (MC4R), and the Amylin receptor, which respond to endogenous hormones like GLP-1, leptin, and cholecystokinin. These signals converge in the hypothalamus and brainstem to activate anorexigenic neurons (e.g., POMC) and inhibit orexigenic neurons (e.g., AgRP/NPY). Clinically, satiety promotion is the primary mechanism of action for several weight-loss and anti-diabetic medications, such as semaglutide and liraglutide, which mimic natural satiety signals to treat obesity and metabolic disorders.

Other names

Appetite suppressionSatiation inductionAnorexigenic signalingFood intake reduction

Satiety is promoted through the activation of G protein-coupled receptors (GPCRs) like GLP-1R and MC4R in the arcuate nucleus of the hypothalamus and the nucleus tractus solitarius in the hindbrain, leading to the stimulation of anorexigenic pathways and the inhibition of orexigenic signaling, often accompanied by a delay in gastric emptying.