Satiety

Satiety refers to the sensation of being full and the inhibition of further eating following food consumption. It results from complex interactions between gut-derived peptide hormones—such as leptin ("the satiety hormone"), cholecystokinin (CCK), glucagon-like peptide‑1 (GLP‑1), peptide YY—and central nervous system pathways primarily involving the hypothalamus[1][3][4]. These signals integrate information about nutrient intake and energy stores to regulate appetite and maintain energy balance. Disruption in these signaling pathways can contribute to overeating and obesity[1][3].\n\nWhile drugs may be developed to enhance feelings of satiety by targeting these hormonal systems—for example, GLP‑1 receptor agonists used in obesity treatment—the term “satiety” itself does not refer to any single druggable entity or molecular target.\n\nSatiety relies on signals from gut hormones acting on brain centers such as the hypothalamus. Key molecules include leptin—which suppresses appetite—and others like CCK and GLP‑1 that promote fullness after meals[3][4]. \n\nIn summary: “Satiety” should not be listed as a canonical therapeutic target because it represents an integrated physiological response rather than an individual molecular entity amenable to direct pharmacological modulation.

Other names

fullnesssatiation