Feelings of fullness

“Feelings of fullness” refers to the subjective sensation known as satiety—the state after eating when further food intake is suppressed. This sensation results from complex interactions between peripheral signals from the gut and adipose tissue—such as hormones like leptin, cholecystokinin (CCK), glucagon-like peptide 1 (GLP‑1)—and central processing within brain regions like the hypothalamus. These signals collectively regulate meal size and frequency by modulating neural circuits that control appetite. While “feelings of fullness” itself cannot be targeted therapeutically, many anti-obesity medications work by enhancing these natural signaling pathways through their respective molecular targets[2][3][5].

Other names

SatietyFullnessFeeling full

Mechanisms relate to modulation of satiety-mediating pathways: - Agonism at GLP‑1 receptor increases satiety and reduces food intake. - Agonism at CCK-A receptor slows gastric emptying and promotes satiety. - Leptin replacement signals energy sufficiency via hypothalamic pathways. All mechanisms ultimately enhance central nervous system signaling that leads to reduced hunger and increased feelings of fullness