Satiety response

The satiety response refers to the intricate physiological and behavioral process that signals fullness and leads to the cessation of food intake. This complex system is governed by the gut-brain axis, where peripheral signals—including hormones like glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), and peptide YY (PYY)—are integrated by the central nervous system, primarily within the hypothalamus and brainstem [10, 11, 17]. These signals activate anorexigenic pathways, such as the pro-opiomelanocortin (POMC) neurons, while simultaneously inhibiting orexigenic (hunger-stimulating) signals to maintain energy homeostasis [5, 11]. In metabolic diseases like obesity and type 2 diabetes, the satiety response is often blunted or impaired, contributing to chronic overconsumption of calories [11, 18]. Modern therapeutic strategies focus on amplifying these responses using pharmacological agents, such as GLP-1 receptor agonists, which mimic natural satiety hormones to reduce appetite and promote weight loss [1, 8, 9]. Understanding and monitoring the satiety response is critical for the development of effective treatments for eating disorders and metabolic syndrome [12, 19].

Other names

Satiation [2, 10, 19]Feeling of fullness [6, 10, 13]Postprandial satiety [12, 17]Anorexigenic response [3, 5, 11]

Drugs targeting this response work by activating anorexigenic neurons in the hypothalamus, inhibiting orexigenic NPY/AgRP neurons, delaying gastric emptying to prolong gastric distension, and enhancing signaling via the vagus nerve to the brain's satiety centers [3, 5, 9, 11].