Satiety centers

The term **"satiety centers"** describes interconnected regions in the central nervous system that process hormonal and neural signals indicative of energy sufficiency, leading to the cessation of eating. Critical brain structures involved in satiety include the arcuate nucleus (ARC) and paraventricular nucleus (PVN) of the hypothalamus, the nucleus tractus solitarius (NTS) and area postrema (AP) in the brainstem, and the parabrachial nucleus (PBN). These areas integrate peripheral signals (such as leptin, cholecystokinin, peptide YY, GLP-1, and gut distension) as well as neural signals (such as vagal input from gastric stretch receptors)[1][3][5]. Unlike a molecular target, satiety centers are composed of multiple cell types and signal through a variety of neurotransmitters and neuropeptides, including pro-opiomelanocortin (POMC) neurons and their subsequent action on melanocortin receptors (notably MC4R). Disruption or dysfunction in satiety neurocircuits can contribute to disorders of food intake, notably obesity and certain eating disorders[2][3][5]. **Summary for database structuring:** - “Satiety centers” are not a molecular target, are not a receptor or enzyme, and cannot be mapped to a single protein or gene. - They are composed of diverse neural circuits and cell types within the central nervous system that act together to integrate satiety signals and terminate eating[2][3][5]. - The most relevant specific molecular targets are certain receptors and cell types within these regions (e.g., MC4R, POMC neurons), but "satiety centers" itself is not a canonical molecular entity[2].

Other names

Satiety centerfeeding inhibition centerssatiety neurocircuitshypothalamic satiety centers