metthetsignaler

Metthetsignaler, often translated as satiety signals, are the physiological cues that reduce hunger and terminate meals. They originate in the gastrointestinal tract, adipose tissue, the pancreas, and other organs, and reach the brain through neural and hormonal pathways. The primary centers that interpret these signals are the hypothalamus and brainstem, especially the nucleus tractus solitarius (NTS) and the arcuate nucleus.

Short-term signals arise during a meal. Gastric distension activates stretch receptors and vagal afferent fibers, contributing to early fullness. Hormones released in response to nutrients also promote satiety: cholecystokinin (CCK) from the small intestine; peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) from the ileum and colon; amylin from the pancreas; and insulin from the pancreas. Leptin and other adipose-derived signals reflect longer-term energy stores and modulate appetite over days to weeks. Ghrelin, secreted mainly by the stomach during fasting, acts as a hunger signal and counterbalances these satiety cues.

The brain integrates these cues to regulate meal size. In the hypothalamus, POMC/CART neurons promote satiety, whereas NPY/AgRP neurons stimulate hunger; insulin and leptin act on these networks to suppress appetite. GLP-1 and CCK also influence reward circuits, helping to reduce the pleasure of eating.

Clinical relevance: disturbances in satiety signaling can contribute to obesity or eating disorders. Therapeutic strategies include drugs that enhance satiety signaling, such as GLP-1 receptor agonists, and surgical interventions that alter gut hormone profiles after bariatric procedures. Understanding metthetsignaler highlights the complex gut–brain communication that governs energy balance.