Satiety signalling (revision 4)
Old revision·00:36, 14 Sep 2024·HalfLifeHavel
| Satiety signalling | |
|---|---|
| Satiation | Termination of a meal in progress |
| Satiety | Suppression of intake between meals |
| Principal relay | Nucleus of the solitary tract, area postrema |
| Topic infobox · conventions | |
Satiety signalling comprises the peripheral signals and central circuits that end a meal and delay the next one. The literature distinguishes satiation — the process terminating an eating episode — from satiety, the inter-meal suppression of appetite; the distinction matters because different signals dominate each.[1]
Peripheral signals include gastric distension relayed by vagal mechanoreceptors, nutrient-sensing hormones from the small intestine such as cholecystokinin, GLP-1, peptide YY and amylin, and longer-term adiposity signals such as leptin and insulin. These converge on the caudal brainstem and on hypothalamic circuits including the arcuate nucleus.[1]
Peripheral signals
[edit]Gastric distension is the most immediate satiation signal, relayed by vagal afferents in the stomach wall. It is volume-dependent rather than calorie-dependent, which is why delayed gastric emptying produces satiation out of proportion to the nutrient consumed.[1]
Intestinal hormones add nutrient specificity. Cholecystokinin is released from duodenal I cells in response to fat and protein and acts largely within a meal. GLP-1 and peptide YY are released from more distal L cells and act over a longer window. Amylin, co-secreted with insulin from the pancreas, acts at the area postrema.[2]