Satiety signalling: difference between revisions
Diff·revision 7 → 8·15:26, 24 Nov 2024
Difference between revision 7 and revision 8 of Satiety signalling. 5 lines changed; the page grew by 704 bytes.
| Revision 7 — 01:05, 3 Nov 2024 CiteBot (talk) bot: normalise citation format 3,234 bytes ±0 | Revision 8 — 15:26, 24 Nov 2024 CiteBot (talk) bot: sort category members 3,938 bytes +704 | ||
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| 19 | Adiposity signals set the background against which meal-related signals are read. Leptin and insulin circulate in proportion to fat mass and modulate the sensitivity of the hypothalamic circuits to meal-related input rather than terminating meals themselves.{{r|schwartz2000}} | 19 | Adiposity signals set the background against which meal-related signals are read. Leptin and insulin circulate in proportion to fat mass and modulate the sensitivity of the hypothalamic circuits to meal-related input rather than terminating meals themselves.{{r|schwartz2000}} |
| 20 | 20 | ||
| + | 21 | == Central integration == | |
| + | 22 | The nucleus of the solitary tract in the caudal brainstem receives vagal afferent input and is adjacent to the area postrema, a circumventricular organ lacking a blood-brain barrier and therefore able to sample circulating peptides directly. Both structures express the [[GLP-1 receptor]].{{r|schwartz2000}} | |
| + | 23 | ||
| + | 24 | The [[Arcuate nucleus|arcuate nucleus]] of the hypothalamus contains two opposing neuronal populations — those expressing pro-opiomelanocortin, which suppress intake, and those expressing agouti-related peptide and neuropeptide Y, which promote it. The arcuate lies adjacent to the median eminence, where fenestrated capillaries allow access to circulating signals. | |
| + | 25 | ||
| 21 | == References == | 26 | == References == |
| 22 | {{reflist}} | 27 | {{reflist}} |