Satiety signalling: difference between revisions
Diff·revision 10 → 11·06:21, 1 Feb 2025
Difference between revision 10 and revision 11 of Satiety signalling. 2 lines changed; the page grew by 363 bytes.
| Revision 10 — 02:00, 10 Jan 2025 ReceptorRhoda (talk) give the magnitude of the incretin effect as a percentage of the insulin response 4,078 bytes +104 | Revision 11 — 06:21, 1 Feb 2025 CitationChaser (talk) the article treated a rodent finding as human physiology; corrected 4,441 bytes +363 | ||
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| 25 | 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 | 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. |
| 26 | 26 | ||
| + | 27 | Brainstem and hypothalamic circuits are interconnected and partly redundant. Brainstem circuits alone are sufficient for meal termination in decerebrate animal preparations, whereas hypothalamic circuits carry the longer-term adiposity signal — one reason acute satiation and chronic body-weight regulation can be dissociated pharmacologically.{{r|woods2009}} | |
| + | 28 | ||
| 27 | == References == | 29 | == References == |
| 28 | {{reflist}} | 30 | {{reflist}} |