Arcuate nucleus: difference between revisions
Diff·revision 17 → 18·13:03, 13 Jul 2025
Difference between revision 17 and revision 18 of Arcuate nucleus. 5 lines changed; the page grew by 654 bytes.
| Revision 17 — 14:38, 19 Jun 2025 BPC_Bramwell (talk) add see also to the sister hormone 4,363 bytes ±0 | Revision 18 — 13:03, 13 Jul 2025 ReceptorRhoda (talk) expand §Neuronal populations 5,017 bytes +654 | ||
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| 27 | Whether a given peptide agonist acts principally at the arcuate, at the brainstem, or through vagal afferents differs between molecules and doses, and the relative contributions in humans are inferred from animal work rather than measured directly.{{r|drucker2018}} | 27 | Whether a given peptide agonist acts principally at the arcuate, at the brainstem, or through vagal afferents differs between molecules and doses, and the relative contributions in humans are inferred from animal work rather than measured directly.{{r|drucker2018}} |
| 28 | 28 | ||
| + | 29 | == Relevance to incretin pharmacology == | |
| + | 30 | [[GLP-1 receptor|GLP-1 receptors]] are expressed in the arcuate and in downstream hypothalamic sites. Agonist administration activates POMC neurons and inhibits AgRP/NPY neurons in animal models, which is the expected signature of an anorexigenic drug.{{r|drucker2018}} | |
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| + | 32 | The clinically interesting question is whether sustained agonism produces adaptation in these circuits. Weight regain after discontinuation is rapid and largely complete, which is consistent with the circuits returning to their prior set point rather than being reset by the period of treatment; see [[Weight regain after discontinuation]]. | |
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| 29 | == References == | 34 | == References == |
| 30 | {{reflist}} | 35 | {{reflist}} |