Satiety signalling: difference between revisions
Diff·revision 4 → 5·16:34, 27 Sep 2024
Difference between revision 4 and revision 5 of Satiety signalling. 4 lines changed; the page grew by 576 bytes.
| Revision 4 — 00:36, 14 Sep 2024 HalfLifeHavel (talk) ce, tighten prose 2,170 bytes ±0 | Revision 5 — 16:34, 27 Sep 2024 RepackRadek (talk) add the enteroendocrine cell type responsible for secretion 2,746 bytes +576 | ||
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| 10 | Peripheral signals include gastric distension relayed by vagal mechanoreceptors, nutrient-sensing hormones from the small intestine such as cholecystokinin, [[Glucagon-like peptide-1|GLP-1]], peptide YY and [[Amylin|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|arcuate nucleus]].{{r|woods2009}} | 10 | Peripheral signals include gastric distension relayed by vagal mechanoreceptors, nutrient-sensing hormones from the small intestine such as cholecystokinin, [[Glucagon-like peptide-1|GLP-1]], peptide YY and [[Amylin|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|arcuate nucleus]].{{r|woods2009}} |
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| + | 12 | Pharmacological exploitation of this system is what [[GLP-1 receptor agonist|GLP-1 receptor agonists]] do. They produce a sustained supraphysiological signal in a system evolved for episodic signalling, and the great majority of the weight loss they produce is attributable to reduced energy intake rather than to increased expenditure.{{r|drucker2018}} | |
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| 12 | == Peripheral signals == | 14 | == Peripheral signals == |
| 13 | 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|gastric emptying]] produces satiation out of proportion to the nutrient consumed.{{r|woods2009}} | 15 | 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|gastric emptying]] produces satiation out of proportion to the nutrient consumed.{{r|woods2009}} |
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| 18 | {{reflist}} | 20 | {{reflist}} |
| 19 | <ref name="woods2009">Woods SC. "The control of food intake: behavioral versus molecular perspectives." ''Cell Metabolism'' 9(6):489–498 (2009). DOI:10.1016/j.cmet.2009.04.007. PMID 19490904.</ref> | 21 | <ref name="woods2009">Woods SC. "The control of food intake: behavioral versus molecular perspectives." ''Cell Metabolism'' 9(6):489–498 (2009). DOI:10.1016/j.cmet.2009.04.007. PMID 19490904.</ref> |
| + | 22 | <ref name="drucker2018">Drucker DJ. "Mechanisms of action and therapeutic application of glucagon-like peptide-1." ''Cell Metabolism'' 27(4):740–756 (2018). PMID 29617641.</ref> | |
| 20 | <ref name="holst2007">Holst JJ. "The physiology of glucagon-like peptide 1." ''Physiological Reviews'' 87(4):1409–1439 (2007). PMID 17928588.</ref> | 23 | <ref name="holst2007">Holst JJ. "The physiology of glucagon-like peptide 1." ''Physiological Reviews'' 87(4):1409–1439 (2007). PMID 17928588.</ref> |
| 21 | 24 | ||
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| 23 | [[Category:Appetite regulation]] | 26 | [[Category:Appetite regulation]] |
| 24 | [[Category:Incretin biology]] | 27 | [[Category:Incretin biology]] |
| + | 28 | [[Category:Gastrointestinal physiology]] | |
| 25 | 29 |