Amylin: difference between revisions
Diff·revision 3 → 4·14:25, 19 Sep 2024
Difference between revision 3 and revision 4 of Amylin. 5 lines changed; the page grew by 705 bytes.
| Revision 3 — 17:13, 7 Sep 2024 CagriCass (talk) the half-life in the lead was the terminal figure; label it as such 1,269 bytes ±0 | Revision 4 — 14:25, 19 Sep 2024 SarcopeniaSefa (talk) add the year of first marketing authorisation, with the regulator named 1,974 bytes +705 | ||
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| 10 | Amylin does not have a dedicated receptor. It acts at the calcitonin receptor in complex with one of three receptor-activity-modifying proteins, RAMP1, RAMP2 or RAMP3, which together constitute the AMY1, AMY2 and AMY3 receptors. The principal site of action for the satiety effect is the area postrema, outside the blood-brain barrier.{{r|hay2015}} | 10 | Amylin does not have a dedicated receptor. It acts at the calcitonin receptor in complex with one of three receptor-activity-modifying proteins, RAMP1, RAMP2 or RAMP3, which together constitute the AMY1, AMY2 and AMY3 receptors. The principal site of action for the satiety effect is the area postrema, outside the blood-brain barrier.{{r|hay2015}} |
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| + | 12 | == Physiology == | |
| + | 13 | Amylin is co-packaged with insulin in the beta-cell secretory granule and released by the same stimuli, so its plasma profile mirrors that of insulin. Fasting concentrations are in the low picomolar range and rise several-fold after a meal.{{r|hay2015}} | |
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| + | 15 | Its three principal actions all restrain nutrient entry rather than promoting disposal. Gastric emptying slows, which flattens the postprandial glucose excursion. Glucagon secretion is suppressed in the postprandial state — but not during hypoglycaemia, where counter-regulation is preserved. Food intake falls through hindbrain signalling that is distinct from, and additive to, the [[Satiety signalling|GLP-1 satiety pathway]]. | |
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| 12 | == References == | 17 | == References == |
| 13 | {{reflist}} | 18 | {{reflist}} |