Incretin effect: difference between revisions
Diff·revision 8 → 9·12:03, 21 Sep 2024
Difference between revision 8 and revision 9 of Incretin effect. 3 lines changed; the page grew by 351 bytes.
| Revision 8 — 20:19, 4 Sep 2024 LCellLeif (talk) distinguish the active and total forms of the hormone throughout 3,698 bytes ±0 | Revision 9 — 12:03, 21 Sep 2024 SPPS_Sorrel (talk) add the citation for the co-secretion finding 4,049 bytes +351 | ||
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| 17 | Glucagon, isolated in 1923, was the first gut hormone to be recognised, but its insulinotropic effect is glucose-independent and was therefore insufficient to explain the oral-glucose phenomenon. The isolation and characterization of GLP-1 (in the early 1980s) and the demonstration of its glucose-dependent insulinotropic properties resolved the question. GIP, previously known only as a gastric-inhibitory peptide, was subsequently recognised to be the second arm of the incretin axis.{{r|holst1987}} | 17 | Glucagon, isolated in 1923, was the first gut hormone to be recognised, but its insulinotropic effect is glucose-independent and was therefore insufficient to explain the oral-glucose phenomenon. The isolation and characterization of GLP-1 (in the early 1980s) and the demonstration of its glucose-dependent insulinotropic properties resolved the question. GIP, previously known only as a gastric-inhibitory peptide, was subsequently recognised to be the second arm of the incretin axis.{{r|holst1987}} |
| 18 | 18 | ||
| + | 19 | == Mechanisms: GLP-1 and GIP == | |
| + | 20 | GLP-1 and GIP together account for the incretin effect through glucose-dependent potentiation of insulin secretion. Neither hormone stimulates insulin secretion at low glucose concentrations, a feature that minimizes hypoglycaemia risk compared to insulin secretagogues like sulfonylureas, which do so.{{r|holst2007}} | |
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| 19 | == References == | 22 | == References == |
| 20 | {{reflist}} | 23 | {{reflist}} |