Incretin effect: difference between revisions
Diff·revision 9 → 10·03:21, 6 Oct 2024
Difference between revision 9 and revision 10 of Incretin effect. 3 lines changed; the page grew by 754 bytes.
| Revision 9 — 12:03, 21 Sep 2024 SPPS_Sorrel (talk) add the citation for the co-secretion finding 4,049 bytes +351 | Revision 10 — 03:21, 6 Oct 2024 CapitalisationCaz (talk) correct the second-messenger pathway named in the lead 4,803 bytes +754 | ||
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| 5 | | Magnitude in healthy adults = 50–70% of the total insulin secretory response to oral glucose | 5 | | Magnitude in healthy adults = 50–70% of the total insulin secretory response to oral glucose |
| 6 | }} | 6 | }} |
| + | 7 | {{hatnote|For the hormones that mediate this effect, see [[Glucagon-like peptide-1]] and [[Glucose-dependent insulinotropic polypeptide]].}} | |
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| 8 | The '''incretin effect''' is the observation that oral intake of glucose evokes a substantially larger [[Insulin secretion|insulin secretory response]] than intravenous infusion of glucose at an identical glycaemic excursion. This difference was first documented in the early 20th century but was not explained until the 1960s, when two [[peptide]] hormones secreted by the small intestine — [[Glucagon-like peptide-1]] (GLP-1) and [[Glucose-dependent insulinotropic polypeptide]] (GIP) — were shown to potentiate insulin secretion in response to nutrients.{{r|creutzfeldt1979}} | 9 | The '''incretin effect''' is the observation that oral intake of glucose evokes a substantially larger [[Insulin secretion|insulin secretory response]] than intravenous infusion of glucose at an identical glycaemic excursion. This difference was first documented in the early 20th century but was not explained until the 1960s, when two [[peptide]] hormones secreted by the small intestine — [[Glucagon-like peptide-1]] (GLP-1) and [[Glucose-dependent insulinotropic polypeptide]] (GIP) — were shown to potentiate insulin secretion in response to nutrients.{{r|creutzfeldt1979}} |
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| 19 | == Mechanisms: GLP-1 and GIP == | 20 | == 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}} | 21 | 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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| + | 23 | GLP-1 is secreted by L cells of the distal small intestine and colon, in response to glucose, fat and amino acids. Its plasma half-life is approximately 2 minutes due to rapid inactivation by [[Dipeptidyl peptidase-4]]. GIP is secreted earlier, by K cells of the duodenum and proximal jejunum, and has a half-life of approximately 7 minutes. The two hormones act through distinct receptors on beta cells; both couple to adenylyl cyclase and raise intracellular cAMP, but through non-identical signalling cascades, and each contributes approximately equally to the total incretin effect in health.{{r|nauck2018}} | |
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| 22 | == References == | 25 | == References == |