Incretin effect (revision 11)
Old revision·00:55, 24 Jul 2024·HalfLifeHavel
| Incretin effect | |
|---|---|
| Also known as | Incretin phenomenon |
| Components | GLP-1 and GIP secretion in response to oral glucose |
| Magnitude in healthy adults | 50–70% of the total insulin secretory response to oral glucose |
| Topic infobox · conventions | |
The incretin effect is the observation that oral intake of glucose evokes a substantially larger 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.[1]
In healthy adults, the incretin effect accounts for approximately 50–70% of the total insulin secretion that follows oral glucose intake. The remaining 30–50% comes from direct stimulation of beta cells by the rising blood glucose itself, termed the glucose-stimulated response. This dual-mechanism design — nutrient-sensing via hormones, plus direct glucose sensing — confers tight glycaemic control in the postprandial state while minimizing the risk of hypoglycaemia when glucose is low.[2]
Historical discovery
[edit]The observation that oral glucose intake provokes a larger insulin response than intravenous glucose at matched glycaemic levels was documented in the 1920s, but the mechanism was unknown for over 40 years. Early hypotheses included a direct effect of the intestinal mucosa on the pancreas (Loewi's "enteroinsular axis") and nervous reflexes, but these remained speculative until the insulin-secreting peptide hormones of the gut were isolated and characterized.[1]