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Incretin effect: difference between revisions

Diff·revision 7 → 8·07:59, 9 Jul 2024

Difference between revision 7 and revision 8 of Incretin effect. 3 lines changed; the page grew by 512 bytes.

Revision 7 — 08:17, 4 Jul 2024
LCellLeif (talk)
expand §Quantification and measurement
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Revision 8 — 07:59, 9 Jul 2024
HalfLifeHavel (talk)
undo good-faith edit: the source does not say this
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10In 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.{{r|holst2007}}10In 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.{{r|holst2007}}
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+12== Historical discovery ==
+13The 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.{{r|creutzfeldt1979}}
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12== References ==15== References ==
13{{reflist}}16{{reflist}}