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Incretin effect: difference between revisions

Diff·revision 3 → 4·23:11, 7 Jul 2024

Difference between revision 3 and revision 4 of Incretin effect. 3 lines changed; the page grew by 512 bytes.

Revision 3 — 02:51, 28 Jun 2024
AmylinAmos (talk)
the article treated a rodent finding as human physiology; corrected
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Revision 4 — 23:11, 7 Jul 2024
ProglucagonPia (talk)
rm the sentence implying the hormone is a drug
2,353 bytes +512
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}}