Incretin effect: difference between revisions
Diff·revision 24 → 25·15:00, 18 Sep 2025
Difference between revision 24 and revision 25 of Incretin effect. 2 lines changed; the page grew by 224 bytes.
| Revision 24 — 20:54, 22 Aug 2025 SatietySunniva (talk) add category for receptor pharmacology 7,134 bytes ±0 | Revision 25 — 15:00, 18 Sep 2025 ThymosinTamsin (talk) state that the enzyme inhibitor class works by raising endogenous levels 7,358 bytes +224 | ||
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| 38 | The defect is asymmetric: GIP-mediated insulin secretion is lost disproportionately, whereas GLP-1 responsiveness is better preserved, though also impaired. This asymmetry is clinically important: it explains why GLP-1-directed drugs work as monotherapy in type 2 diabetes whereas GIP-directed drugs do not, and why the later addition of GIP agonism to GLP-1 monotherapy produces further benefit.{{r|nauck2018}} | 38 | The defect is asymmetric: GIP-mediated insulin secretion is lost disproportionately, whereas GLP-1 responsiveness is better preserved, though also impaired. This asymmetry is clinically important: it explains why GLP-1-directed drugs work as monotherapy in type 2 diabetes whereas GIP-directed drugs do not, and why the later addition of GIP agonism to GLP-1 monotherapy produces further benefit.{{r|nauck2018}} |
| 39 | 39 | ||
| + | 40 | In type 1 diabetes, the incretin effect is preserved in those with residual beta-cell function, suggesting the lesion in T2D is beta-cell-intrinsic rather than a defect in hormone secretion or action at the receptor level. | |
| + | 41 | ||
| 40 | == References == | 42 | == References == |
| 41 | {{reflist}} | 43 | {{reflist}} |