Glucagon-like peptide-1: difference between revisions
Diff·revision 53 → 54·04:07, 12 Jun 2025
Difference between revision 53 and revision 54 of Glucagon-like peptide-1. 2 lines changed; the page grew by 201 bytes.
| Revision 53 — 13:12, 4 Jun 2025 DPP4_Dagmar (talk) typo 11,229 bytes ±0 | Revision 54 — 04:07, 12 Jun 2025 ArcuateArt (talk) move table to the section it supports 11,430 bytes +201 | ||
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| 76 | In type 2 diabetes the incretin effect is markedly attenuated. The dominant lesion appears to be loss of beta-cell responsiveness to GIP rather than deficient GLP-1 secretion, since pharmacological GLP-1 concentrations restore much of the insulin response whereas GIP does not.{{r|nauck1986,nauck2018}} This asymmetry is the reason the GLP-1 arm of the axis, and not the GIP arm, was pursued first as a monotherapy target — and it is also why the later demonstration that GIP co-agonism ''adds'' clinical benefit in [[Dual incretin agonist|dual agonists]] was regarded as surprising. | 76 | In type 2 diabetes the incretin effect is markedly attenuated. The dominant lesion appears to be loss of beta-cell responsiveness to GIP rather than deficient GLP-1 secretion, since pharmacological GLP-1 concentrations restore much of the insulin response whereas GIP does not.{{r|nauck1986,nauck2018}} This asymmetry is the reason the GLP-1 arm of the axis, and not the GIP arm, was pursued first as a monotherapy target — and it is also why the later demonstration that GIP co-agonism ''adds'' clinical benefit in [[Dual incretin agonist|dual agonists]] was regarded as surprising. |
| 77 | 77 | ||
| + | 78 | Whether GLP-1 secretion itself is reduced in obesity and type 2 diabetes has been contested for two decades; meta-analytic work suggests differences are small and heterogeneous between studies.{{cn}} | |
| + | 79 | ||
| 78 | == References == | 80 | == References == |
| 79 | {{reflist}} | 81 | {{reflist}} |