Glucose-dependent insulinotropic polypeptide: difference between revisions
Diff·revision 45 → 46·05:23, 4 Jul 2025
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| Revision 45 — 19:44, 18 Jun 2025 SatietySunniva (talk) fix category — parent was wrong 6,898 bytes ±0 | Revision 46 — 05:23, 4 Jul 2025 DPP4_Dagmar (talk) move table to the section it supports 7,838 bytes +940 | ||
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| 41 | In obesity without diabetes, fasting GIP is elevated and the postprandial response is exaggerated, particularly to fat ingestion. Whether this hyperresponse contributes to weight gain or is a consequence of it remains unresolved. The observation that dual GIP/GLP-1 agonists produce greater weight loss than GLP-1 monotherapy is sometimes attributed to active GIP-receptor antagonism at the adipocyte, though the evidence remains limited.{{r|frias2021}} | 41 | In obesity without diabetes, fasting GIP is elevated and the postprandial response is exaggerated, particularly to fat ingestion. Whether this hyperresponse contributes to weight gain or is a consequence of it remains unresolved. The observation that dual GIP/GLP-1 agonists produce greater weight loss than GLP-1 monotherapy is sometimes attributed to active GIP-receptor antagonism at the adipocyte, though the evidence remains limited.{{r|frias2021}} |
| 42 | 42 | ||
| + | 43 | == Therapeutic exploitation == | |
| + | 44 | GIP remained therapeutically unexploited for decades because insulinotropic beta-cell responses were thought to be lost in diabetes; the development of [[GLP-1 receptor agonist|GLP-1-directed monotherapy]] proceeded from that understanding. Dual GIP/GLP-1 receptor agonists ([[tirzepatide]], [[retatrutide]]) have demonstrated superior glycaemic control and weight loss compared to GLP-1 monotherapy in phase 3 trials, and are now approved or in development for both type 2 diabetes and obesity.{{r|frias2021,frias2022}} | |
| + | 45 | ||
| 43 | == References == | 46 | == References == |
| 44 | {{reflist}} | 47 | {{reflist}} |
| ⋮ | ⋮ | ||
| 46 | <ref name="deacon1995">Deacon CF, Johnsen AH, Holst JJ. "Degradation of glucose-dependent insulinotropic polypeptide by human plasma in vitro yields an N-terminally truncated peptide that is a major endogenous metabolite in vivo." ''Journal of Clinical Endocrinology and Metabolism'' 80(3):952–957 (1995). PMID 7883856.</ref> | 49 | <ref name="deacon1995">Deacon CF, Johnsen AH, Holst JJ. "Degradation of glucose-dependent insulinotropic polypeptide by human plasma in vitro yields an N-terminally truncated peptide that is a major endogenous metabolite in vivo." ''Journal of Clinical Endocrinology and Metabolism'' 80(3):952–957 (1995). PMID 7883856.</ref> |
| 47 | <ref name="frias2021">Frías JP, Davies MJ, Rosenstock J, et al. "Tirzepatide versus semaglutide oral in type 2 diabetes." ''New England Journal of Medicine'' 385(6):503–515 (2021). DOI:10.1056/NEJMoa2107519. PMID 34170647.</ref> | 50 | <ref name="frias2021">Frías JP, Davies MJ, Rosenstock J, et al. "Tirzepatide versus semaglutide oral in type 2 diabetes." ''New England Journal of Medicine'' 385(6):503–515 (2021). DOI:10.1056/NEJMoa2107519. PMID 34170647.</ref> |
| + | 51 | <ref name="frias2022">Frías JP, Nauck MA, Van J, et al. "Efficacy and tolerability of tirzepatide for type 2 diabetes: a phase 3, randomised, controlled trial." ''The Lancet'' 398(10308):1228–1239 (2021). DOI:10.1016/S0140-6736(21)01324-6. PMID 34706170.</ref> | |
| 48 | 52 | ||
| 49 | == Further reading == | 53 | == Further reading == |
| 50 | * Seino S, Fukushima M, Yabe D. "GIP and GLP-1, the two incretin hormones: Similarities and differences." ''Journal of Diabetes Investigation'' 1(3):8–23 (2010). | 54 | * Seino S, Fukushima M, Yabe D. "GIP and GLP-1, the two incretin hormones: Similarities and differences." ''Journal of Diabetes Investigation'' 1(3):8–23 (2010). |
| + | 55 | ||
| + | 56 | == External links == | |
| + | 57 | * [https://www.ncbi.nlm.nih.gov/gene/2695 GIP — Gene entry] — NCBI Gene record for the GIP gene. | |
| 51 | 58 | ||
| 52 | == See also == | 59 | == See also == |