Glucose-dependent insulinotropic polypeptide: difference between revisions
Diff·revision 7 → 8·23:18, 10 Sep 2024
Difference between revision 7 and revision 8 of Glucose-dependent insulinotropic polypeptide. 4 lines changed; the page grew by 688 bytes.
| Revision 7 — 13:32, 28 Aug 2024 ReceptorRhoda (talk) attribute the gastric-emptying effect to the study that measured it 4,346 bytes +829 | Revision 8 — 23:18, 10 Sep 2024 GsCouplingGil (talk) clarify that concentrations differ substantially between assay platforms 5,034 bytes +688 | ||
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| 1 | {{Infobox concept | 1 | {{Infobox concept |
| 2 | | name = Glucose-dependent insulinotropic polypeptide | 2 | | name = Glucose-dependent insulinotropic polypeptide |
| + | 3 | | image = peptide-chain.svg | |
| + | 4 | | caption = GIP is a 42-residue peptide processed from pro-GIP in the duodenum and proximal jejunum. | |
| 3 | | Abbreviation = GIP | 5 | | Abbreviation = GIP |
| 4 | | Precursor = [[Proglucagon|Pro-GIP]] (gene {{math|GIP}}) | 6 | | Precursor = [[Proglucagon|Pro-GIP]] (gene {{math|GIP}}) |
| ⋮ | ⋮ | ||
| 25 | == Receptor signalling and cellular actions == | 27 | == Receptor signalling and cellular actions == |
| 26 | GIP acts through the GIP receptor (GIPR), a class B G-protein-coupled receptor structurally related to [[GLP-1 receptor|the GLP-1 receptor]]. Like GLP-1, GIP coupling is glucose-dependent at the beta cell: the same concentration of GIP that stimulates insulin secretion at 8 mM glucose is ineffective at 2 mM, the physiological basis for avoiding hypoglycaemia in the fasting state.{{r|frias2021}} | 28 | GIP acts through the GIP receptor (GIPR), a class B G-protein-coupled receptor structurally related to [[GLP-1 receptor|the GLP-1 receptor]]. Like GLP-1, GIP coupling is glucose-dependent at the beta cell: the same concentration of GIP that stimulates insulin secretion at 8 mM glucose is ineffective at 2 mM, the physiological basis for avoiding hypoglycaemia in the fasting state.{{r|frias2021}} |
| + | 29 | ||
| + | 30 | GIP receptors are expressed on pancreatic beta cells, enteroendocrine cells, neural tissue and adipocytes. Beyond the beta cell, GIP inhibits gastric acid secretion and slows gastric emptying. In adipose tissue, GIP promotes triglyceride uptake and storage — a pathway that was hypothesised to mediate the modest weight gain sometimes observed in early GLP-1 monotherapy and is now thought to explain some of the superior weight loss seen with dual agonists, if GIP signal inhibition at the adipocyte level reduces energy storage.{{r|frias2021}} | |
| 27 | 31 | ||
| 28 | == References == | 32 | == References == |