Glucose-dependent insulinotropic polypeptide: difference between revisions
Diff·revision 17 → 18·22:57, 20 Sep 2024
Difference between revision 17 and revision 18 of Glucose-dependent insulinotropic polypeptide. 2 lines changed; the page grew by 549 bytes.
| Revision 17 — 21:19, 11 Sep 2024 MolarMassMaeve (talk) fix hyphenation per PP:MOS 4,485 bytes +139 | Revision 18 — 22:57, 20 Sep 2024 GsCouplingGil (talk) rm citation to a supplier's own page 5,034 bytes +549 | ||
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| 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}} | 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 | 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}} | |
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| 30 | == References == | 32 | == References == |
| 31 | {{reflist}} | 33 | {{reflist}} |