Glucose-dependent insulinotropic polypeptide: difference between revisions
Diff·revision 13 → 14·07:15, 21 Aug 2024
Difference between revision 13 and revision 14 of Glucose-dependent insulinotropic polypeptide. 9 lines changed; the page grew by 937 bytes.
| Revision 13 — 21:03, 11 Aug 2024 IncretinIvo (talk) restructure 3,409 bytes +41 | Revision 14 — 07:15, 21 Aug 2024 DrTitration (talk) add PMID 4,346 bytes +937 | ||
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| 4 | | Precursor = [[Proglucagon|Pro-GIP]] (gene {{math|GIP}}) | 4 | | Precursor = [[Proglucagon|Pro-GIP]] (gene {{math|GIP}}) |
| 5 | | Principal source = Intestinal K cells (duodenum, proximal jejunum) | 5 | | Principal source = Intestinal K cells (duodenum, proximal jejunum) |
| + | 6 | <!-- Molecular data --> | |
| + | 7 | | Residues = 42 | |
| + | 8 | | Monoisotopic mass = ≈4,972 Da | |
| + | 9 | | Plasma half-life = 7 minutes | |
| 6 | }} | 10 | }} |
| 7 | 11 | ||
| ⋮ | ⋮ | ||
| 16 | 20 | ||
| 17 | K cells are found predominantly in the duodenum and jejunum, extending into the ileum in smaller numbers. They are open-type epithelial cells with an apical surface exposed to the lumen, allowing direct contact with nutrient-induced secretagogues. Secretion is biphasic: an early phase within 15 minutes of ingestion, followed by a later more sustained phase as nutrients pass through the intestine.{{r|nauck2019}} | 21 | K cells are found predominantly in the duodenum and jejunum, extending into the ileum in smaller numbers. They are open-type epithelial cells with an apical surface exposed to the lumen, allowing direct contact with nutrient-induced secretagogues. Secretion is biphasic: an early phase within 15 minutes of ingestion, followed by a later more sustained phase as nutrients pass through the intestine.{{r|nauck2019}} |
| + | 22 | ||
| + | 23 | Fasting concentrations of total GIP in healthy adults are typically 40–60 pmol/L, rising 5–10-fold postprandially. The response to glucose is monophasic, reaching a peak around 30–60 minutes after a meal. This distinct timing profile — earlier than GLP-1 and independent of the distal small intestine — means GIP is the first incretin to encounter the portal circulation. | |
| + | 24 | ||
| + | 25 | == 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}} | |
| 18 | 27 | ||
| 19 | == References == | 28 | == References == |