Glucose-dependent insulinotropic polypeptide: difference between revisions
Diff·revision 12 → 13·23:06, 23 Dec 2024
Difference between revision 12 and revision 13 of Glucose-dependent insulinotropic polypeptide. 4 lines changed; the page grew by 654 bytes.
| Revision 12 — 22:28, 1 Dec 2024 BacWaterBarnaby (talk) rm the sentence implying the hormone is a drug 5,577 bytes +118 | Revision 13 — 23:06, 23 Dec 2024 ArcuateArt (talk) expand §Biosynthesis and secretion 6,231 bytes +654 | ||
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| 36 | 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}} | 36 | 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}} |
| 37 | 37 | ||
| + | 38 | == Impaired GIP response in obesity and type 2 diabetes == | |
| + | 39 | In type 2 diabetes, the incretin effect is attenuated primarily because beta cells are unresponsive to GIP — even pharmacological GIP concentrations fail to stimulate insulin secretion, whereas GLP-1-directed drugs remain effective. This loss of GIP potency has been termed ''GIP-incompetence'' and is distinct from deficient GIP secretion, which does not occur. The mechanism remains unclear; current hypotheses include altered receptor expression, impaired downstream signalling and altered beta-cell function secondary to chronic hyperglycaemia.{{r|nauck2019}} | |
| + | 40 | ||
| 38 | == References == | 41 | == References == |
| 39 | {{reflist}} | 42 | {{reflist}} |
| ⋮ | ⋮ | ||
| 47 | * [[Incretin effect]] | 50 | * [[Incretin effect]] |
| 48 | * [[Dipeptidyl peptidase-4]] | 51 | * [[Dipeptidyl peptidase-4]] |
| + | 52 | * [[Dual incretin agonist]] | |
| 49 | 53 | ||
| 50 | {{DEFAULTSORT:Glucose-dependent insulinotropic polypeptide}} | 54 | {{DEFAULTSORT:Glucose-dependent insulinotropic polypeptide}} |