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Glucose-dependent insulinotropic polypeptide: difference between revisions

Diff·revision 32 → 33·08:33, 5 Feb 2025

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Revision 32 — 12:00, 26 Jan 2025
OralSemaOswin (talk)
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Revision 33 — 08:33, 5 Feb 2025
ITT_Imelda (talk)
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39In 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}}39In 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}}
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+41In 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}}
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41== References ==43== References ==
42{{reflist}}44{{reflist}}