Enteroendocrine L cell: difference between revisions
Diff·revision 7 → 8·08:45, 5 Oct 2024
Difference between revision 7 and revision 8 of Enteroendocrine L cell. 2 lines changed; the page grew by 305 bytes.
| Revision 7 — 14:31, 21 Sep 2024 LCellLeif (talk) state that the receptor is a class B G-protein-coupled receptor 3,046 bytes +425 | Revision 8 — 08:45, 5 Oct 2024 CDMO_Caradoc (talk) rm the causal claim about appetite — the cited work is associative 3,351 bytes +305 | ||
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| 13 | [[Proglucagon]], the precursor peptide, is expressed in L cells and processed post-translationally to generate GLP-1. Secretion is triggered by nutrient ingestion and follows a biphasic time course: an early phase (10–15 minutes) mediated by neural and hormonal signals from the proximal gut, and a later phase (30–120 minutes) as nutrients reach the distal intestine.{{r|holst2007}} | 13 | [[Proglucagon]], the precursor peptide, is expressed in L cells and processed post-translationally to generate GLP-1. Secretion is triggered by nutrient ingestion and follows a biphasic time course: an early phase (10–15 minutes) mediated by neural and hormonal signals from the proximal gut, and a later phase (30–120 minutes) as nutrients reach the distal intestine.{{r|holst2007}} |
| 14 | 14 | ||
| + | 15 | Once secreted, GLP-1 enters the portal blood and is rapidly inactivated by [[Dipeptidyl peptidase-4]] (DPP-4), which cleaves the N-terminal dipeptide. This short plasma half-life of 1–2 minutes is why GLP-1-directed drugs use either DPP-4 inhibitors or engineered peptides resistant to DPP-4 cleavage. | |
| + | 16 | ||
| 15 | == References == | 17 | == References == |
| 16 | {{reflist}} | 18 | {{reflist}} |