Insulin secretion (revision 2)
Old revision·16:15, 7 Aug 2024·ReceptorRhoda
| Insulin secretion | |
|---|---|
| Cell type | Pancreatic islet beta cell |
| Threshold | ≈5 mM glucose |
| Pattern | Biphasic; superimposed 5–10 min pulses |
| Topic infobox · conventions | |
Insulin secretion is the regulated release of insulin from the beta cells of the pancreatic islets. It is triggered by glucose metabolism within the beta cell rather than by glucose binding to a receptor, and it is amplified by a second set of signals — among them the incretin hormones — that have no effect in the absence of the trigger.[1]
The distinction between triggering and amplifying pathways is the single most important idea for understanding why GLP-1 receptor agonists rarely cause hypoglycaemia while sulfonylureas frequently do. Sulfonylureas act on the triggering pathway and initiate secretion regardless of glucose; incretins act on the amplifying pathway and can only enlarge a response that glucose has already begun.[2]
References
- ^ Rorsman P, Braun M. "Regulation of insulin secretion in human pancreatic islets." Annual Review of Physiology 75:155–179 (2013). DOI:10.1146/annurev-physiol-030212-183754. PMID 22974438.
- ^ Drucker DJ. "Mechanisms of action and therapeutic application of glucagon-like peptide-1." Cell Metabolism 27(4):740–756 (2018). PMID 29617641.