The difference is explained by the gut: on detecting nutrients it releases hormones (the incretins) that alert the pancreas before glucose reaches the blood. The two main ones are GLP-1, made by L cells in the ileum and colon, and GIP, made by K cells in the duodenum.
In healthy people, incretins account for a large share of the insulin released after a meal. Their action is glucose-dependent: they amplify insulin secretion when glucose is high and stop doing so when it falls, which limits the risk of hypoglycaemia.
The discovery that this effect is reduced in type 2 diabetes opened the whole line of research that led to GLP-1 agonists and later to dual and triple agonists.
The incretin effect is the conceptual starting point of the whole metabolic family in the catalogue. Understanding it explains why receptors are combined (GLP-1, GIP, glucagon, amylin) instead of acting on just one.
Related terms
Learn it in depth at the Peptide University
- Incretin physiology · Module 3
- Metabolic and repair (1–5) · Module 14
- Pharmacology of agonists: single, dual and triple · Module 3
- Pharmacokinetics: ADME and parameters · Module 2
- Amylin, the oral route and the next generation · Module 3
Related catalogue compounds
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