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Incretins are gut hormones released in response to food intake that amplify the metabolic response to nutrients. The main ones are GLP-1 (L cells, ileum and colon) and GIP (K cells, duodenum).
The founding phenomenon is the incretin effect: oral glucose induces a much greater insulin response than the same glucose given intravenously, because the gut, on detecting nutrients, releases incretins that prime the pancreas.
Actions of GLP-1
- Glucose-dependent insulin secretion: only with elevated blood glucose; the stimulus switches off at normal glucose, which limits hypoglycemia.
- Glucagon suppression, reducing hepatic glucose production.
- Slowing of gastric emptying, which moderates the postprandial peak and prolongs satiety.
- Central action on hypothalamic appetite nuclei.
GIP shares the glucose-dependent insulin potentiation and adds effects on adipose tissue and, according to emerging evidence, on central nausea and satiety signaling. The half-life of native GLP-1 is minutes because of DPP-4; the whole class solves that limit with the modifications of Module 2.
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