Glucagon-like peptide-1 (GLP-1)
Also known as: GLP-1, incretin, GIP, glucose-dependent insulinotropic polypeptide
An incretin hormone secreted by L cells of the distal small intestine and colon after meals that amplifies glucose-dependent insulin secretion, suppresses glucagon, slows gastric emptying and promotes satiety.
Overview
L cells of the ileum and colon process proglucagon into GLP-1, GLP-2 and oxyntomodulin. Nutrients in the lumen (and neural/hormonal signals from the duodenum) trigger release within minutes of eating. GLP-1 acts on the GLP-1 receptor, a Gs-coupled GPCR on β cells, α cells (indirectly via somatostatin), gastric and vagal neurons and the hypothalamus.
Together with GIP (glucose-dependent insulinotropic polypeptide, from K cells of the duodenum and jejunum), GLP-1 produces the incretin effect: an oral glucose load releases ≈50–70 % more insulin than the same glucose given intravenously. Crucially, its insulinotropic action is glucose-dependent, so it causes little hypoglycaemia. Native GLP-1 is degraded within ≈2 min by dipeptidyl peptidase-4 (DPP-4).
- Location
Source: L cells of the ileum and colon (GIP: K cells of the duodenum/jejunum). Targets: β and α cells, stomach, brain.
Function
- Amplifies glucose-stimulated insulin secretion.
- Suppresses glucagon secretion.
- Slows gastric emptying.
- Reduces appetite and food intake.
- Physiology
Class: peptide (GLP-1 7–36 amide, 30 aa). Receptor: GLP-1R — Gs/cAMP. Half-life ≈2 min (DPP-4).
- Regulation
Released by carbohydrate, fat and protein in the gut lumen; secretion is enhanced after bariatric surgery (rapid nutrient delivery to the distal gut).
Clinical significance
Incretin-based therapy
GLP-1 receptor agonists (liraglutide, semaglutide, dulaglutide) and the dual GIP/GLP-1 agonist tirzepatide lower glucose and body weight and reduce cardiovascular events; side effects include nausea, vomiting and gallstones. DPP-4 inhibitors (sitagliptin, linagliptin) prolong endogenous incretins and are weight-neutral.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.