The incretin effect accounts for the greater insulin response to oral glucose versus intravenous glucose (at equivalent glucose levels). The two primary incretins and their respective stimulus-secretion patterns are:

• A Insulin and glucagon from beta and alpha cells; both stimulated by nutrient ingestion
• B CCK from I-cells and secretin from S-cells; both stimulate insulin by vagal reflex
• C GLP-2 from L cells and motilin from M cells; both stimulate pancreatic beta cells directly
• D GLP-1 (glucagon-like peptide-1) from intestinal L cells (distal small bowel/colon) and GIP (glucose-dependent insulinotropic polypeptide) from K cells (proximal small intestine); both stimulated by nutrient contact with gut mucosa, enhancing beta-cell insulin secretion in a glucose-dependent manner ✓

Explanation

The incretin effect — the augmentation of insulin secretion that occurs with oral versus intravenous glucose — is mediated by two primary gut hormones: GIP (glucose-dependent insulinotropic polypeptide, formerly gastric inhibitory polypeptide) secreted by K cells in the duodenum and proximal jejunum in response to carbohydrate and fat ingestion; and GLP-1 (glucagon-like peptide-1) secreted by L cells in the distal ileum and colon in response to nutrient delivery. Both act via Gs-cAMP-PKA pathways on pancreatic beta cells to potentiate glucose-stimulated insulin secretion (they have no effect at low glucose — 'glucose-dependent'). GLP-1 also suppresses glucagon, slows gastric emptying, and promotes satiety. GLP-1 receptor agonists (semaglutide, liraglutide) exploit this physiology for diabetes and obesity treatment.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.