An oral glucose load elicits a greater insulin response than the same dose given intravenously. Which hormone accounts for most of this 'incretin' contribution, and where is it produced?
- A Glucagon-like peptide-1 from pancreatic alpha cells
- B Cholecystokinin from I cells of the terminal ileum
- C Gastric inhibitory peptide (glucose-dependent insulinotropic peptide) from K cells of the duodenum and jejunum ✓
- D Somatostatin from D cells of the gastric fundus
Explanation
GIP is released from K cells of the duodenum and upper jejunum in response to oral glucose, fatty acids and amino acids. It potentiates glucose-stimulated insulin secretion from beta cells, producing the augmented response to enteral versus parenteral glucose known as the incretin effect. GLP-1 also contributes but is produced by intestinal L cells, not alpha cells. CCK arises from I cells of the duodenum and jejunum, not the ileum.
Reference: Ganong's Review of Medical Physiology, 26th ed.
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