Cholecystokinin (CCK) released from I cells of the duodenum and jejunum acts on the pancreas to stimulate enzyme secretion. Through which receptor and intracellular pathway does CCK exert its effect on pancreatic acinar cells?
- A CCK-A (CCK1) receptor → Gs → cAMP → PKA → zymogen granule exocytosis
- B CCK-B (CCK2) receptor → Gi → reduced cAMP → paradoxical enzyme release
- C CCK acts through enteric neurons only (vagal afferents) and has no direct acinar cell receptor
- D CCK-A (CCK1) receptor → Gq → PLC → IP3 + DAG → IP3-mediated Ca²⁺ release from ER + PKC activation → zymogen exocytosis ✓
Explanation
CCK binds CCK-A (CCK1) receptors on pancreatic acinar cells. These receptors couple to Gq protein → activates phospholipase C (PLC) → generates IP3 (inositol-1,4,5-trisphosphate) and DAG. IP3 triggers Ca²⁺ release from ER → rise in cytosolic Ca²⁺ → activation of calmodulin-dependent kinases. DAG activates PKC. Together these signals drive zymogen granule fusion and exocytosis. cAMP (Gs pathway) is the mechanism for secretin on pancreatic ductular cells (causing HCO3⁻ secretion), not for CCK on acinar cells. CCK does also activate vagal afferents, but direct acinar cell receptors exist and mediate enzyme secretion.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.