Effects of CCK on pancreatic function and morphology

Area of Science:

• Gastroenterology
• Endocrinology
• Neuroscience

Background:

• Cholecystokinin (CCK) is released from the small intestine post-meal, influencing pancreatic secretion and growth via specific receptors.
• CCK receptors are found on pancreatic acinar cells and gastrointestinal cholinergic neurons, suggesting diverse physiological roles.
• The exact physiological importance of CCK and its dual role as a hormone or neurotransmitter remained unclear.

Purpose of the Study:

• To review the effects of CCK on pancreatic function and morphology.
• To analyze studies using CCK receptor antagonists to elucidate CCK's physiological role.
• To investigate the pathways through which CCK modulates pancreatic activity.

Main Methods:

• Review of studies utilizing CCK receptor antagonists (e.g., loxiglumide, L-364,718) in various species.
• Analysis of the impact of CCK antagonists on meal-stimulated pancreatic enzyme and bicarbonate secretion.
• Evaluation of CCK antagonist effects on pancreatic growth, insulin, and pancreatic polypeptide (PP) release.

Main Results:

• CCK-A antagonists partially reduced meal-stimulated pancreatic enzyme secretion (~50%) but had minimal effect on bicarbonate secretion.
• Atropine, a cholinergic antagonist, abolished postprandial pancreatic secretion, indicating a significant role for cholinergic pathways.
• CCK antagonists did not affect postprandial insulin but reduced PP release; long-term CCK-A receptor blockade in mice showed minimal pancreatic morphological changes.

Conclusions:

• CCK influences pancreatic secretion and growth, potentially acting as a neurotransmitter on cholinergic neurons at low doses.
• Cholinergic pathways are crucial for postprandial pancreatic secretion, with CCK playing a modulatory role.
• Further research is needed to clarify the controversial findings regarding CCK's role in pancreatic tumor development.