Food ingestion stimulates cholecystokinin (CCK) release from the proximal intestine, but the mechanisms involved are not well understood. To investigate this effect in vivo in intact rats, plasma CCK was measured after orogastric feeding of proteins, protein hydrolysates, amino acids, glucose, and starch. Intact proteins were the only nutrients to stimulate CCK release. The possibility of direct interaction between different dietary constituents and intestinal CCK-secreting endocrine cells was then examined using a perifusion system containing isolated mucosal cells from the rat duodenojejunum. The functional validity of this system was established by demonstrating that monitor peptide and bombesin both stimulated CCK release in a dose-dependent manner. The stimulatory effect of bombesin required extracellular calcium and was not inhibited by addition of tetrodotoxin. Perifusion of proteins, protein digests, and carbohydrates did not stimulate CCK release. These results indicate that proteins stimulate CCK release postprandially via an indirect mechanism, most likely related to inhibition of intraluminal trypsin. Perifusion of dispersed mucosal cells constitutes a reproducible model to investigate hormonal and peptidergic regulation of CCK release in vitro.
|Original language||English (US)|
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|Issue number||1 28-1|
|State||Published - 1993|
- gastrointestinal hormone
ASJC Scopus subject areas
- Physiology (medical)