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Effect of intraduodenal bile salt on pancreaticobiliary responses to bombesin and to cholecystokinin in humans
Author(s) -
Thimister Paul W.,
Hopman Wim P.,
Tangerman Albert,
Rosenbusch Gerd,
Willems Hans L.,
Jansen Jan B.
Publication year - 1998
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510280602
Subject(s) - cholecystokinin , medicine , postprandial , endocrinology , gastrointestinal hormone , bombesin , gallbladder , ceruletide , chemistry , peptide hormone , neuropeptide , receptor , insulin
Bile salts modulate postprandial gallbladder emptying and pancreatic enzyme secretion, possibly by interfering with plasma cholecystokinin (CCK) responses. The regulatory role of bile salts in the absence of nutrients from the gut is poorly understood. Therefore, we studied the effect of intraduodenal sodium chenodeoxycholate on bombesin (BBS)‐ or CCK‐stimulated plasma CCK levels, plasma pancreatic polypeptide levels, gallbladder motility, and pancreatic enzyme secretion. In a crossover design, saline without or with chenodeoxycholate was perfused intraduodenally for 3 hours in healthy volunteers. During the last hour, either BBS (n = 9) or CCK (n = 10) was infused intravenously. Chenodeoxycholate inhibited BBS‐stimulated gallbladder emptying from 59% ± 4% to 34% ± 6% ( P < .05) and intraduodenal bilirubin output from 41 ± 9 to 21 ± 5 μmol/h ( P < .05), but it increased integrated plasma CCK levels from 157 ± 19 to 184 ± 19 pmol/L · 60 min ( P = .01). Similarly, chenodeoxycholate administration inhibited gallbladder emptying and bilirubin output in response to intravenous CCK. Chenodeoxycholate also tended to reduce pancreatic polypeptide release and intraduodenal amylase output in response to intravenous BBS or CCK. It is concluded that intraduodenal chenodeoxycholate administration inhibits BBS‐ or CCK‐stimulated gallbladder emptying, probably by diminishing target organ sensitivity to circulating CCK.