Bile salt dependent inhibition of gallbladder emptying.
Lin, Henry C., Xiao-Tuan Zhao, Greg M. Kwok, Yu-Guo Gu, and Janet D.
Elashoff.
Department of Medicine, Cedars-Sinai Research Institute, Cedars
-Sinai Medical Center, Los Angeles, California 90048; and School of
Medicine, University of California, Los Angeles, California 90024
APStracts 2:0134G, 1995.
Little is known about the inhibitory controls of gallbladder emptying.
Since cholestyramine, a binding agent that reduces luminal
concentration of bile salt, has been reported to accelerate
gallbladder emptying suggesting that bile salt is inhibitory, we
hypothesized that fat-stimulated gallbladder emptying is inhibited by
a bile salt dependent mechanism. To test this idea, we compared
gallbladder emptying in 10 dogs equipped with duodenal and jejunal
fistulas that allowed for complete diversion of the native bile while
varying concentrations of bile salt were perfused into the small
intestine. In 6 dogs, 30 mM oleate and 5, 10, or 20 mM sodium
taurocholate was perfused into the whole intestine. Since bile salt
availability alters fat absorption, in a separate experiment in 7
dogs, we also compared gallbladder emptying while 30 mM oleate and 5
mM taurocholate were perfused between fistula and 0, 5, 10, or 20 mM
taurocholate were perfused beyond jejunal fistula to separate fat
from varying concentration of bile salt. We found that intestinal
taurocholate inhibited fat-stimulated gallbladder emptying in a dose
-dependent fashion (P<0.01, ANOVA, significant linear dose
effect) and the inhibitory effect of bile salt persisted when 5-20 mM
taurocholate was perfused beyond the jejunal fistula. (0 vs. average
of 5-20 mM taurocholate, p<0.05, paired t-test). We conclude
that fat-stimulated gallbladder emptying is inhibited by a bile salt
dependent inhibitory mechanism.
Received 16 December 1994; accepted in final form 14 June 1995.
APS Manuscript Number G492-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.