AJP - Gastrointestinal and Liver Physiology, Vol 269, Issue 6 988-G993, Copyright © 1995 by American Physiological Society
Bile salt-dependent inhibition of gallbladder emptying
H. C. Lin, X. T. Zhao, G. M. Kwok, Y. G. Gu and J. D. Elashoff
Department of Medicine, Cedars-Sinai Research Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
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 six 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 seven 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 concentrations of bile salt. We found that intestinal taurocholate
inhibited fat-stimulated gallbladder emptying in a dose-dependent fashion
(P < 0.01; analysis of variance, significant linear dose effect) and
that 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.
