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Research Article Free access | 10.1172/JCI114703

Protective action of luminal bile salts in necrotizing acute pancreatitis in mice.

G Gomez, C M Townsend Jr, D W Green, S Rajaraman, T Uchida, G H Greeley Jr, R D Soloway, and J C Thompson

Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Department of Surgery, University of Texas Medical Branch, Galveston 77550.

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Published July 1, 1990 - More info

Published in Volume 86, Issue 1 on July 1, 1990
J Clin Invest. 1990;86(1):323–331. https://doi.org/10.1172/JCI114703.
© 1990 The American Society for Clinical Investigation
Published July 1, 1990 - Version history
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Abstract

Bile salts in the intestinal lumen act to inhibit the release of cholecystokinin (CCK). Recent studies have shown that CCK may play a permissive role in the development of acute pancreatitis. In this study, the amount of luminal bile salts in female Swiss Webster mice was either decreased by feeding 4% (wt/wt) cholestyramine or increased by feeding 0.5% sodium taurocholate for 1 wk. Plasma levels of CCK were stimulated by cholestyramine and inhibited by taurocholate. Then, acute pancreatitis was induced either by caerulein injections, or by feeding a choline-deficient, ethionine-supplemented (CDE) diet. Feeding of cholestyramine significantly decreased survival from 25% to 0% in the CDE pancreatitis, and increased the magnitude of elevation of serum amylase levels and the extent of pancreatic necrosis in both models of pancreatitis; CCK-receptor blockade with CR-1409 completely abolished the adverse effects of cholestyramine. In contrast, feeding of taurocholate significantly increased survival to 100% and decreased the elevation of serum amylase and pancreatic necrosis; CCK-8 antagonized these actions of taurocholate. Luminal bile salts appear to provide a physiologic protection against necrotizing pancreatitis, at least in part, both by inhibiting the release of CCK and by promoting resistance of the pancreas to CCK excessive stimulation in vivo.

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