J. Lipid Res.
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A more recent version of this article appeared on January 1, 2006

Papers In Press, published online ahead of print October 13, 2005
J. Lipid Res., doi:10.1194/jlr.M500180-JLR200
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Submitted on May 9, 2005
Revised on October 6, 2005
Accepted on October 13, 2005

Gallbladder histopathology during murine gallstone formation: relation to motility and concentrating function

Karel J van Erpecum, David Q. H. Wang, Antonio Moschetta, Domenico Ferri, Maria Svelto, Piero Portincasa, Jan-Jaap Hendrickx, Marguérite Schipper, and Giuseppe Calamita

Department of Gastroenterology F.02.618, University Medical Center Utrecht, Utrecht 3508 GA

Corresponding Author: k.j.vanerpecum{at}azu.nl

C57L mice are susceptible and AKR mice are resistant to gallstone formation. We studied in male mice of both strains, gallbladder histopathology, cholecystokinin-induced emptying and concentrating function at 0, 14, 28 and 56 days on lithogenic diet. Gallbladder wall thickness increased during diet, with stromal granulocyte infiltration, progressive fibrosis, edema and epithelial cell indentation, particularly in C57L. Strong basal CCK-induced gallbladder emptying (70% of fasting volumes) occurred in both strains, but fasting gallbladder volumes were significantly larger in C57L (14.8±2.2 mu L vs 8.8±1.0 mu L). During diet, fasting volumes increased exclusively in C57L (28.6±2.9 mu L on day 56) with progressively decreased emptying (27% of fasting volumes on day 56). Gallbladder emptying remained normal in AKR. Gallbladder concentrating function decreased during lithogenic diet (especially in C57L), coinciding with decreased Aquaporin-1 and -8 expression at mRNA and protein level. In additional experiments, similar downregulation of Aquaporin-1-and -8 mRNA expression occurred in farnesoid X receptor -/- mice after one week lithogenic diet, without difference from corresponding wild type mice. In conclusion, during murine lithogenesis, altered gallbladder histology is associated with impaired motility, reduced concentrating function and decreased Aquaporin-1 and -8 expression, the latter without involvement of farnesoid X nuclear receptor.


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