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Originally published In Press as doi:10.1194/jlr.M500215-JLR200 on October 19, 2005

Papers In Press, published online ahead of print January 1, 2006
J. Lipid Res., doi:10.1194/jlr.M500215-JLR200
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Journal of Lipid Research, Vol. 47, 42-50, January 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology

Apical sodium bile acid transporter and ileal lipid binding protein in gallstone carriersboxs

Ina Bergheim*, Simone Harsch*, Oliver Mueller{dagger}, Silke Schimmel*, Peter Fritz{dagger} and Eduard F. Stange1,{dagger}

* Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, Germany
{dagger} Robert-Bosch-Hospital, Stuttgart, Germany

boxs This article contains supplemental data in the form of 3 figures.

Published, JLR Papers in Press, October 19, 2005.

1 To whom correspondence should be addressed. e-mail: eduard.stange{at}rbk.de

Although a cholesterol supersaturation of gallbladder bile has been identified as the underlying pathophysiologic defect, the molecular pathomechanism of gallstone formation in humans remains poorly understood. A deficiency of the apical sodium bile acid transporter (ASBT) and ileal lipid binding protein (ILBP) in the small intestine may result in bile acid loss into the colon and might promote gallstone formation by reducing the bile acid pool and increasing the amount of hydrophobic bile salts. To test this hypothesis, protein levels and mRNA expression of ASBT and ILBP were assessed in ileal mucosa biopsies of female gallstone carriers and controls. Neither ASBT nor ILBP levels differed significantly between gallstone carriers and controls. However, when study participants were subgrouped by body weight, ASBT and ILBP protein were 48% and 67% lower in normal weight gallstone carriers than in controls (P < 0.05); similar differences were found for mRNA expression levels. The loss of bile transporters in female normal weight gallstone carriers was coupled with a reduction of protein levels of hepatic nuclear factor 1{alpha} and farnesoid X receptor. In conclusion, in normal weight female gallstone carriers, the decreased expression of ileal bile acid transporters may form a molecular basis for gallstone formation.

Supplementary key words gallstone • intestine • nuclear receptor

Abbreviations: ASBT, apical sodium bile acid transporter; FXR, farnesoid X receptor; HNF1{alpha}, hepatic nuclear factor 1{alpha}; ILBP, ileal lipid binding protein; PPAR{alpha}, peroxisome proliferator-activated receptor {alpha}


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Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.