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Originally published In Press as doi:10.1074/jbc.M206522200 on July 8, 2002

J. Biol. Chem., Vol. 277, Issue 37, 33870-33877, September 13, 2002
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Increased Hepatobiliary and Fecal Cholesterol Excretion upon Activation of the Liver X Receptor Is Independent of ABCA1*

Torsten PlöschDagger §, Tineke KokDagger §, Vincent W. BloksDagger , Martin J. Smit||, Rick HavingaDagger , Giovanna Chimini**, Albert K. GroenDagger Dagger , and Folkert KuipersDagger

From the Dagger  Center for Liver, Digestive, and Metabolic Diseases, Groningen University Institute for Drug Exploration, Department of Pediatrics, University Hospital Groningen, Groningen 9713 GZ, The Netherlands, the || Department of Pharmacology, Organon BV, Oss 5340 AM, The Netherlands, the ** Centre de Immunologie, INSERM-CNRS, Marseille 13288, France, and the Dagger Dagger  Department of Gastroenterology, Academic Medical Center, Amsterdam 1105 BK, The Netherlands

The ATP-binding cassette transporter ABCA1 is essential for high density lipoprotein (HDL) formation and considered rate-controlling for reverse cholesterol transport. Expression of the Abca1 gene is under control of the liver X receptor (LXR). We have evaluated effects of LXR activation by the synthetic agonist T0901317 on hepatic and intestinal cholesterol metabolism in C57BL/6J and DBA/1 wild-type mice and in ABCA1-deficient DBA/1 mice. In wild-type mice, T0901317 increased expression of Abca1 in liver and intestine, which was associated with a ~60% rise in HDL. Biliary cholesterol excretion rose 2.7-fold upon treatment, and fecal neutral sterol output was increased by 150-300%. Plasma cholesterol levels also increased in treated Abca1-/- mice (+120%), but exclusively in very low density lipoprotein-sized fractions. Despite the absence of HDL, hepatobiliary cholesterol output was stimulated upon LXR activation in Abca1-/- mice, leading to a 250% increase in the biliary cholesterol/phospholipid ratio. Most importantly, fecal neutral sterol loss was induced to a similar extent (+300%) by the LXR agonist in DBA/1 wild-type and Abca1-/- mice. Expression of Abcg5 and Abcg8, recently implicated in biliary excretion of cholesterol and its intestinal absorption, was induced in T0901317-treated mice. Thus, activation of LXR in mice leads to enhanced hepatobiliary cholesterol secretion and fecal neutral sterol loss independent of (ABCA1-mediated) elevation of HDL and the presence of ABCA1 in liver and intestine.

* This work was supported by Grants 902-23-191 and 902-23-193 from the Netherlands Organization for Scientific Research.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Both authors contributed equally to this work.

To whom correspondence should be addressed: Groningen University Inst. for Drug Exploration, Lab. of Pediatrics, CMC IV, Academic Hospital Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. Tel.: 31-50-3611732; Fax: 31-50-3611746; E-mail: t.ploesch@med.rug.nl.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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