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J. Lipid Res.
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A more recent version of this article appeared on February 1, 2009

Papers In Press, published online ahead of print September 23, 2008
J. Lipid Res., doi:10.1194/jlr.M800376-JLR200
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Submitted on July 18, 2008
Revised on August 14, 2008
Accepted on September 23, 2008

Synthetic LXR agonist attenuates plaque formation in apoE-deficient mice without inducing liver steatosis and hypertriglyceridemia

Adelheid Kratzer, Marlene Buchebner, Thomas Pfeifer, Tatjana M. Becker, Georg Uray, Makoto Miyazaki, Shinobu Miyazaki-Anzai, Birgit Ebner, Prakash G. Chandak, Rajendra S. Kadam, Emine Calayir, Nora Rathke, Helmut Ahammer, Branislav Radovic, Michael Trauner, Gerald Hoefler, Uday B. Kompella, Guenter Fauler, Moshe Levi, Sanja Levak-Frank, Gerhard M. Kostner, and Dagmar Kratky

Institute of Molecular Biology and Biochemistry, Medical University of Graz, Graz 8010

Corresponding Author: dagmar.kratky{at}meduni-graz.at

Liver X receptors are important regulators of cholesterol and lipid metabolism. LXR agonists have been shown to limit the cellular cholesterol content by inducing reverse cholesterol transport, increasing bile acid production, and inhibiting intestinal cholesterol absorption. Most of them, however, also increase lipogenesis via sterol regulatory element-binding protein-1c (SREBP1c) and carbohydrate response element-binding protein activation resulting in hypertriglyceridemia and liver steatosis. We report on the antiatherogenic properties of the steroidal liver X receptor agonist N,N-dimethyl-3beta-hydroxy-cholenamide (DMHCA) in apolipoprotein E (apoE)-deficient mice. Long-term administration of DMHCA (11 weeks) significantly reduced lesion formation in both male and female apoE-null mice. Notably, DMHCA neither increased hepatic triglyceride levels in male nor female apoE-deficient mice. ATP binding cassette transporter A1 and G1 and cholesterol 7alpha-hydroxylase mRNA abundances were increased, while SREBP1c mRNA expression was unchanged in liver, and even decreased in macrophages and intestine. Acute short term treatment revealed similar effects on mRNA regulation with even higher changes. Our data provide evidence that DMHCA is a strong candidate as therapeutic agent for the treatment or prevention of atherosclerosis, circumventing the negative side effects of other LXR agonists.


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