NDLI: Synthetic LXR agonist attenuates plaque formation in apoE-/- mice without inducing liver steatosis and hypertriglyceridemia.

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kratzer, Adelheid Buchebner, Marlene Pfeifer, Thomas Becker, Tatjana M. Uray, Georg Miyazaki, Makoto Miyazaki-Anzai, Shinobu Ebner, Birgit Chandak, Prakash G. Kadam, Rajendra S. Calayir, Emine Rathke, Nora Ahammer, Helmut Radovic, Branislav Trauner, Michael Hoefler, Gerald Kompella, Uday B. Fauler, Guenter Levi, Moshe Levak-Frank, Sanja Kostner, Gerhard M. Kratky, Dagmar
Description	Country affiliation: Austria Author Affiliation: Kratzer A ( Institute of Molecular Biology and Biochemistry, Center of Molecular Medicine, Medical University of Graz, Harrachgasse 21/3, 8010 Graz, Austria.)
Abstract	Liver X receptors (LXRs) 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 male and female apoE-null mice. Notably, DMHCA neither increased hepatic triglyceride (TG) levels in male nor female apoE-deficient mice. ATP binding cassette transporter A1 and G1 and cholesterol 7alpha-hydroxylase mRNA abundances were increased, whereas SREBP1c mRNA expression was unchanged in liver, and even decreased in macrophages and intestine. Short-term treatment revealed even higher changes on mRNA regulation. 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.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M800376-JLR200
Journal	The Journal of Lipid Research
Issue Number	2
Volume Number	50
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2009-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Atherosclerosis Drug Therapy Cholic Acids Therapeutic Use Dna-binding Proteins Agonists Receptors, Cytoplasmic And Nuclear Atp Binding Cassette Transporter 1 Atp-binding Cassette Transporters Genetics Metabolism Animals Apolipoproteins E Pathology Fatty Liver Chemically Induced Foam Cells Hypertriglyceridemia Macrophages Mice Mice, Inbred C57bl Mice, Transgenic Orphan Nuclear Receptors Rna, Messenger Sterol Regulatory Element Binding Protein 1 Time Factors Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

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

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