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Originally published In Press as doi:10.1074/jbc.M204887200 on July 3, 2002

J. Biol. Chem., Vol. 277, Issue 37, 34182-34190, September 13, 2002
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Stimulation of Lipogenesis by Pharmacological Activation of the Liver X Receptor Leads to Production of Large, Triglyceride-rich Very Low Density Lipoprotein Particles*

Aldo GrefhorstDagger §, Baukje M. ElzingaDagger §, Peter J. Voshol||, Torsten PlöschDagger , Tineke KokDagger , Vincent W. BloksDagger , Fjodor H. van der SluijsDagger , Louis M. Havekes**, Johannes A. Romijn||, Henkjan J. VerkadeDagger , and Folkert KuipersDagger Dagger Dagger

From the Dagger  Laboratory of Pediatrics, Center for Liver, Digestive and Metabolic Diseases, University Hospital Groningen, 9700 RB Groningen, the  Gaubius Laboratory, TNO Prevention and Health, 2301 CE Leiden, and the Departments of || Endocrinology and Diabetes and ** Internal Medicine, Leiden University Medical Center, 2300 RA Leiden, The Netherlands

The oxysterol-activated liver X receptor (LXR) provides a link between sterol and fatty acid metabolism; activation of LXR induces transcription of lipogenic genes. This study shows that induction of the lipogenic genes Srebp-1c, Fas, and Acc1 upon administration of the synthetic LXR agonist T0901317 to C57BL/6J mice (10 mg/kg/day, 4 days) is associated with massive hepatic steatosis along the entire liver lobule and a 2.5-fold increase in very low density lipoprotein-triglyceride (VLDL-TG) secretion. The increased VLDL-TG secretion was fully accounted for by formation of larger (129 ± 9 nm versus 94 ± 12 nm, a 2.5-fold increase of particle volume) TG-rich particles. Stimulation of VLDL-TG secretion did not lead to elevated plasma TG levels in C57BL/6J mice, indicating efficient particle metabolism and clearance. However, T0901317 treatment did lead to severe hypertriglyceridemia in mouse models of defective TG-rich lipoprotein clearance, i.e. APOE*3-Leiden transgenic mice (3.2-fold increase) and apoE-/- LDLr-/- double knockouts (12-fold increase). Incubation of rat hepatoma McA-RH7777 cells with T0901317 also resulted in intracellular TG accumulation and enhanced TG secretion. We conclude that, in addition to raising high density lipoprotein cholesterol concentrations, pharmacological LXR activation in mice leads to development of hepatic steatosis and secretion of atherogenic, large TG-rich VLDL particles.

* This work was supported by Grants 903-39-291 (to A. G.) and 902-23-244 (to B. M. E.) 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.

§ These authors contributed equally to this work.

Dagger Dagger To whom correspondence should be addressed: Laboratory of Pediatrics, Center for Liver, Digestive and Metabolic Diseases, Rm. Y2115, CMC IV, University Hospital Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. Tel.: 31-50-363-2669; Fax: 31-50-361-1746; E-mail: f.kuipers@med.rug.nl.

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