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Originally published In Press as doi:10.1194/jlr.M400448-JLR200 on March 1, 2005

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Journal of Lipid Research, Vol. 46, 1285-1294, June 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Hypolipidemic action of the SERM acolbifene is associated with decreased liver MTP and increased SR-BI and LDL receptors

Christian Lemieux*, Yves Gélinas*, Josée Lalonde*, Fernand Labrie{dagger}, Katherine Cianflone§ and Yves Deshaies1,*

* Laval Hospital Research Center, Department of Anatomy and Physiology, Faculty of Medicine, Laval University, Quebec City, Quebec, Canada G1K 7P4
{dagger} Laval University Molecular and Oncology Endocrinology Research Center, Department of Anatomy and Physiology, Faculty of Medicine, Laval University, Quebec City, Quebec, Canada G1K 7P4
§ McGill Unit for the Prevention of Cardiovascular Disease, Royal Victoria Hospital, Montréal, Quebec, Canada H3A 1A1

Published, JLR Papers in Press, March 1, 2005. DOI 10.1194/jlr.M400448-JLR200

1 To whom correspondence should be addressed. e-mail: yves.deshaies{at}phs.ulaval.ca

This study aimed to identify the mechanisms of the hypolipidemic action of the selective estrogen receptor modulator (SERM) acolbifene (ACOL). Four weeks of treatment with ACOL reduced fasting and postprandial plasma triglycerides (TGs), an effect associated with lower VLDL-TG secretion rate (–25%), and decreased mRNA of microsomal triglyceride transfer protein (MTP; –29%). ACOL increased liver TG concentration (+100%) and amplified the feeding-induced increase in the master lipogenic regulators sterol-regulatory element binding protein-1a (SREBP-1a) and SREBP-1c. ACOL decreased total, HDL, and non-HDL cholesterol (CHOL) by 50%. SREBP-2 mRNA and HMG-CoA reductase activity were minimally affected by ACOL. However, in the fasted state, liver concentration of scavenger receptor class B type I (SR-BI) protein, but not mRNA, was 3-fold higher in ACOL-treated than in control animals and correlated with plasma HDL-CHOL levels (r = 0.80, P < 0.002). Liver LDL receptor (LDLR) protein, but not mRNA, was increased 2-fold by ACOL, independently of the nutritional status.

This study demonstrates that ACOL possesses the unique ability among SERMs to reduce VLDL-TG secretion, likely by reducing MTP expression, and strongly suggests that the robust hypocholesterolemic action of ACOL is related to increased removal of CHOL from the circulation as a consequence of enhanced liver SR-BI and LDLR abundance.

Supplementary key words cholesterol • triglycerides • selective estrogen receptor modulator • liver lipoprotein receptors • hypocholesterolemic drug • microsomal triglyceride transfer protein • scavenger receptor class B type I • low density lipoprotein receptor


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