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Molecular Pharmacology

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Research ArticleArticle

Metabolic Effects of Rexinoids: Tissue-Specific Regulation of Lipoprotein Lipase Activity

Peter J. A. Davies, Stacey A. Berry, Gregory L. Shipley, Robert H. Eckel, Nathalie Hennuyer, Diane L. Crombie, Kathleen M. Ogilvie, Julia Peinado-Onsurbe, Catherine Fievet, Mark D. Leibowitz, Richard A. Heyman and Johan Auwerx
Molecular Pharmacology February 2001, 59 (2) 170-176; DOI: https://doi.org/10.1124/mol.59.2.170
Peter J. A. Davies
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Stacey A. Berry
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Gregory L. Shipley
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Robert H. Eckel
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Nathalie Hennuyer
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Diane L. Crombie
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Kathleen M. Ogilvie
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Julia Peinado-Onsurbe
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Catherine Fievet
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Mark D. Leibowitz
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Richard A. Heyman
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Johan Auwerx
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Abstract

Hypertriglyceridemia is a frequent complication accompanying the treatment of patients with either retinoids or rexinoids, [retinoid X receptor (RXR)-selective retinoids]. To investigate the cellular and molecular basis for this observation, we have studied the effects of rexinoids on triglyceride metabolism in both normal and diabetic rodents. Administration of a rexinoid such as LG100268 (LG268) to normal or diabetic rats results in a rapid increase in serum triglyceride levels. LG268 has no effect on hepatic triglyceride production but suppresses post-heparin plasma lipoprotein lipase (LPL) activity suggesting that the hypertriglyceridemia results from diminished peripheral processing of plasma very low density lipoproteins particles. Treatment of diabetic rats with rexinoids suppresses skeletal and cardiac muscle but not adipose tissue LPL activity. This effect is independent of changes in LPL mRNA. In C2C12 myocytes, LG268 suppresses the level of cell surface (i.e., heparin-releasable) LPL activity without altering LPL mRNA. This effect is very rapid (t 1/2 = 2 h) and is blocked by the transcriptional inhibitor actinomycin D. These studies demonstrate that RXR ligands can have dramatic effects on the post-translational processing of LPL and suggest that skeletal muscle may be an important target of rexinoid action. In addition, these data underscore that the metabolic consequences of RXR activation are distinct from either retinoic acid receptor or peroxisome proliferator-activated receptor activation.

Footnotes

    • Received July 18, 2000.
    • Accepted October 10, 2000.
  • Send reprint requests to: Dr. Peter J. A. Davies, Dept. of Integrative Biology and Pharmacology, University of Texas School of Medicine, P.O. Box 20708, Houston, TX 77225. E-mail:peter.j.davies{at}uth.tmc.edu

  • This work was supported by grants from Ligand Pharmaceuticals, the National Institutes of Health (DK26356), the Fondation de France, the European Union (Grant QLG1-CT-1999-00674), CNRS, INSERM, and Hôpitaux Universitaires de Strasbourg. J.A. and C.F. are research directors with CNRS and INSERM, respectively.

  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 59 (2)
Molecular Pharmacology
Vol. 59, Issue 2
1 Feb 2001
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Research ArticleArticle

Metabolic Effects of Rexinoids: Tissue-Specific Regulation of Lipoprotein Lipase Activity

Peter J. A. Davies, Stacey A. Berry, Gregory L. Shipley, Robert H. Eckel, Nathalie Hennuyer, Diane L. Crombie, Kathleen M. Ogilvie, Julia Peinado-Onsurbe, Catherine Fievet, Mark D. Leibowitz, Richard A. Heyman and Johan Auwerx
Molecular Pharmacology February 1, 2001, 59 (2) 170-176; DOI: https://doi.org/10.1124/mol.59.2.170

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Research ArticleArticle

Metabolic Effects of Rexinoids: Tissue-Specific Regulation of Lipoprotein Lipase Activity

Peter J. A. Davies, Stacey A. Berry, Gregory L. Shipley, Robert H. Eckel, Nathalie Hennuyer, Diane L. Crombie, Kathleen M. Ogilvie, Julia Peinado-Onsurbe, Catherine Fievet, Mark D. Leibowitz, Richard A. Heyman and Johan Auwerx
Molecular Pharmacology February 1, 2001, 59 (2) 170-176; DOI: https://doi.org/10.1124/mol.59.2.170
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