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Molecular Pharmacology

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Research ArticleArticle

ABCD2 Alters Peroxisome Proliferator-Activated Receptor α Signaling In Vitro, but Does Not Impair Responses to Fenofibrate Therapy in a Mouse Model of Diet-Induced Obesity

Xiaoxi Liu, Jingjing Liu, Shuang Liang, Agatha Schlüter, Stephane Fourcade, Stella Aslibekyan, Aurora Pujol and Gregory A. Graf
Molecular Pharmacology November 2014, 86 (5) 505-513; DOI: https://doi.org/10.1124/mol.114.092742
Xiaoxi Liu
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Jingjing Liu
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Shuang Liang
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Agatha Schlüter
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Stephane Fourcade
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Stella Aslibekyan
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Aurora Pujol
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Gregory A. Graf
Department of Pharmaceutical Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky (X.L., J.L., S.L., G.A.G.); Neurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, Barcelona, Spain (A.S., S.F., A.P.); Center for Biomedical Research on Rare Diseases, Instituto de Salud Carlos III (ISCIII), Valencia, Spain (A.S., S.F., A.P.); Catalan Institution of Research and Advanced Studies, Barcelona, Spain (A.P.); and Department of Epidemiology, University of Alabama, Birmingham, Alabama (S.A.)
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Abstract

Fenofibrate is a peroxisome proliferator-activated receptor (PPAR) α ligand that has been widely used as a lipid-lowering agent in the treatment of hypertriglyceridemia. ABCD2 (D2) is a peroxisomal long-chain acyl-CoA transporter that is highly induced by fenofibrate in the livers of mice. To determine whether D2 is a modifier of fibrate responses, wild-type and D2-deficient mice were treated with fenofibrate for 14 days. The absence of D2 altered expression of gene clusters associated with lipid metabolism, including PPARα signaling. Using 3T3-L1 adipocytes, which express high levels of D2, we confirmed that knockdown of D2 modified genomic responses to fibrate treatment. We next evaluated the impact of D2 on effects of fibrates in a mouse model of diet-induced obesity. Fenofibrate treatment opposed the development of obesity, hypertriglyceridemia, and insulin resistance. However, these effects were unaffected by D2 genotype. We concluded that D2 can modulate genomic responses to fibrates, but that these effects are not sufficiently robust to alter the effects of fibrates on diet-induced obesity phenotypes.

Footnotes

    • Received March 13, 2014.
    • Accepted August 14, 2014.
  • This work was supported by National Institutes of Health National Institute of Diabetes and Digestive and Kidney Diseases [Grants DK080874 and DK100892], National Institute of General Medical Sciences [Grant 8 P20 GM103527-05], and National Heart, Lung, and Blood Institute [Grant R01 HL 09135704]. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

  • dx.doi.org/10.1124/mol.114.092742.

  • ↵Embedded ImageThis article has supplemental material available at molpharm.aspetjournals.org.

  • Copyright © 2014 by The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 86 (5)
Molecular Pharmacology
Vol. 86, Issue 5
1 Nov 2014
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Research ArticleArticle

D2 Influences Fenofibrate Efficacy

Xiaoxi Liu, Jingjing Liu, Shuang Liang, Agatha Schlüter, Stephane Fourcade, Stella Aslibekyan, Aurora Pujol and Gregory A. Graf
Molecular Pharmacology November 1, 2014, 86 (5) 505-513; DOI: https://doi.org/10.1124/mol.114.092742

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Research ArticleArticle

D2 Influences Fenofibrate Efficacy

Xiaoxi Liu, Jingjing Liu, Shuang Liang, Agatha Schlüter, Stephane Fourcade, Stella Aslibekyan, Aurora Pujol and Gregory A. Graf
Molecular Pharmacology November 1, 2014, 86 (5) 505-513; DOI: https://doi.org/10.1124/mol.114.092742
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