CD36 is important for adipocyte recruitment and affects lipolysis

Authors

  • Irene O.C.M. Vroegrijk,

    1. Department of General Internal Medicine, Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
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    • Disclosure: The authors have no competing interests.

      Funding Agencies: This work was supported by grants from the Netherlands Organization for Scientific Research (NWO Zon-MW;917.76.301 to P.J.V.) and by grants from the Center of Medical Systems Biology (CMSB), the Netherlands Consortium for Systems Biology (NCSB) established by The Netherlands Genomics Initiative/Netherlands Organization for Scientific Research (NGI/NWO), the Dutch Diabetes Research Foundation (2005.01.003 to P.J.V.), the seventh framework program of the EU-funded “LipidomicNet” (proposal number 202272) and was performed within the framework of CTMM, the Center for Translational Molecular Medicine (www.ctmm.nl), project PREDICCt (grant 01C-104), and supported by the Netherlands Heart Foundation, Dutch Diabetes Research Foundation, and Dutch Kidney Foundation. P.C.N.R. is an Established Investigator of the Netherlands Heart Foundation (2009T038).

  • Jan Bert van Klinken,

    1. Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
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  • Janna A. van Diepen,

    1. Department of General Internal Medicine, Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
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  • Sjoerd A.A. van den Berg,

    1. Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
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  • Maria Febbraio,

    1. Division Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA
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  • Laura K.M. Steinbusch,

    1. Department of Molecular Genetics, Maastricht University, Maastricht, The Netherlands
    Current affiliation:
    1. Metabolic Research Laboratories, Institute of Metabolic Science, University of Cambridge, Cambridge, UK
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  • Jan F.C. Glatz,

    1. Department of Molecular Genetics, Maastricht University, Maastricht, The Netherlands
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  • Louis M. Havekes,

    1. Department of General Internal Medicine, Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
    2. Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
    3. TNO Metabolic Health Research, Gaubius Laboratory, Leiden, The Netherlands
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  • Peter J. Voshol,

    1. Department of General Internal Medicine, Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
    Current affiliation:
    1. Metabolic Research Laboratories, Institute of Metabolic Science, University of Cambridge, Cambridge, UK
    2. Center for Integrative Genomics, Université de Lausanne, Lausanne, Switzerland
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  • Patrick C.N. Rensen,

    1. Department of General Internal Medicine, Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
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  • Ko Willems van Dijk,

    1. Department of General Internal Medicine, Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
    2. Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
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  • Vanessa van Harmelen

    Corresponding author
    1. Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
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Abstract

Objective: The scavenger receptor CD36 facilitates the cellular uptake of long-chain fatty acids. As CD36-deficiency attenuates the development of high fat diet (HFD)-induced obesity, the role of CD36-deficiency in preadipocyte recruitment and adipocyte function was set out to characterize.

Design and Methods: Fat cell size and number were determined in gonadal, visceral, and subcutaneous adipose tissue of CD36−/− and WT mice after 6 weeks on HFD. Basal lipolysis and insulin-inhibited lipolysis were investigated in gonadal adipose tissue.

Results: CD36−/− mice showed a reduction in adipocyte size in all fat pads. Gonadal adipose tissue also showed a lower total number of adipocytes because of a lower number of very small adipocytes (diameter <50 μm). This was accompanied by an increased pool of preadipocytes, which suggests that CD36-deficiency reduces the capacity of preadipocytes to become adipocytes. Regarding lipolysis, in adipose tissue from CD36−/− mice, cAMP levels were increased and both basal and 8-bromo-cAMP stimulated lipolysis were higher. However, insulin-mediated inhibition of lipolysis was more potent in CD36−/− mice.

Conclusions: These results indicate that during fat depot expansion, CD36-deficiency negatively affects preadipocyte recruitment and that in mature adipocytes, CD36-deficiency is associated with increased basal lipolysis and insulin responsiveness.

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