Resistin affects lipid metabolism during adipocyte maturation of 3T3-L1 cells

Authors

  • Yoshito Ikeda,

    1. Department of Biophysical Chemistry, Kyoto Pharmaceutical University, Japan
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  • Hiroyuki Tsuchiya,

    1. Department of Biophysical Chemistry, Kyoto Pharmaceutical University, Japan
    Current affiliation:
    1. Departments of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA
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  • Susumu Hama,

    1. Department of Biophysical Chemistry, Kyoto Pharmaceutical University, Japan
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  • Kazuaki Kajimoto,

    1. Laboratory of Innovative Nanomedicine, Graduate School of Pharmaceutical Sciences, Hokkaido University, Japan
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  • Kentaro Kogure

    Corresponding author
    1. Department of Biophysical Chemistry, Kyoto Pharmaceutical University, Japan
    • Correspondence

      K. Kogure, Department of Biophysical Chemistry, Kyoto Pharmaceutical University, 5 Nakauchi-cho, Misasagi, Yamashina-ku, Kyoto 607-8414, Japan

      Fax: +81 75 595 4762

      Tel: +81 75 595 4663

      E-mail: kogure@mb.kyoto-phu.ac.jp

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Abstract

Resistin, an adipose-tissue-specific secretory factor, aggravates metabolic syndrome through impairment of glucose metabolism. Previously, we demonstrated that resistin expression was induced in both 3T3-L1 cells and primary pre-adipocytes derived from Zucker obese rats during the process of differentiation and maturation (Ikeda Y, Hama S, Kajimoto K, Okuno T, Tsuchiya H & Kogure K (2011) Biol Pharm Bull 34, 865–870). However, the biological function of resistin in adipocytes is poorly understood. In the present study, we examined the effects of resistin knockdown on the biological features of 3T3-L1 cells. We found that lipid content was significantly decreased in 3T3-L1 cells transfected with anti-resistin small interfering RNA (siRNA) after adipocyte differentiation. While expression of peroxisome proliferator activated receptor γ and CCAAT/enhancer-binding protein α was not affected, protein expression and transcriptional activity levels of carbohydrate response element binding protein (ChREBP), which upregulates transcription of lipogenic genes, decreased after anti-resistin siRNA treatment. Moreover, gene expression of fatty acid synthase and acetyl-CoA carboxylase 2, which are known to be regulated by ChREBP, were also suppressed by resistin knockdown. In contrast, activity of the fatty acid β-oxidation-regulating protein carnitine palmitoyltransferase 1 increased. These results suggest that resistin knockdown induces suppression of lipid production and activation of fatty acid β-oxidation. Consequently, resistin may affect lipid metabolism during adipocyte maturation.

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