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All-trans retinoic acid displays multiple effects on the growth, lipogenesis and adipokine gene expression of AML-I preadipocyte cell line

Authors

  • Keiko Morikawa,

    Corresponding author
    • Division of Clinical Nutrition, Department of Nutritional Science, Sagami Women's University, 2-1-1 Bunkyo, Sagamihara, Kanagawa 228-8533, Japan
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  • Haruka Hanada,

    1. Division of Clinical Nutrition, Department of Nutritional Science, Sagami Women's University, 2-1-1 Bunkyo, Sagamihara, Kanagawa 228-8533, Japan
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  • Kaori Hirota,

    1. Division of Clinical Nutrition, Department of Nutritional Science, Sagami Women's University, 2-1-1 Bunkyo, Sagamihara, Kanagawa 228-8533, Japan
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  • Mitsuko Nonaka,

    1. Division of Clinical Nutrition, Department of Nutritional Science, Sagami Women's University, 2-1-1 Bunkyo, Sagamihara, Kanagawa 228-8533, Japan
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  • Chiharu Ikeda

    1. Division of Clinical Nutrition, Department of Nutritional Science, Sagami Women's University, 2-1-1 Bunkyo, Sagamihara, Kanagawa 228-8533, Japan
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Corresponding author: e-mail: keikomorika@m8.gyao.ne.jp

Abstract

Adipose tissue is a potential site of retinoic acid (RA) action, but its physiological significance remains to be clarified. We have examined the effect of all-trans retinoic acid (ATRA) on growth and differentiation of preadipocytes, and on adipokine gene expression in mature adipocytes using human preadipocyte cell model, AML-I. Both ATRA and 9-cis RA induced growth arrest in AML-I preadipocyte at between 50 and 100 µM, which was accompanied by apoptosis. Western blotting showed a loss of NF-κB, Bcl-2 and p-Akt, and the accumulation of Bad and Akt in cytoplasm of ATRA-treated AML-I preadipocytes. Exposure of AML-I to ATRA or 9-cis RA increased intracellular lipid accumulation in a time-dependent manner compared to vehicle-treated cells. Expression of fatty acid synthase (FAS) and peroxisome proliferator-activated receptor-γ (PPAR-γ) proteins was increased in ATRA-treated cells. Thus, both ATRA and 9-cis RA promoted differentiation, inhibited proliferation and induced apoptosis in AML-I preadipocytes. ATRA also modulated adipokine expression by increasing the mRNA level of adipocytokines (adiponectin, leptin and LPL), and by inhibiting PAI-1 mRNA expression in mature AML-I adipocytes. The data suggest that ATRA exerts a wide range of effects—growth arrest, apoptosis, lipogenesis and modulation of adipokine gene expression—during the maturation of preadipocytes into adipocytes.

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