Antihyperglycemic effect of equol, a daidzein derivative, in cultured L6 myocytes and ob/ob mice

Authors

  • Sun Hee Cheong,

    1. Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan
    2. Department of Biotechnology, Konkuk University, Chungju, Republic of Korea
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  • Keisuke Furuhashi,

    1. Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan
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  • Katsuki Ito,

    1. Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan
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  • Masato Nagaoka,

    1. Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan
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  • Takayuki Yonezawa,

    1. Graduate School of Medicine, The University of Tokyo, Bunkyo-Ku, Tokyo, Japan
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  • Yutaka Miura,

    1. Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan
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  • Kazumi Yagasaki

    Corresponding author
    1. Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan
    2. Graduate School of Medicine, The University of Tokyo, Bunkyo-Ku, Tokyo, Japan
    • Correspondence: Professor Kazumi Yagasaki, Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo 183–8509, Japan

      E-mail: yagasaki@cc.tuat.ac.jp

      Fax: +81-42-367-5714

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Abstract

Scope

Molecular mechanisms for the potential antihyperglycemic effect of equol remain to be elucidated. In this study, we investigated the in vitro effect of equol on glucose uptake, AMP-activated protein kinase (AMPK) phosphorylation, and glucose transporter 4 (GLUT4) translocation to plasma membrane in L6 myocytes, and its in vivo antihyperglycemic effect in obese-diabetic model ob/ob mice.

Methods and results

Equol was found to promote glucose uptake, AMPK phosphorylation, and GLUT4 translocation detected by Western blotting analyses in L6 myotubes under a condition of insulin absence. Equol (0.05% in diet) suppressed the rise in serum glucose, cholesterol, triglyceride, and lipid peroxide concentrations and the hepatic triglyceride level as compared with those in the control group. Moreover, equol treatment suppressed the rises in fasting blood glucose level and improved the impaired glucose tolerance in ob/ob mice. Furthermore, equol treatment was demonstrated to improve expression of hepatic gluconeogenesis- and lipogenesis-related genes in terms of glucose and lipid metabolism.

Conclusion

The hypoglycemic effect of equol is related to increased GLUT4 translocation to the plasma membrane via AMPK activation. In addition, equol suppresses the fasting blood glucose level and gene expression of hepatic enzymes related to glucose metabolism. These results strongly suggest that equol has antidiabetic potential.

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