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ASK1 signalling regulates brown and beige adipocyte function

Author

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  • Kazuki Hattori

    (The laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo)

  • Isao Naguro

    (The laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo)

  • Kohki Okabe

    (The laboratory of Bioanalytical Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo
    JST, PRESTO)

  • Takashi Funatsu

    (The laboratory of Bioanalytical Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo)

  • Shotaro Furutani

    (The laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo)

  • Kohsuke Takeda

    (Graduate School of Biomedical Sciences, Nagasaki University)

  • Hidenori Ichijo

    (The laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo)

Abstract

Recent studies suggest that adult humans have active brown or beige adipocytes, the activation of which might be a therapeutic strategy for the treatment of diverse metabolic diseases. Here we show that the protein kinase ASK1 regulates brown and beige adipocytes function. In brown or white adipocytes, the PKA-ASK1-p38 axis is activated in response to cAMP signalling and contributes to the cell-autonomous induction of genes, including Ucp1. Global and fat-specific ASK1 deficiency leads to impaired metabolic responses, including thermogenesis and oxygen consumption, at the cell and whole-body levels, respectively. Our data thus indicate that the ASK1 signalling axis is a regulator of brown and beige adipocyte gene expression and function.

Suggested Citation

  • Kazuki Hattori & Isao Naguro & Kohki Okabe & Takashi Funatsu & Shotaro Furutani & Kohsuke Takeda & Hidenori Ichijo, 2016. "ASK1 signalling regulates brown and beige adipocyte function," Nature Communications, Nature, vol. 7(1), pages 1-10, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11158
    DOI: 10.1038/ncomms11158
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