SYK kinase mediates brown fat differentiation and activation

Marko Knoll, Sally Winther, Anirudh Natarajan, Huan Yang, Mengxi Jiang, Prathapan Thiru, Aliakbar Shahsafaei, Tony E. Chavarria, Dudley W. Lamming, Lei Sun, Jacob B. Hansen and Harvey F. Lodish ()
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Marko Knoll: Whitehead Institute for Biomedical Research
Sally Winther: Whitehead Institute for Biomedical Research
Anirudh Natarajan: Whitehead Institute for Biomedical Research
Huan Yang: Whitehead Institute for Biomedical Research
Mengxi Jiang: Whitehead Institute for Biomedical Research
Prathapan Thiru: Whitehead Institute for Biomedical Research
Aliakbar Shahsafaei: Brigham and Women’s Hospital
Tony E. Chavarria: Whitehead Institute for Biomedical Research
Dudley W. Lamming: Whitehead Institute for Biomedical Research
Lei Sun: Whitehead Institute for Biomedical Research
Jacob B. Hansen: University of Copenhagen
Harvey F. Lodish: Whitehead Institute for Biomedical Research

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Brown adipose tissue (BAT) metabolism influences glucose homeostasis and metabolic health in mice and humans. Sympathetic stimulation of β-adrenergic receptors in response to cold induces proliferation, differentiation, and UCP1 expression in pre-adipocytes and mature brown adipocytes. Here we show that spleen tyrosine kinase (SYK) is upregulated during brown adipocyte differentiation and activated by β-adrenergic stimulation. Deletion or inhibition of SYK, a kinase known for its essential roles in the immune system, blocks brown and white pre-adipocyte proliferation and differentiation in vitro, and results in diminished expression of Ucp1 and other genes regulating brown adipocyte function in response to β-adrenergic stimulation. Adipocyte-specific SYK deletion in mice reduces BAT mass and BAT that developed consisted of SYK-expressing brown adipocytes that had escaped homozygous Syk deletion. SYK inhibition in vivo represses β-agonist-induced thermogenesis and oxygen consumption. These results establish SYK as an essential mediator of brown fat formation and function.

Date: 2017
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DOI: 10.1038/s41467-017-02162-3

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