Research ArticleMetabolism

Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

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Science Signaling  24 Apr 2018:
Vol. 11, Issue 527, eaai7838
DOI: 10.1126/scisignal.aai7838

Committing progenitors to adipogenesis

Promoting the “browning” of white fat has been proposed as a strategy to combat obesity. Beige adipocytes, which are intermediate between fat-storing white adipocytes and thermogenic brown adipocytes, can emerge from the differentiation of adipocyte progenitors in adipose tissue in response to β3-adrenergic stimulation. Using primary human and mouse cells and ex vivo mouse models, Babaei et al. (see also the Focus by Sun et al.) found that the Jak family of kinases promoted the commitment of adipocyte progenitors to beige adipogenesis. Through the downstream transcription factor Stat3, Jak inhibited TGFβ signaling and prevented adipocyte progenitors from differentiating into smooth muscle cells. β3-Adrenergic stimulation of lipolysis, which transiently triggers inflammation, induced the production of the cytokines IL-6 and IL-11, which activated the Jak/Stat3 pathway. These results delineate a pathway that is activated by transient inflammation in adipose tissue that steers adipocyte progenitors toward differentiation into a thermogenically active form of fat.

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