Research ArticleMetabolism

Mitophagy controls beige adipocyte maintenance through a Parkin-dependent and UCP1-independent mechanism

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Science Signaling  24 Apr 2018:
Vol. 11, Issue 527, eaap8526
DOI: 10.1126/scisignal.aap8526

A whitener for beige fat

White fat can undergo “browning” and acquire some of the energy-burning properties of brown fat in response to various stimuli, such as β3-adrenergic receptor activation. Mitophagy, a specialized autophagic process that degrades mitochondria, causes these beige adipocytes to reacquire the fat-storing characteristics of white adipocytes. Using mouse models and cultured beige adipocytes, Lu et al. (see also the Focus by Sarraf and Youle) found that Parkin, a factor that promotes the autophagy of damaged mitochondria, was also responsible for mitophagy in beige adipocytes, which triggered their reversion to white adipocytes. β3-Adrenergic receptor activation triggered the PKA-mediated phosphorylation of Parkin and prevented the recruitment of Parkin to mitochondria. These results not only identify a mechanism that could be targeted to maintain beige fat but also demonstrate that Parkin induces the mitophagy of undamaged mitochondria and thus has a role in adipose tissue under physiological conditions.

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