| First Author | Abe I | Year | 2022 |
| Journal | Dev Cell | Volume | 57 |
| Issue | 23 | Pages | 2623-2637.e8 |
| PubMed ID | 36473459 | Mgi Jnum | J:347576 |
| Mgi Id | MGI:7410767 | Doi | 10.1016/j.devcel.2022.11.007 |
| Citation | Abe I, et al. (2022) Lipolysis-derived linoleic acid drives beige fat progenitor cell proliferation. Dev Cell 57(23):2623-2637.e8 |
| abstractText | De novo beige adipocyte biogenesis involves the proliferation of progenitor cells in white adipose tissue (WAT); however, what regulates this process remains unclear. Here, we report that in mouse models but also in human tissues, WAT lipolysis-derived linoleic acid triggers beige progenitor cell proliferation following cold acclimation, beta3-adrenoceptor activation, and burn injury. A subset of adipocyte progenitors, as marked by cell surface markers PDGFRalpha or Sca1 and CD81, harbored cristae-rich mitochondria and actively imported linoleic acid via a fatty acid transporter CD36. Linoleic acid not only was oxidized as fuel in the mitochondria but also was utilized for the synthesis of arachidonic acid-derived signaling entities such as prostaglandin D(2). Oral supplementation of linoleic acid was sufficient to stimulate beige progenitor cell proliferation, even under thermoneutral conditions, in a CD36-dependent manner. Together, this study provides mechanistic insights into how diverse pathophysiological stimuli, such as cold and burn injury, promote de novo beige fat biogenesis. |
