| First Author | Acharya A | Year | 2019 |
| Journal | Genes Dev | Volume | 33 |
| Issue | 19-20 | Pages | 1367-1380 |
| PubMed ID | 31488578 | Mgi Jnum | J:284175 |
| Mgi Id | MGI:6390687 | Doi | 10.1101/gad.328955.119 |
| Citation | Acharya A, et al. (2019) miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19. Genes Dev 33(19-20):1367-1380 |
| abstractText | Fat storage in adult mammals is a highly regulated process that involves the mobilization of adipocyte progenitor cells (APCs) that differentiate to produce new adipocytes. Here we report a role for the broadly conserved miR-26 family of microRNAs (miR-26a-1, miR-26a-2, and miR-26b) as major regulators of APC differentiation and adipose tissue mass. Deletion of all miR-26-encoding loci in mice resulted in a dramatic expansion of adipose tissue in adult animals fed normal chow. Conversely, transgenic overexpression of miR-26a protected mice from high-fat diet-induced obesity. These effects were attributable to a cell-autonomous function of miR-26 as a potent inhibitor of APC differentiation. miR-26 blocks adipogenesis, at least in part, by repressing expression of Fbxl19, a conserved miR-26 target without a previously known role in adipocyte biology that encodes a component of SCF-type E3 ubiquitin ligase complexes. These findings have therefore revealed a novel pathway that plays a critical role in regulating adipose tissue formation in vivo and suggest new potential therapeutic targets for obesity and related disorders. |
