MiR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

Asha Acharya, Daniel C. Berry, He Zhang, Yuwei Jiang, Benjamin T. Jones, Robert E. Hammer, Jonathan M Graff, Joshua T. Mendell

Research output: Contribution to journalArticlepeer-review

31 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1367-1380
Number of pages14
JournalGenes and Development
Issue number19-20
StatePublished - Oct 1 2019


  • Adipocyte progenitor cell
  • Adipogenesis
  • Fbxl19
  • MiR-26
  • MicroRNA
  • Obesity
  • White adipose tissue

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology


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