Conquering obesity has become a major socioeconomic challenge.
Scientists show that reduced expression of themiR-25-93-106bcluster, ormiR-93alone, increases fat mass and, subsequently, insulin resistance.
Mechanistically, authors discovered an intricate interplay between enhanced adipocyte precursor turnover and increased adipogenesis. First, miR-93 controlsTbx3, thereby limiting self-renewal in early adipocyte precursors.
Second, miR-93 inhibits the metabolic targetSirt7, which they identified as a major driver of in vivo adipogenesis via induction of differentiation and maturation of early adipocyte precursors.
Downregulation ofmiR-93also occurred in obeseob/obmice, and this phenocopy ofmir-25-93-106b–/–was partially reversible with injection of miR-93 mimics.
These data establish miR-93 as a negative regulator of adipogenesis and a potential therapeutic option for obesity and the metabolic syndrome.