Loss of MyoD Promotes Fate Transdifferentiation of Myoblasts Into Brown Adipocytes.

ABSTRACT: Brown adipose tissue (BAT) represents a promising agent to ameliorate obesity and other metabolic disorders. However, the abundance of BAT decreases with age and BAT paucity is a common feature of obese subjects. As brown adipocytes and myoblasts share a common Myf5 lineage origin, elucidating the molecular mechanisms underlying the fate choices of brown adipocytes versus myoblasts may lead to novel approaches to expand BAT mass. Here we identify MyoD as a key negative regulator of brown adipocyte development. CRISPR/CAS9-mediated deletion of MyoD in C2C12 myoblasts facilitates their adipogenic transdifferentiation. MyoD knockout downregulates miR-133 and upregulates the miR-133 target Igf1r, leading to amplification of PI3K-Akt signaling. Accordingly, inhibition of PI3K or Akt abolishes t

SUBMITTER: Wang C 

PROVIDER: S-EPMC5474440 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature