Silencing miR-106b improves palmitic acid-induced mitochondrial dysfunction and insulin resistance in skeletal myocytes.

MicroRNA‑106b (miR‑106b) is reported to correlate closely with skeletal muscle insulin resistance. In the current study the effect of miR‑106b on palmitic acid (PA)‑induced mitochondrial dysfunction and insulin resistance was investigated in C2C12 myotubes via the silencing of miR‑106b. MiR‑106b expression was increased under PA treatment, while miR‑106b loss of function improved insulin sensitivity by upregulating its target mitofusin‑2 (Mfn2) in C2C12 myocytes. Furthermore, miR‑106b loss of function partly improved mitochondrial morphological lesions and increased the levels of mitochondial DNA and intracellular adenosine triphosphate that had been impaired by PA exposure in C2C12 myocytes. MiR‑106b loss of function attenuated the levels of intracellular reactive oxygen species (ROS), and upregulated the expression levels of the estrogen‑related receptor (ERR)‑α/peroxisome proliferative activated receptor γ coactivator (PGC)‑1α/Mfn2 axis under PA exposure. In addition, miR‑106b negatively regulated skeletal muscle mitochondrial function and insulin sensitivity under PA‑induced insulin resistance by targeting Mfn2, which may be associated with reduced ROS and upregulation of the ERR‑α/PGC‑1α/Mfn2 axis.