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To investigate the role of microRNA (miRNA) in muscle atrophy, we performed microarray analysis of miRNA expression in skeletal muscles of Sham, orchiectomized (ORX) mice, and ORX mice treated with androgen and identified that the expression of  miR-23b-3p  in ORX mice was significantly higher than that in Sham mice ( P  = 0.007); however,  miR-23b-3p  expression in ORX mice treated with androgen was lower ( P  = 0.001). We also investigated the mechanism by which overexpression or knockdown of  miR-23b-3p  influences the expression of myosin heavy chain, muscle protein synthesis, ATP activity, and glucose uptake in C2C12 myotube cells. Moreover, we examined the serum  miR-23b-3p  levels among male subjects with type 2 diabetes and whether the serum  miR-23b-3p  levels could be a biomarker for muscle atrophy. The overexpression of  miR-23b-3p  in C2C12 myotube cells significantly upregulated the expression of myosin heavy chain, protein synthesis, ATP activity, and glucose uptake. Reporter assays raised a possible direct post-transcriptional regulation involving  miR-23b-3p  and the 3′-UTR of  PTEN  mRNA. Among subjects with type 2 diabetes, serum  miR-23b-3p  levels in the subjects with decreased muscle mass were significantly higher compared to the levels in the subjects without. Our results indicate that  miR-23b-3p  downregulates the expression of  PTEN  in myotube cells and induces the growth of myosin heavy chain. In addition, the serum level of  miR-23b-3p  can be used as a diagnostic marker for muscle atrophy.

miR-23b-3p acts as a counter-response against skeletal muscle atrophy