miR‐183 and miR‐96 orchestrate both glucose and fat utilization in skeletal muscle

A

Relative expression of miR‐183 and miR‐96 in GAS, TA and SOL muscles of WT and DKO mice (n = 5).

B

SDH staining of GAS and SOL muscles in WT and DKO mice (n = 5). Scale bars: 100 μm.

C

Representative photographs of GAS and SOL muscles dissected from WT and DKO mice (n = 5). Scale bar: 1 cm.

D

ATPase staining of GAS and SOL muscles of WT and DKO mice (left). Corresponding percentage of type I fibers were determined (right) (n = 5). Scale bars: 100 μm.

E

Relative mRNA expression of MHC isoforms in GAS muscles of WT and DKO mice (n = 3).

F

Oxygen consumption rate of WT and DKO mice in light and dark phases (n = 5).

G

Relative mRNA expression of PGC1α and PLIN5 in GAS muscles of WT and DKO mice (n = 3 for PGC1α analysis; n = 5 for PLIN5 analysis).

H

Relative mRNA expression of PGC1α and PLIN5 in C2C12 cells transfected with miR‐183 and miR‐96 agomirs (Ago‐183/96) or antagomirs (Ant‐183/96) (n = 3).

I

Western blot analysis of PLIN5 in C2C12 cells transfected with Ago‐183/96 or Ant‐183/96.

J, K

Mitochondrial respiration profile of C2C12 cells transfected with Ago‐183/96 (J) or Ant‐183/96 (K). Cellular oxygen consumption rate (OCR) was measured in real time, and corresponding basal and maximal respiration were analyzed by overall OCR (n = 3 or 4 per group).

Figure 1. Loss of miR‐183 and miR‐96 enhances muscle oxidative phenotype.