Fig. 7. Sdhaf2 overexpression restores fatty acid oxidation and insulin action in Drp^KD myocytes.

(A) Immunoblot of Sdhaf2 in control (Scr), Drp1^KD, and Drp1^KD and Sdhaf2^OE myocytes. Densitometric quantification of Sdhaf2 protein normalized to GAPDH (n = 3 biological replications). (B) Fatty acid oxidation analysis of control (Scr), Drp1^KD, and Drp1^KD and Sdhaf2^OE myocytes (n = 4 biological replicates). (C) Immunoblot of phospho-Akt serine-473 and total-Akt in control (Scr), Drp1^KD, and Drp1^KD and Sdhaf2^OE myotubes with and without insulin (n = 3 biological replications). Respiratory control ratio (RCR) of control (Scr) versus Drp1^KD versus Drp1^KD and Sdhaf2^OE myocytes with (D) pyruvate and malate or (E) succinate and rotenone (n = 4 to 5 per genotype). (F) Schematic overview of Drp1-Sdhaf2 interaction promoting mitochondrial translocation to enhance fatty acid oxidation (FAO) and insulin sensitivity in skeletal muscle. All values are presented as means ± SEM; *P < 0.05 determined by unpaired Student’s t test, two-tailed.