Research Paper Volume 12, Issue 19 pp 19677—19700

Increase in fatty acid oxidation and respiratory capacity can compensate for reduced mitochondrial biogenesis in the liver but not skeletal muscle. Oxygen consumption for Leak State (L), OXPHOS capacity (P) and ET-capacity (ET) was measured and the spare respiratory capacity (sc) was calculated (P-ET) in liver NCD or HFD (A) and the skeletal muscle of NCD or HFD (B) fed Ptcd1^+/+ and Ptcd1^+/- mice using an OROBOROS oxygen electrode supplemented with succinate (S pathway control state) as the substrate in the presence of inhibitors and FCCP. FAO controlled pathway oxygen consumption was measured in the liver (C) and skeletal muscle (D) of NCD or HFD Ptcd1^+/+ and Ptcd1^+/- mice using palmitoyl carnitine as the substrate in the presence of inhibitors to measure FAO Leak State (F_L), FAO controlled OXPHOS Capacity (F_P) FAO controlled OXPHOS capacity in the presence of a succinate (FS_P) and FAO ET-capacity in the presence of succinate and FCCP (FS_E). Data are from 5 mice from each genotype run in technical duplicates. Error bars indicated SEM. *P<0.05, Student’s t test.