Figure 4.

Mitochondrial Respiratory Dysfunction Is Not Required for the Development of Obesity. (A–C) Mitochondrial respiration was not reduced in mitochondria isolated from the heart, liver, or skeletal muscle of obese animals. (D, E) With the exception of a reduction in OXPHOS within the liver, mitochondrial content was not altered in obese mice. (F) Respiration in permeabilized eWAT was not influenced by obesity. (G, H) Mitochondrial lipid-supported ROS emission rates and 4HNE protein content were increased in eWAT of obese mice, indicating oxidative stress. (I, J) In permeabilized muscle fibers, maximal respiration and ADP sensitivity were not affected by obesity. Data expressed as mean ± SEM of results obtained from n = 5–10 per genotype. *P < .05 versus lean (unpaired two-tailed Student’s t-test). DNP, dinitrophenol; JH₂O₂, rate of hydrogen peroxide production; JO₂, rate of oxygen utilization; Km, Michaelis–Menten constant; L, lean mice; L-Carn, L-carnitine; M, malate; M-CoA, malonyl-CoA; Ob, obese mice; P, pyruvate; P/O, the content of ADP utilized relative to oxygen; S, succinate; Vmax, maximal respiration rate.