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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: Cell Metab. 2010 Aug 4;12(2):154–165. doi: 10.1016/j.cmet.2010.07.003

Figure 7. Enhanced mitochondrial complex I activity, fatty acid oxidation, and trifunctional protein (TFP) expression in liver of ALCAT1−/− mice.

Figure 7

A, mitochondrial complex I activity and B, citrate synthase activity were analyzed in C2C12 cells as used in Figure 1. C, mitochondrial complex I activity and D, citrate synthase activity were analyzed in isolated liver mitochondria from ALCAT1−/− (−/−) and wild type control (+/+) mice. E, palmitoylcarnitine oxidation rate was analyzed from C2C12 cells used in Figure 1, and F, from isolated mitochondria from the liver of the ALCAT1−/− mice (−/−) and the wild type controls (+/+) mice. G, lipid peroxidation levels, as indicated by the level of malonaldehyde (MDA), were analyzed in tissue lysate from liver, skeletal muscle, and fat of the ALCAT1−/− mice and the controls by a TBARS kit, N=4. D, western blot analysis of TFP from C2C12 cells used in Figure 1, or D, from liver lysates of wild type (WT) and the ALCAT1−/− (KO) mice on high fat diet (HFD), using anti-β-actin antibodies (internal control). J, a schematic diagram depicts a causative role of ALCAT1 in mitochondrial dysfunction and insulin resistance. N=6–8. *P < 0.05, ** P < 0.01.