Nonalcoholic fatty liver disease and mitochondrial dysfunction

Figure 1 An illustration of mitochondrial fatty acid β-oxidation. LCFA: long-chain fatty acid; TCA: tricarboxylic acid.

Figure 2 Representative electron micrograph of hepatocytes from control wild-type mice (MTPa^+/+) (A) and mice heterozygous for a mitochondrial trifunctional protein defect (MTPa^+/-) (B) at 11 700 × magnification. The MTPa^+/- mice develop hepatic steatosis (see Figure 3). The mitochondria from the MTPa^+/- mice were swollen with hypodense matrix and disrupted cristae. Reproduced with permission from Gastroenterology. 2005; 128: 1381-1390.

Figure 3 Representative liver sections obtained from control wild-type mice (MTPa^+/+) (A and C) and mice with a defect in mitochondrial trifunctional protein (MTPa^+/-) (B and D) littermates stained with hematoxylin-eosin (A and B) and oil red O (C and D) (20 ×). Reproduced with permission from Gastroenterology. 2005; 128: 1381-1390.