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Review
. 2008 Jan 14;14(2):193-9.
doi: 10.3748/wjg.14.193.

Nonalcoholic fatty liver disease and mitochondrial dysfunction

Yongzhong Wei  1 , R Scott Rector, John P Thyfault, Jamal A Ibdah
Affiliations
Review

Nonalcoholic fatty liver disease and mitochondrial dysfunction

Yongzhong Wei et al. World J Gastroenterol. .

Abstract

Nonalcoholic fatty liver disease (NAFLD) includes hepatic steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. NAFLD is the most common liver disorder in the United States and worldwide. Due to the rapid rise of the metabolic syndrome, the prevalence of NAFLD has recently dramatically increased and will continue to increase. NAFLD has also the potential to progress to hepatocellular carcinoma (HCC) or liver failure. NAFLD is strongly linked to caloric overconsumption, physical inactivity, insulin resistance and genetic factors. Although significant progress in understanding the pathogenesis of NAFLD has been achieved in years, the primary metabolic abnormalities leading to lipid accumulation within hepatocytes has remained poorly understood. Mitochondria are critical metabolic organelles serving as "cellular power plants". Accumulating evidence indicate that hepatic mitochondrial dysfunction is crucial to the pathogenesis of NAFLD. This review is focused on the significant role of mitochondria in the development of NAFLD.

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Figures

Figure 1
Figure 1
An illustration of mitochondrial fatty acid β-oxidation. LCFA: long-chain fatty acid; TCA: tricarboxylic acid.
Figure 2
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
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.
See this image and copyright information in PMC

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