Nonalcoholic Fatty Liver Disease: Pathogenesis and Therapeutics from a Mitochondria-Centric Perspective

Vitamin E therapy is only recommended in nondiabetic Nonalcoholic fatty liver disease patients with biopsy proven nonalcoholic steatohepatitis

Aaron M. Gusdon; Ke-xiu Song; Shen Qu


Scholarcy highlights

  • Nonalcoholic fatty liver disease is a broad term used to encompass a range of disorders ranging in severity from excess triglyceride accumulation in the liver to hepatic steatosis and eventually fibrosis, cirrhosis, and hepatocellular carcinoma
  • While many of the molecular mechanisms involved in the pathogenesis of NAFLD are still being worked out, mitochondria lie at the core of NAFLD
  • This increase in mitochondrial reactive oxygen species production likely plays an important role in the development of insulin resistance and leads to the function decline in activity of the electron transport chain seen in the later stages of NALD
  • Mitochondrial functional decline leads to a mismatch between fatty acid beta-oxidation and oxidative phosphorylation leading to the accumulation of partially oxidized intermediates which further exacerbate insulin resistance and leads to the progression of NAFLD
  • While several compounds have been tested which are known to upregulate beta-oxidation, without concomitant improvement in the mitochondrial ETC, this approach may further exacerbate insulin resistance and NAFLD
  • Future treatments will likely need to be developed with greater specificity and their efficacy may vary based on the stage in the pathogenesis of NAFLD

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