Oxidative stress triggers lipid droplet accumulation in primary cultured hepatocytes by activating fatty acid synthesis

Biochem Biophys Res Commun. 2015 Aug 14;464(1):229-35. doi: 10.1016/j.bbrc.2015.06.121. Epub 2015 Jun 23.

Abstract

Despite the impaired intestinal lipid absorption and low level of visceral fat, the Sod1-deficient mouse is susceptible to developing liver steatosis. To gain insights into the mechanism responsible for this abnormal lipid metabolism, we analyzed primary cultured hepatocytes obtained from Sod1-deficient and wild-type mice. Lipid droplets began to accumulate in the cultured hepatocytes and was further increased by a Sod1 deficiency. Levels of enzymes involved in lipogenesis were elevated. It thus appears that lipogenesis is activated by oxidative stress, which is more prominent in the case of Sod1 deficiency, and appears to participate in liver steatosis.

Keywords: Lipogenesis; Liver steatosis; Oxidative stress; Superoxide dismutase.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Fatty Acids / biosynthesis*
  • Fatty Liver / genetics
  • Fatty Liver / metabolism*
  • Fatty Liver / pathology
  • Gene Expression
  • Hepatocytes / metabolism*
  • Hepatocytes / pathology
  • Intestinal Absorption
  • Lipid Droplets / metabolism*
  • Lipid Metabolism / genetics
  • Lipogenesis / genetics
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Oxidative Stress
  • Primary Cell Culture
  • Superoxide Dismutase / deficiency
  • Superoxide Dismutase / genetics*
  • Superoxide Dismutase-1

Substances

  • Fatty Acids
  • Sod1 protein, mouse
  • Superoxide Dismutase
  • Superoxide Dismutase-1