A malfunction in triglyceride transfer from the intracellular lipid pool to apoB in enterocytes of SOD1-deficient mice

FEBS Lett. 2012 Dec 14;586(24):4289-95. doi: 10.1016/j.febslet.2012.09.047. Epub 2012 Oct 23.

Abstract

We compared lipid metabolism in the intestines of Sod1-knockout mice with that found in wild-type mice to elucidate the impact of oxidative stress in vivo. A high-fat diet in wild-type mice induced postprandial hypertriglyceridemia, but this adaptive response was impaired in Sod1-knockout mice. While fewer triglycerides were secreted to the blood in the form of triglyceride-rich lipoprotein, more lipid droplets accumulated in the enterocytes of Sod1-knockout mice fed a high-fat diet. These data collectively suggest that high-fat diet induces oxidative stress, inhibits lipid secretion to the blood, and ultimately leads to dysfunctional lipid metabolism in enterocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins B / metabolism*
  • Diet, High-Fat / adverse effects
  • Enterocytes / metabolism*
  • Hypertriglyceridemia / metabolism
  • Intestinal Absorption / physiology
  • Lipid Metabolism
  • Lipoproteins / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism*
  • Superoxide Dismutase-1
  • Triglycerides / blood
  • Triglycerides / metabolism*

Substances

  • Apolipoproteins B
  • Lipoproteins
  • Triglycerides
  • lipoprotein triglyceride
  • Sod1 protein, mouse
  • Superoxide Dismutase
  • Superoxide Dismutase-1