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A malfunction in triglyceride transfer from the intracellular lipid pool to apoB in enterocytes of SOD1‐deficient mice
Author(s) -
Kurahashi Toshihiro,
Konno Tasuku,
Otsuki Noriyuki,
Kwon Myoungsu,
Tsunoda Satoshi,
Ito Junitsu,
Fujii Junichi
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.09.047
Subject(s) - endocrinology , medicine , lipid metabolism , oxidative stress , knockout mouse , triglyceride , sod1 , apolipoprotein b , hypertriglyceridemia , chemistry , lipoprotein , postprandial , secretion , lipid droplet , biology , biochemistry , cholesterol , superoxide dismutase , gene , insulin
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.