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activation and ROS production
1 Division of Clinical Nutrition, National Institute of Health and Nutrition, 1-23-1, Toyama, Shinjuku-ku, Tokyo 162-8636; and 2 Research Center for Advanced Science and Technology, University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8904, Japan
Fish oil rich in n-3
polyunsaturated fatty acids has been shown to reduce the risk of
cardiovascular diseases partly by reduction of blood triglyceride
concentration. This favorable effect mainly results from the combined
effects of inhibition of lipogenesis by decrease of SREBP-1 and
stimulation of fatty acid oxidation by activation of peroxisome
proliferator-activated receptor-
(PPAR) in liver. However,
because fish oil is easily peroxidized to form hydroperoxides and
increases oxidative stress, some defense mechanism(s) against oxidative
stress might occur. To understand these complex effects of fish oil
diet, the gene expression profile of mice liver was analyzed using
high-density oligonucleotide arrays. High-fat diet (60% of total
energy intake) as either safflower oil or fish oil (tuna) was given to
mice. After 6 mo of feeding, expression levels of a total of 6,521 genes were analyzed. In fish oil diet compared with safflower oil diet,
immune reaction-related genes, antioxidant genes (several glutathione
transferases, uncoupling protein 2, and Mn-superoxide dismutase), and
lipid catabolism-related genes upregulated, whereas cholesterol and
fatty acid synthesis-related genes and 17-alpha hydroxylase/C17-20
lyase and sulfotransferases related to production of endogenous PPAR
ligands and reactive oxygen species (ROS) downregulated markedly.
Because upregulation of these antioxidant genes and downregulation of
sulfotransferases were also observed in mice administered fenofibrate,
altered gene expression related to antioxidant system observed in fish
oil feeding was mediated directly and indirectly by PPAR activation. However, downregulation of 17-alpha hydroxylase/C17-20 lyase was not due to PPAR activation. These data indicate that fish oil feeding downregulated the endogenous PPAR-activation system and increased antioxidant gene expressions to protect against ROS excess.
n-3 fatty acids; fibrate; sulfotransferase; glutathione transferase; dehydroepiandrosterone
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