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Articles in PresS, published online ahead of print October 24, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00376.2001
Submitted on August 24, 2001
Accepted on October 3, 2001
activation and ROS production
1 Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan
2 Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: ezaki{at}nih.go.jp.
Fish oil rich in n-3 polyunsaturated fatty acids has 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 PPAR in liver. However, since 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 month feeding, expression levels of total 6521 genes were analyzed. In fish oil diet compared with safflower oil diet, immune-reaction related genes, anti-oxidant genes (several glutathione transferases, uncoupling protein 2, and Mn-superoxide dismutase), and lipid catabolism-related genes up-regulated, while cholesterol and fatty acids synthesis related genes, and 17-alpha hydroxylase/C17-20 lyase and sulfotransferases related to production of endogenous PPAR ligands and reactive oxygen species (ROS) down-regulated markedly. Since up-regulation of these antioxidant genes and down-regulation of sulfotransferases were also observed in fenofibrate administrated mice, altered gene expression related to anti-oxidant system observed in fish oil feeding was mediated directly and indirectly by PPAR activation. However, down-regulation of 17-alpha hydroxylase/C17-20 lyase was not due to PPAR activation. These data indicate that fish oil feeding down-regulated the endogenous PPAR activation system and increased anti-oxidant gene expressions to protect against ROS excess.
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