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Am J Physiol Endocrinol Metab 282: E395-E401, 2002. First published October 23, 2001; doi:10.1152/ajpendo.00414.2001
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Vol. 282, Issue 2, E395-E401, February 2002

Contrasting effects of fish oil and safflower oil on hepatic peroxisomal and tissue lipid content

Susanne Neschen1, Irene Moore2, Werner Regittnig2, Chun Li Yu1, Yanlin Wang1, Marc Pypaert3, Kitt Falk Petersen2, and Gerald I. Shulman1,2

1 Howard Hughes Medical Institute and the Departments of 2 Internal Medicine, Cellular and Molecular Physiology, and 3 Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06520-8020

To examine the mechanism by which fish oil protects against fat-induced insulin resistance, we studied the effects of control, fish oil, and safflower oil diets on peroxisomal content, fatty acyl-CoA, diacylglycerol, and ceramide content in rat liver and muscle. We found that, in contrast to control and safflower oil-fed rats, fish oil feeding induced a 150% increase in the abundance of peroxisomal acyl-CoA oxidase and 3-ketoacyl-CoA thiolase in liver but lacked similar effects in muscle. This was paralleled by an almost twofold increase in hepatic peroxisome content (both P < 0.002 vs. control and safflower). These changes in the fish oil-fed rats were associated with a more than twofold lower hepatic triglyceride/diacylglycerol, as well as intramuscular triglyceride/fatty acyl-CoA, content. In conclusion, these data strongly support the hypothesis that n-3 fatty acids protect against fat-induced insulin resistance by serving as peroxisome proliferator-activated receptor-alpha ligands and thereby induce hepatic, but not intramuscular, peroxisome proliferation. In turn, an increased hepatic beta -oxidative capacity results in lower hepatic triglyceride/diacylglycerol and intramyocellular triglyceride/fatty acyl-CoA content.

peroxisome proliferator-activating receptor-alpha ; beta -oxidation; diacylglycerol; acyl-CoA oxidase; 3-ketoacyl-CoA thiolase


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