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Journal of Lipid Research, Vol 38, 1851-1858, Copyright © 1997 by Lipid Research, Inc.
L Froyland, L Madsen, H Vaagenes, GK Totland, J Auwerx, H Kryvi, B Staels and RK Berge
Fish oil polyunsaturated fatty acids and fibrate hypolipidemic drugs are
potent hypotriglyceridemic agents that act by increasing fatty acid
catabolism and decreasing triglyceride synthesis and secretion by the
liver. A major unresolved issue is whether this hypotriglyceridemic effect
can occur independent of induction of peroxisomal beta- oxidation, a
predisposing factor for hepatocarcinogenesis. The present study was
undertaken to determine which component of fish oil, eicosapentaenoic acid
(EPA) or docosahexaenoic acid (DHA), is responsible for its
triglyceride-lowering effect. We demonstrate that EPA and not DHA is the
hypotriglyceridemic component of fish oil and that mitochondria and not
peroxisomes are the principal target. Results obtained by fenofibrate
feeding support the hypothesis that the mitochondrion is the primary site
for the hypotriglyceridemic effect. In contrast to fibrates, EPA did not
affect hepatic apolipoprotein C- III gene expression. Therefore, increased
mitochondrial beta-oxidation with a concomitant decrease in triglyceride
synthesis and secretion seems to be the primary mechanism underlying the
hypotriglyceridemic effect of EPA and fibrates in rats, rabbits and
possibly also in humans. In addition, these data show that lowering of
plasma triglycerides can occur independently of any deleterious peroxisome
proliferation.
ARTICLES
Mitochondrion is the principal target for nutritional and pharmacological control of triglyceride metabolism
Department of Clinical Biology, University of Bergen, Haukeland Hospital, Norway.
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