Affiliations: Laboratory of Nutrition Biochemistry, National Food
Research Institute, Ministry of Agriculture, Forestry and Fisheries, Tsukuba
305-8642, Japan
Note: [] Laboratory of Nutrition Biochemistry, National Food Research
Institute, Ministry of Agriculture, Forestry and Fisheries, 2-1-2 Kannondai,
Tsukuba Science City 305-8642, Japan. Tel.: +81 298 38 8083; Fax: +81 298 38
7996; E-mail: idetaka@nfri.affrc.go.jp
Abstract: The activities of hepatic fatty acid oxidation enzymes in rats fed
linseed and perilla oils rich in \alpha-linolenic acid
(\alpha-18:3) were compared with those in the animals fed
safflower oil rich in linoleic acid (18:2) and saturated fats (coconut or palm
oil). Mitochondrial and peroxisomal palmitoyl-CoA (16:0-CoA) oxidation rates in
the liver homogenates were significantly higher in rats fed linseed and perilla
oils than in those fed saturated fats and safflower oil. The fatty oxidation
rates increased as dietary levels of \alpha-18:3 increased.
Dietary \alpha-18:3 also increased the activity of fatty
acid oxidation enzymes except for 3-hydroxyacyl-CoA dehydrogenase.
Unexpectedly, dietary \alpha-18:3 caused great reduction in
the activity of 3-hydroxyacyl-CoA dehydrogenase measured with short- and
medium-chain substrates but not with long-chain substrate. Dietary
\alpha-18:3 significantly increased the mRNA levels of
hepatic fatty acid oxidation enzymes including carnitine palmitoyltransferase I
and II, mitochondrial trifunctional protein, acyl-CoA oxidase, peroxisomal
bifunctional protein, mitochondrial and peroxisomal 3-ketoacyl-CoA thiolases,
2, 4-dienoyl-CoA reductase and \Delta ^3, \Delta
^2-enoyl-CoA isomerase. Fish oil rich in very long-chain
n-3 fatty acids caused similar changes in hepatic fatty acid
oxidation. Regarding the substrate specificity of
\beta-oxidation pathway, mitochondrial and peroxisomal
\beta-oxidation rate of \alpha-18:3-CoA,
relative to 16:0- and 18:2-CoAs, was higher irrespective of the
substrate/albumin ratios in the assay mixture or dietary fat sources. The
substrate specificity of carnitine palmitoyltransferase I appeared to be
responsible for the differential mitochondrial oxidation rates of these
acyl-CoA substrates. Dietary fats rich in \alpha-18:3-CoA
relative to safflower oil did not affect the hepatic activity of fatty acid
synthase and glucose 6-phosphate dehydrogenase. It was suggested that both
substrate specificities and alterations in the activities of the enzymes in
\beta-oxidation pathway play a significant role in the
regulation of the serum lipid concentrations in rats fed
\alpha-18:3.
