Ide T
Laboratory of Nutrition Biochemistry, National Food Research Institute, Ministry of Agriculture, Forestry and Fisheries, Tsukuba, Japan.
Biofactors. 2000;13(1-4):9-14. doi: 10.1002/biof.5520130103.
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 delta3, delta2-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.
将富含α-亚麻酸（α-18:3）的亚麻籽和紫苏油喂养的大鼠肝脏脂肪酸氧化酶活性，与富含亚油酸（18:2）的红花油和饱和脂肪（椰子油或棕榈油）喂养的动物进行比较。肝脏匀浆中线粒体和过氧化物酶体棕榈酰辅酶A（16:0-CoA）氧化率，在喂食亚麻籽和紫苏油的大鼠中显著高于喂食饱和脂肪和红花油的大鼠。脂肪酸氧化率随膳食中α-18:3水平的增加而增加。膳食中的α-18:3还增加了除3-羟酰基辅酶A脱氢酶外的脂肪酸氧化酶活性。出乎意料的是，膳食中的α-18:3导致用短链和中链底物测量的3-羟酰基辅酶A脱氢酶活性大幅降低，但用长链底物测量时则没有。膳食中的α-18:3显著增加了肝脏脂肪酸氧化酶的mRNA水平，包括肉碱棕榈酰转移酶I和II、线粒体三功能蛋白、酰基辅酶A氧化酶、过氧化物酶体双功能蛋白、线粒体和过氧化物酶体3-酮酰基辅酶A硫解酶、2,4-二烯酰基辅酶A还原酶和δ3,δ2-烯酰基辅酶A异构酶。富含极长链n-3脂肪酸的鱼油对肝脏脂肪酸氧化也有类似影响。关于β-氧化途径的底物特异性，无论测定混合物中的底物/白蛋白比例或膳食脂肪来源如何，相对于16:0-和18:2-CoAs，α-18:3-CoA的线粒体和过氧化物酶体β-氧化率都更高。肉碱棕榈酰转移酶I的底物特异性似乎是这些酰基辅酶A底物线粒体氧化率差异的原因。相对于红花油，富含α-18:3-CoA的膳食脂肪不会影响脂肪酸合酶和葡萄糖6-磷酸脱氢酶的肝脏活性。研究表明，底物特异性和β-氧化途径中酶活性的改变在调节喂食α-18:3的大鼠血清脂质浓度中起重要作用。
