THE EFFECT OF FEEDING FISH OILS, VEGETABLE-OILS AND CLOFIBRATE ON THE KETOGENESIS FROM LONG-CHAIN FATTY-ACIDS IN HEPATOCYTES
THE EFFECT OF FEEDING FISH OILS, VEGETABLE-OILS AND CLOFIBRATE ON THE KETOGENESIS FROM LONG-CHAIN FATTY-ACIDS IN HEPATOCYTES
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DOI：
10.1007/bf02535638
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发表时间：
1986-08-01
期刊：
影响因子：
1.9
通讯作者：
BREMER, J
中科院分区：
文献类型：
--
作者：
BERGSETH, S;CHRISTIANSEN, EN;BREMER, J
各组大鼠分别饲喂含25%鱼油（FO）、25%豆油、25%部分氢化鱼油（PHFO）、25%部分氢化豆油（PHSO）、25%部分氢化椰子油或0.3%氯贝特的饲料3 wk。动物禁食24小时后，分离肝细胞，并测量添加的棕榈酸酯、顺式和反式亚油酸酯、花生四烯酸酯和二十二碳六烯酸酯的生酮作用。仅在PHFO和PHSO喂养大鼠的细胞中，油喂养后的生酮作用受到显著刺激（2 - 3倍）。以长链不饱和脂肪酸为底物时，刺激作用最明显。这些脂肪酸是对照肝细胞中相对较差的酮体前体。必需脂肪酸缺乏似乎不是这种刺激的原因。氯贝特还显著刺激生酮（1.5- 3倍）。刺激的程度随着链长和底物的不饱和度而增加。还在相同组中研究了酶2，4-二烯酰-CoA还原酶的活性。其活性在氯贝酯处理的大鼠中被刺激约四倍，并且在较小程度上被PHFO、PHSO和FO饮食刺激。该活性与饲料中不饱和脂肪酸的含量或其在离体肝细胞中的氧化程度无关。因此，2，4-二烯酰辅酶A还原酶似乎不是膳食多不饱和脂肪酸代谢的调节酶。可以得出结论，过氧化物酶体β-氧化系统最有可能参与报道的来自极长链多不饱和脂肪酸的酮生成增加。
Groups of rats were fed diets containing 25% fish oil (FO), 25% soybean oil, 25% partially hydrogenated fish oil (PHFO), 25% partially hydrogenated soybean oil (PHSO), 25% partially hydrogenated coconut oil or 0.3% clofibrate for 3 wk. After the animals were fasted for 24 hr, hepatocytes were isolated and ketogenesis from added palmitate, linoleate cis and trans, arachidonate and docosahexaenoate was measured. Ketogenesis after oil feeding was significantly stimulated (two- to threefold) only in cells from the PHFO- and PHSO-fed rats. The stimulation was most apparent with the long chain unsaturated fatty acids as substrates. These fatty acids were relatively poor ketone body precursors in control hepatocytes. Essential fatty acid deficiency did not seem to be the reason for this stimulation. Clofibrate also stimulated ketogenesis significantly (1.5- to 3-fold). The degree of stimulation increased with chain length and degree of unsaturation of the substrate. The activity of the enzyme 2,4-dienoyl-CoA reductase was also studied in the same groups. Its activity was stimulated about fourfold in the clofibrate-treated rats and to a lesser extent by the PHFO, PHSO and FO diets. The activity showed no correlation with the content of unsaturated fatty acids in the diet or their oxidation in isolated hepatocytes. The 2,4-dienoyl-CoA reductase, therefore, does not seem to be a regulatory enzyme in the metabolism of dietary polyunsaturated fatty acids. It is concluded that an induction of the peroxisomal .beta.-oxidation system most likely is involved in the reported increases in ketogenesis from very long chain polyunsaturated fatty acids.