Luthria D L, Sprecher H
Department of Medical Biochemistry, Ohio State University, Columbus 43210, USA.
J Lipid Res. 1995 Sep;36(9):1897-904.
Male weanling rats were fed a diet that contained 2.1% ethyl oleate, 1% ethyl linoleate, and 0.2% ethyl linolenate. After 4 weeks all the linoleate was replaced by the deuterium-labeled analog and the animals were killed 4 days later. The molar fraction of total 20:4(n-6) in liver, heart, and kidney phospholipids containing deuterium was 33.9, 8.9, and 13.3%, respectively. Second, animals were preconditioned by incorporating either 0.2% of 18:3(n-6), 20:3(n-6), or 20:4(n-6) into the above diet and again after 4 weeks all the linoleate was replaced with the labeled analog. Now the molar fraction of labeled 20:4(n-6) in liver phospholipids from these three groups of animals was reduced from 33.9 to 27.1, 23.9, and 24.1% respectively. In contrast, there was little change in the specific activity of 20:4(n-6) in heart and kidney phospholipids. The third protocol was a direct crossover study in that again unlabeled linoleate was fed during the entire period. Four days prior to killing the unlabeled 18:3(n-6), 20:3(n-6), and 20:4(n-6) were replaced with the deuterium-labeled analogs. The mole % of total esterified 20:4(n-6) in liver phospholipids was now 24.6, 32.0, and 26.2%, respectively. Even though 18:3(n-6), 20:3(n-6), and 20:4(n-6) were all fed at only 20% of the level of 18:2(n-6), it can be calculated that the molar fraction of esterified 20:4(n-6) in liver phospholipids was between 65 to 77% of that found when 18:2(n-6) was the only dietary (n-6) acid as under these conditions 33.9 mol % of the 20:4(n-6) was labeled. Interestingly, when deuterium-labeled 18:3(n-6), 20:3(n-6), or 20:4(n-6) was fed, the specific activity of esterified 20:4(n-6) in kidney and heart phospholipids was always equal to or greater than what was derived from deuterium-labeled 18:2(n-6). The results show that under steady-state dietary conditions, (n-6) dietary fatty acids are processed in different ways by liver, heart, and kidney.
给雄性断奶大鼠喂食一种含有2.1%油酸乙酯、1%亚油酸乙酯和0.2%亚麻酸乙酯的饮食。4周后,所有亚油酸酯被氘标记的类似物取代,4天后处死动物。肝脏、心脏和肾脏磷脂中含氘的总20:4(n-6)的摩尔分数分别为33.9%、8.9%和13.3%。其次,通过在上述饮食中加入0.2%的18:3(n-6)、20:3(n-6)或20:4(n-6)对动物进行预处理,4周后同样将所有亚油酸酯替换为标记的类似物。现在,这三组动物肝脏磷脂中标记的20:4(n-6)的摩尔分数分别从33.9%降至27.1%、23.9%和24.1%。相比之下,心脏和肾脏磷脂中20:4(n-6)的比活性变化不大。第三个方案是直接交叉研究,即在整个期间再次喂食未标记的亚油酸酯。在处死前4天,将未标记的18:3(n-6)、20:3(n-6)和20:4(n-6)替换为氘标记的类似物。肝脏磷脂中总酯化20:4(n-6)的摩尔百分比现在分别为24.6%、32.0%和26.2%。尽管18:3(n-6)、20:3(n-6)和20:4(n-6)的喂食量仅为18:2(n-6)水平的20%,但可以计算出,肝脏磷脂中酯化20:4(n-6)的摩尔分数是当18:2(n-6)是唯一膳食(n-6)酸时所发现值的65%至77%,因为在这些条件下,20:4(n-6)的33.9摩尔%被标记。有趣的是,当喂食氘标记的18:3(n-6)、20:3(n-6)或20:4(n-6)时,肾脏和心脏磷脂中酯化20:4(n-6)的比活性总是等于或大于来自氘标记的18:2(n-6)的比活性。结果表明,在稳态饮食条件下,肝脏、心脏和肾脏对膳食(n-6)脂肪酸的处理方式不同。