NUTRITIONAL EFFECTS ON ESSENTIAL FATTY ACID COMPOSITION

我们的研究表明，酗酒会导致 花生四烯酸等长链多不饱和脂肪酸的水平 (20：4n6)和二十二碳六烯酸(22：6n3)。例如，有一个 选择性降低患者肝脏中22：6n3水平 酒精性肝病后进行移植的。它是 假设这些重要细胞膜的水平降低 成分导致细胞功能的变化，这可能是基础 酒精引起的器官损伤的某些方面以及预防或 恢复这种必需脂肪酸的减少可能是 对酗酒者的治疗益处。这一观点得到了 发现血浆22：6N3与血浆中 早发性脑脊液中5-羟色胺代谢产物5-HIAA 酗酒者。最近的研究主要集中在阐明这种能力。 人类在体内从18-碳中生物合成这些脂肪酸 前体以及对这一途径的调控。一直以来 首次证明人类可以在体内生物合成20：4N6 这种能力是在妊娠33周时发展起来的 在婴儿身上。20：4N6和22：6N3的生物合成能力不同 似乎足以满足神经系统的需求 生命的第一周。在一项相关的研究中，甚至证明了 非常高的18：3N3水平不能支持神经系统的水平 22：6N3在早期营养良好的水坝饲养大鼠幼鼠中的观察 发展。迄今为止进行的最大规模的对照饮食研究 研究表明，长链n-3脂肪酸水平的增加 日粮中的20：5n3和22：6n3会导致较低的氢化n-3积累量 体内的代谢物。这些研究支持这样一种观点，即 22：6n3对神经系统的正常发育和功能是必不可少的 酒精产生不良影响的一个重要机制 是通过这种脂肪酸的拮抗作用。

Our studies have demonstrated that alcohol abuse leads to a decrease in the level of long chain polyunsaturated fatty acids like arachidonate (20:4n6) and docosahexaenoate (22:6n3). For example, there is a selective decrease in the level of 22:6n3 in the livers of patients undergoing transplantation subsequent to alcoholic liver disease. It is hypothesized that the lowered level of these important cell membrane constituents leads to alterations in cellular function that may underlie some aspects of alcohol-induced organ injuries and that prevention or restoration of this decrement in essential fatty acids may be of therapeutic benefit to alcoholics. This view was supported by the finding that plasma 22:6n3 was (inversely) correlated with the level of the serotonin metabolite 5-HIAA in the cerebrospinal fluid of early onset alcoholics. Recent studies have focused upon elucidating the ability of humans to biosynthesize these fatty acids in vivo from their 18-carbon precursors as well as the regulation of this pathway. It has been demonstrated for the first time that humans can biosynthesize 20:4n6 in vivo and that this capability has developed by 33 weeks gestational age in infants. The biosynthetic capacity for 20:4n6 and 22:6n3 do not appear to be adequate to supply nervous system requirements during the first week of life. In a related study, it was demonstrated that even very high levels of 18:3n3 could not support the levels of nervous system 22:6n3 observed in well nourished dam-reared rat pups in early development. The largest controlled dietary studies thus far conducted have shown that increased levels of long chain n-3 fatty acids like 20:5n3 and 22:6n3 in the diet lead to a lower accretion of deuterated n-3 metabolites in vivo. These studies support the view that preformed 22:6n3 is essential for proper nervous system development and function and that an important mechanism by which alcohol exerts adverse effects is through the antagonism of this fatty acid.