NUTRITIONAL EFFECTS ON ESSENTIAL FATTY ACID COMPOSITION

我们的假设是酗酒会导致 来自许多组织的多不饱和脂类，并导致代谢改变 二十烷类化合物。肝脏以及其他器官的这种变化 组织可能参与与以下相关的病理变化 酗酒。花生四烯酸(20：4n6)和其他n-6脂肪酸的损失 在我们对酒精暴露大鼠组织的研究中观察到 在酗酒者的血细胞中。这就引出了这样一个问题： 通过饮食替代这些必需的脂肪酸是可能的。 操纵。动物研究表明，供应n-6 前体、18：3N6在饮食中可部分预防酒精诱导的 与18：1n9或长链高饮食相比，肝脏损失20：4n6 N-3脂肪酸。一项酒精戒断过程中的临床研究 表明多不饱和物的组成在络合物中发生了变化 血细胞中的时尚。血小板表现出20：4n6的损失。 酗酒者中几种非必需磷脂种类的增加 在入院时。这些变化大部分在4周后恢复正常 戒烟。在红细胞中，18：2n6的损失和增加 在非必需物种中18：0和18：1n9。没有一个物种 在戒酒开始时不正常，在戒酒后 红细胞减少4周。在PE中花生四烯基物种增加，而 PS降低。磷脂普遍增加。 酒精中毒患者红细胞膜分子种类的不对称性。

It is our hypothesis that alcohol abuse leads to the depletion of polyunsaturated lipids from many tissues and leads to altered metabolism of eicosanoids. Such changes in the liver as well as in other organs and tissues may contribute to the pathological changes associated with alcoholism. Losses in arachidonic acid (20:4n6) and other n-6 fatty acids have been observed in our studies of alcohol exposed rat tissues as well as in the blood cells of alcoholics. This led to the question as to whether it was possible to replace these essential fatty acids by dietary manipulation. Animal studies have indicated that supplying the n-6 precursor, 18:3n6 in the diet can partially prevent the alcohol-induced loss of liver 20:4n6 when compared to diets high in 18:1n9 or long chain n-3 fatty acids. A clinical study of alcoholics during withdrawal has indicated that the composition of polyunsaturates is altered in a complex fashion in blood cells. Platelets exhibited a loss of a 20:4n6 species with increases in several non-essential phospholipid species in alcoholics at admittance. Most of these changes normalized after 4 weeks of withdrawal. In the erythrocyte, there was a loss of 18:2n6 and an increase in the non-essential species 18:0 and 18:1n9. None of the species that were abnormal at the beginning of alcohol withdrawal had normalized in the erythrocyte by 4 weeks. Arachidonyl species increased in PE while decreasing in PS. There was a generalized increase in phospholipid molecular species asymmetry in the erythrocyte membrane in alcoholics.