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肪，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 组织可能导致或促成相关的病理改变 酗酒。此前，我们已经表明，在 酒精暴露大鼠花生四烯酸(20：4n6)等n-6脂肪酸的变化 组织以及酗酒者的血细胞中也是如此。分布情况： 酒精引起的多不饱和脂肪酸(PUFA)和 饮食中特定脂肪酸含量的升高具有预防作用 已经在大鼠肝脂中进行了详细的研究。总脂的变化 萃取物可以归因于磷脂和 胆固醇酯类，但变化不大 甘油三酯或非酯化脂肪酸池中的乙醇吸入。 动物在酒精吸入期间喂食富含18：3n6的萝卜油 (7d)20：4n6的损失没有18：1n9或更长的损失大 链n-3脂肪酸为主的饮食。同样，n-3脂肪酸的损失 在喂食男人的动物中，酒精暴露后的影响不是很大 以油为基础的饮食。补充脂肪酸的这些“保护性”作用 也主要追溯到磷脂和胆固醇酯池。 连续12周每天饮酒一次的猫表现出进行性的LSO长 含20：4N6和22：6N3的链状多不饱和物 血浆中18：2N6和非必需脂肪酸的增加。肝 活组织检查显示，9天后几乎所有的多不饱和物都丢失了。 暴露在酒精中。这项研究表明，猫的饮食习惯是 只能勉强提供足够的脂肪酸，并暴露在慢性 酒精可能为大脑和肝脏的研究提供一个极好的模型 与人类酒精中毒有关的病理学。

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 cause or contribute to the pathological changes associated with alcoholism. Previously, we have shown that there are losses in arachidonic acid (20:4n6) and other n-6 fatty acids in alcohol exposed rat tissues as well as in the blood cells of alcoholics. The distribution of both the alcohol-induced losses in polyunsaturated fatty acids (PUFA) and the preventive effects of dietary elevations in specific fatty acids have been studied in detail in rat liver lipids. Changes in the total lipid extracts can be ascribed to alterations in the phospholipid and cholesterol ester classes but there was little change as a result of ethanol inhalation in the triglyceride or nonesterified fatty acid pools. Animals fed borage oil rich in 18:3n6 during the ethanol inhalation period (7 d) did not have as great a loss in 20:4n6 than those fed 18:1n9 or long chain n-3 fatty acid based diets. Similarly, losses in n-3 fatty acids subsequent to alcohol exposure were not as great in animals fed a menhaden oil based diet. These "protective" effects of fatty acid supplementation were also traced mainly to the phospholipid and cholesterol ester pools. cats fed alcohol once daily for 12 weeks showed a progressive lsos of long chain polyunsaturates including 20:4n6 and 22:6n3 with a concomitant increase in 18:2n6 and non-essential fatty acids in plasma. Liver biopsies showed a loss in nearly all of the polyunsaturates after 9 days of alcohol exposure. This study indicated that cats placed on a diet that is only just adequate in supplying fatty acids and exposed to chronic alcohol may provide an excellent model for the study of brain and liver pathology related to human alcoholism.