NUTRITIONAL EFFECTS ON ESSENTIAL FATTY ACID COMPOSITION

我们的假设是酗酒会导致 多不饱和脂质从许多组织，并导致改变代谢 类花生酸 肝脏和其他器官的这种变化， 组织可能引起或促成与这些疾病相关的病理变化 酗酒 之前，我们已经证明， 酒精暴露大鼠花生四烯酸（20：4 n6）等n-6脂肪酸 组织和酗酒者的血细胞中。 的分布 酒精引起的多不饱和脂肪酸（PUFA）和 膳食中特定脂肪酸的升高的预防作用 在大鼠肝脏脂质中进行了详细研究。 总脂质的变化 提取物可归因于磷脂的改变， 胆固醇酯类，但由于 在甘油三酯或非酯化脂肪酸池中吸入乙醇。 在乙醇吸入期间，动物喂食富含18：3 n6的琉璃苣油 （7 d）在20：4 n6中的损失没有18：1 n9或长时间喂养的损失大 链n-3脂肪酸为基础的饮食。 同样，n-3脂肪酸的损失 酒精暴露后，在喂食鲱鱼的动物中， 油基饮食。 补充脂肪酸的这些“保护”作用 也主要追溯到磷脂和胆固醇酯库。 每天一次喂食酒精12周的猫显示出长时间的渐进性LSO 链多不饱和化合物，包括20：4 n6和22：6 n3， 血浆中18：2n 6和非必需脂肪酸增加。 肝 活组织检查显示9天后几乎所有的多不饱和化合物都丢失了 酒精暴露。 这项研究表明，猫的饮食， 仅能提供足够的脂肪酸， 酒精可能为研究大脑和肝脏提供了一个很好的模型 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.