NUTRITIONAL EFFECTS ON ESSENTIAL FATTY ACID COMPOSITION

我们的假设是酗酒会导致 从许多组织中提取的多不饱和脂肪。肝脏和肝脏的这种变化 大脑以及其他器官和组织可能引起或促成 与酒精中毒有关的病理变化。此前，我们有 表明花生四烯酸(20：4n6)和其他n-6有损失 酒精染毒大鼠组织和血细胞中的脂肪酸 酗酒者。动物在酒精注射过程中喂食富含18：3n6的罗非鱼油 吸入期(7d)，20：4n6无明显损失 喂食18：1n9或长链n-3脂肪酸的饮食，这些损失是 主要追溯到磷脂和胆固醇酯池。同样， 酒精暴露后n-3脂肪酸的损失没有那么大。 在饲喂以男人为基础的油性饮食的动物身上。酒精中毒的啮齿动物模型 通过使用每天12小时的吸入剂而不是 持续暴露，更长的暴露持续时间和控制 饮食，特别是低必需脂肪配方。人文科学 已经表明，我们物种有能力形成完整的 必需脂肪酸代谢和饮食中的多不饱和脂肪酸 调节这一途径的活性。

It is our hypothesis that alcohol abuse leads to the depletion of polyunsaturated lipids from many tissues. Such changes in the liver and brain 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. 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 as those fed 18:1n9 or long chain n-3 fatty acid-based diets and these losses were traced mainly to the phospholipid and cholesterol ester pools. Similarly, losses in n-3 fatty acids subsequent to alcohol exposure were not as great in animals fed a menhaden oil-based diet. The rodent model of alcoholism has been improved with the use of 12 hr per day of inhalation rather than continuous exposure, a longer duration of exposure and the control of the diets, particularly with low essential fat formulation. Human studies have shown that our species are capable of a complete spectrum of essential fatty acid metabolism and that polyunsaturates in the diet regulate the activity of this pathway.