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)。它被假设为 这些重要细胞膜成分水平的降低导致 细胞功能的改变可能是某些方面的基础 酒精所致器官损伤及其预防或恢复 必需脂肪酸的减少可能对治疗有益 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 为了更好地了解前驱体的能力 例如，在肝脏中，人类可以补偿他们的损失。它有 首次证明人类可以生物合成20：4n6 在体内，这种能力至少在33周前形成 婴儿的胎龄。因此，最大的对照饮食研究 目前进行的研究表明，长链n-3脂肪水平的增加 饮食中的20：5n3和22：6n3等酸导致n-3的摄入量较低 体内的代谢物。在培育大鼠方面也取得了进展 人工饲养的极端神经细胞22：6N3缺乏症模型 在那里，饮食可以在几乎整个生命周期中得到控制。 行为研究表明，社交学习任务的表现较差 在大脑水平较低的大鼠中，22：6n3。

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). 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. Recent studies have focused upon elucidating the ability of humans to biosynthesize these fatty acids in vivo from their 18-carbon precursors in order to gain a better understanding of the ability of humans to compensate for their losses, for example, in the liver. It has been demonstrated for the first time that humans can biosynthesize 20:4n6 in vivo and that this capability is developed at least by 33 weeks gestational age in infants. 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 n-3 metabolites in vivo. Progress has also been made in developing a rat model of extreme neural 22:6n3 deficiency using the artificial rearing where the diet may be controlled throughout nearly the entire life cycle. Behavioral studies indicate poorer performance on social learning tasks in rats with lower levels of brain 22:6n3.