NUTRITIONAL EFFECTS ON ESSENTIAL FATTY ACID COMPOSITION

我们的研究表明，酗酒会导致 长链多不饱和脂肪酸如花生四烯酸 (20：4 n6）和二十二碳六烯酸酯（22：6 n3）。 比如有一 恒河猴肝脏中22：6 N3水平的选择性降低 自由饮用酒精， 三年后出现肝纤维化。 也有损失 二十二碳六烯酸（DHA）在猫和恒河猴的大脑中， 慢性酒精暴露 据推测，低水平的 这些重要的细胞膜成分会导致 细胞功能，可能是酒精诱导的器官的某些方面的基础 伤害和预防或恢复这种减少， 必需脂肪酸可能对酗酒者有治疗益处。 在了解酒精的潜在作用方面已经取得了进展 对必需脂肪酸代谢的影响 在对猫和恒河猴的研究中 长期接触酒精的猴子， 脂质过氧化的标志物。 然而，浓缩的增加 长链多不饱和化合物，特别是DHA， 18碳脂肪酸前体表明，必需脂肪酸 体内酸的形成和积累增加。 这一论点是 与通常认为的酒精抑制去饱和酶的观点相反， 内切酶 这些论点在一项人类研究中得到了证实， 证明了酗酒者会积累更多的氘 从d5-亚麻酸标记的DHA。 这些研究支持这样一种观点， 预先形成的22：6 n3对适当的大脑和肝脏功能至关重要， 酒精产生副作用的一个重要机制是 通过这种脂肪酸的拮抗作用。

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). For example, there is a selective decrease in the level of 22:6n3 in the livers of rhesus monkeys given alcohol on an ad libitum basis that was associated with the development of liver fibrosis after three years. There is also a loss of docosahexaenoate (DHA) in the brains of cats and rhesus monkeys after chronic alcohol exposure. 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. Progress has been made in understanding the underlying actions of alcohol on essential fatty acid metabolism. In studies of cats and rhesus monkeys exposed to chronic alcohol, there was a large in increase in markers of lipid peroxidation. However, an increase in the enrichment of long chain polyunsaturates, especially DHA, with deuterium supplied by the 18-carbon fatty acid precursors indicated that essential fatty acid formation and accretion in vivo was increased. This contention is opposite to the commonly held notion that alcohol inhibits desaturase enzymes. These contentions were confirmed in a human study in which it was demonstrated that alcoholics accumulate greater amounts of deuterium- labeled DHA from d5-linolenic acid. These studies support the view that preformed 22:6n3 is essential for proper brain and liver function and that an important mechanism by which alcohol exerts adverse effects is through the antagonism of this fatty acid.