NUTRITIONAL EFFECTS ON ESSENTIAL FATTY ACID COMPOSITION

营养对必需脂肪酸组成的影响

• 批准号: 2565453
• 负责人: N SALEM
• 金额: --
• 依托单位: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2565453
• 关键词: alcoholism /alcohol abuse; arachidonate; dietary lipid; essential fatty acids; ethanol; fatty acid biosynthesis; gas chromatography mass spectrometry; human subject; human tissue; infant human (0-1 year); interview; laboratory rat; lipid structure; liver metabolism; long chain fatty acid; nutrient requirement; nutrition related tag; omega 3 fatty acid; physical chemical interaction; unsaturated fatty acids

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 patients undergoing transplantation subsequent to alcoholic liver disease. 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. This view was supported by the finding that plasma 22:6n3 was (inversely) correlated with the level of the serotonin metabolite 5-HIAA in the cerebrospinal fluid of early onset alcoholics. Recent studies have focused upon elucidating the ability of humans to biosynthesize these fatty acids in vivo from their 18-carbon precursors as well as the regulation of this pathway. It has been demonstrated for the first time that humans can biosynthesize 20:4n6 in vivo and that this capability has developed by 33 weeks gestational age in infants. The biosynthetic capacity for 20:4n6 and 22:6n3 do not appear to be adequate to supply nervous system requirements during the first week of life. In a related study, it was demonstrated that even very high levels of 18:3n3 could not support the levels of nervous system 22:6n3 observed in well nourished dam-reared rat pups in early development. 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 deuterated n-3 metabolites in vivo. These studies support the view that preformed 22:6n3 is essential for proper nervous system development and function and that an important mechanism by which alcohol exerts adverse effects is through the antagonism of this fatty acid.

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 选择性降低患者肝脏22：6 N3水平 在酒精性肝病之后接受移植。 是 假设这些重要的细胞膜水平的降低 成分导致细胞功能的改变， 酒精引起的器官损伤的一些方面， 必需脂肪酸减少的恢复可能是 对酗酒者的治疗效果 这一观点得到了 发现血浆22：6 n3与血浆中的 早发性脑脊髓液中5-羟色胺代谢物5-HIAA 酗酒者 最近的研究集中在阐明 人类在体内从其18-碳合成这些脂肪酸 前体以及该途径的调节。 已经 首次证明人类可以在体内生物合成20：4 n6。 这种能力在胎龄33周时就已经形成 在婴儿身上。 20：4n_6和22：6n_3的生物合成能力不强 似乎足以供应神经系统的要求， 生命的第一周 在一项相关的研究中，研究表明，即使 高水平的18：3 n3不能维持神经系统的水平 22：6 n3在早期营养良好的母鼠幼仔中观察到 发展 迄今为止进行的最大规模的控制饮食研究 已经表明，增加长链n-3脂肪酸， 20：5 n3和22：6 n3的加入降低了氘代n-3的吸积 体内代谢物。 这些研究支持了这样一种观点， 22：6 n3是必要的适当的神经系统发育和功能 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。