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酒精中毒和肝硬化患者血清脂质中多不饱和脂肪酸模式异常:肝硬化患者花生四烯酸缺乏。

Abnormal polyunsaturated fatty acid patterns of serum lipids in alcoholism and cirrhosis: arachidonic acid deficiency in cirrhosis.

作者信息

Johnson S B, Gordon E, McClain C, Low G, Holman R T

出版信息

Proc Natl Acad Sci U S A. 1985 Mar;82(6):1815-8. doi: 10.1073/pnas.82.6.1815.

Abstract

Patterns of polyunsaturated fatty acids of serum phospholipids were measured for groups of alcoholics without cirrhosis, alcoholics with cirrhosis, cirrhotics without alcoholism, and a control population. Alcoholics without cirrhosis showed increased polyunsaturated fatty acids derived from linoleic and linolenic acids, but in cirrhotics these products were decreased. Alcoholism accentuated the abnormal polyunsaturated fatty acid pattern of cirrhosis. In alcohol abuse without cirrhosis, the level of 20:3 omega 9 (20 acyl carbon atoms:3 double bonds, omega, 9 carbon atoms beyond last double bond) was significantly increased, despite adequate levels of linoleic and arachidonic acids. Liver involvement appears necessary for development of deficiencies of polyunsaturated fatty acids in serum phospholipids, of which arachidonic acid deficiency is of the largest magnitude.

摘要

对无肝硬化的酗酒者、有肝硬化的酗酒者、无酗酒的肝硬化患者以及对照人群的血清磷脂多不饱和脂肪酸模式进行了测量。无肝硬化的酗酒者血清中源自亚油酸和亚麻酸的多不饱和脂肪酸增加,但肝硬化患者的这些产物减少。酗酒加剧了肝硬化异常的多不饱和脂肪酸模式。在无肝硬化的酒精滥用中,尽管亚油酸和花生四烯酸水平充足,但20:3 ω9(20个酰基碳原子:3个双键,ω,最后一个双键后的第9个碳原子)水平显著升高。肝脏受累似乎是血清磷脂中多不饱和脂肪酸缺乏发展的必要条件,其中花生四烯酸缺乏最为严重。

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