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人类饮食中α-亚麻酸对亚油酸代谢和前列腺素生物合成的影响。

Effect of alpha-linolenic acid in the human diet on linoleic acid metabolism and prostaglandin biosynthesis.

作者信息

Adam O, Wolfram G, Zöllner N

出版信息

J Lipid Res. 1986 Apr;27(4):421-6.

PMID:2873197
Abstract

The effect of dietary alpha-linolenic acid intake on linoleic acid metabolism and prostaglandin (PG) biosynthesis was investigated in two groups of six healthy females (25-32 yr). They were given isocaloric formula diets (FD) containing linoleic acid at a constant intake (4% of calories), with different amounts of alpha-linolenic acid: 0% (FD4/0), 4% (FD4/4), 8% (FD4/8) (group I) and 12% (FD4/12) or 16% (FD4/16) (group II); the diets were given for 2 weeks each. Comparing diet FD4/0 to FD4/16, enrichment of alpha-linolenic acid was greatest in cholesteryl esters (+6.8% in plasma, +7.1% in low density lipoproteins (LDL), +5.9% in high density lipoproteins (HDL)), less in phosphatidylcholine (+2.5% in plasma, +2.9% in LDL, +2.7% in HDL), and least in platelet lipids (+0.7%). The accumulation of alpha-linolenic acid was compensated by a decrease of oleic acid. Eicosapentaenoic acid (EPA), which was excluded from the diet, increased in all plasma lipids with augmented alpha-linolenic acid intake, indicating a chain elongation and desaturation of alpha-linolenic acid to EPA. However, even at the end of FD4/16, EPA was less than 2% of total fatty acids in all plasma lipids. Plasma linoleic acid levels were constant during all dietary regimes, according to the constant dietary intake of this fatty acid. No replacement of linoleic acid by alpha-linolenic acid could be observed. The percentage of arachidonic acid in all lipids was unaffected by alpha-linolenic acid intake. As arachidonic acid was not provided by the diet, it can be concluded that alpha-linolenic acid does not inhibit chain elongation and desaturation of linoleic acid to arachidonic acid in man.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在两组各六名健康女性(25 - 32岁)中,研究了膳食α-亚麻酸摄入量对亚油酸代谢和前列腺素(PG)生物合成的影响。她们食用等热量配方饮食(FD),亚油酸摄入量恒定(占热量的4%),α-亚麻酸含量不同:0%(FD4/0)、4%(FD4/4)、8%(FD4/8)(第一组)和12%(FD4/12)或16%(FD4/16)(第二组);每种饮食持续给予2周。将饮食FD4/0与FD4/16比较,α-亚麻酸在胆固醇酯中的富集程度最高(血浆中增加6.8%,低密度脂蛋白(LDL)中增加7.1%,高密度脂蛋白(HDL)中增加5.9%),在磷脂酰胆碱中较少(血浆中增加2.5%,LDL中增加2.9%,HDL中增加2.7%),在血小板脂质中最少(增加0.7%)。α-亚麻酸的积累通过油酸的减少得到补偿。饮食中未含有的二十碳五烯酸(EPA),随着α-亚麻酸摄入量增加,在所有血浆脂质中均增加,表明α-亚麻酸发生链延长和去饱和转化为EPA。然而,即使在FD4/16结束时,EPA在所有血浆脂质中仍不到总脂肪酸的2%。根据该脂肪酸恒定的膳食摄入量,在所有饮食方案期间血浆亚油酸水平保持恒定。未观察到α-亚麻酸替代亚油酸的情况。α-亚麻酸摄入量不影响所有脂质中花生四烯酸的百分比。由于饮食中未提供花生四烯酸,可以得出结论,α-亚麻酸在人体中不抑制亚油酸向花生四烯酸的链延长和去饱和。(摘要截短于250字)

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