Koletzko B, Decsi T, Demmelmair H
Kinderpoliklinik, Ludwig-Maximilans-Universität, Munich, Germany.
Lipids. 1996 Jan;31(1):79-83. doi: 10.1007/BF02522415.
Infants need arachidonic acid (AA; C20:4n-6) for eicosanoid synthesis and deposition in growing tissues, including brain. Human milk supplies preformed AA in amounts considered to meet accretion in membrane-rich tissues, but vegetable oil-based infant formulas do not contain AA. We studied two groups of ten healthy infants, each fed human milk or formula, and analyzed plasma lipid composition. Percentage contributions of AA to plasma phospholipids were stable over two months after birth in breast-fed infants, but infants fed formula developed significantly (P < 0.05) lower levels at the ages of two weeks (formula 6.9% vs. breast 9.4%, w/w), one month (6.2 vs. 9.1%), and two months (5.7 vs. 8.4%). In a second trial, we randomized infants to receive (from birth to age four months) formula without or with both AA and docosahexaenoic acid (DHA; C22:6n-3) at levels typical for mature human milk. Infants fed conventional formula showed a continuous decrease of phospholipid AA over time, whereas feeding of formula supplemented with AA and DHA led to significantly higher AA levels, similar to those in breast-fed infants (two months: supplemented 9.6% vs. unsupplemented 7.1%; four months: 8.7 vs. 6.6%). In order to estimate infantile capacity for endogenous synthesis of AA, we fed four term neonates with newly diagnosed phenylketonuria (mean age 18 d) a formula with all fat contributed by corn oil, which has a higher natural 13C-enrichment than European human milk or formula. Analysis of 13C-enrichment in plasma fatty acids over four days allowed us to estimate infantile AA synthesis. We found an increased 13C-value in plasma AA of all infants, which indicates that term neonates can synthesize AA. However, with a simplified isotope balance equation, we estimate that endogenous synthesis contributed only about 23% of total plasma arachidonic acid by day four. We conclude that full-term infants fed formula may require a dietary supply of some preformed AA if the biochemical status of breast-fed infants is to be achieved.
婴儿需要花生四烯酸（AA；C20:4n - 6）用于类二十烷酸的合成以及在包括大脑在内的生长组织中的沉积。母乳提供的现成AA量被认为能满足富含膜的组织中的累积需求，但以植物油为基础的婴儿配方奶粉不含AA。我们研究了两组各10名健康婴儿，一组喂母乳，另一组喂配方奶粉，并分析了血浆脂质组成。在母乳喂养的婴儿中，出生后两个月内AA对血浆磷脂的百分比贡献保持稳定，但喂配方奶粉的婴儿在两周龄（配方奶粉组6.9% vs. 母乳喂养组9.4%，w/w）、一个月龄（6.2% vs. 9.1%）和两个月龄（5.7% vs. 8.4%）时AA水平显著较低（P < 0.05）。在第二项试验中，我们将婴儿随机分为两组，从出生到四个月龄分别接受不含AA或同时含有AA和二十二碳六烯酸（DHA；C22:6n - 3）的配方奶粉，其含量为成熟母乳中的典型水平。喂传统配方奶粉的婴儿随着时间推移血浆磷脂AA持续下降，而喂添加了AA和DHA的配方奶粉的婴儿血浆AA水平显著更高，与母乳喂养的婴儿相似（两个月龄：添加组9.6% vs. 未添加组7.1%；四个月龄：8.7% vs. 6.6%）。为了评估婴儿内源性合成AA的能力，我们给4名新诊断为苯丙酮尿症的足月儿（平均年龄18天）喂一种配方奶粉，其中所有脂肪均由玉米油提供，玉米油的天然13C富集程度高于欧洲母乳或配方奶粉。通过分析四天内血浆脂肪酸中的13C富集情况，我们能够评估婴儿的AA合成。我们发现所有婴儿血浆AA中的13C值都有所增加，这表明足月儿能够合成AA。然而，通过一个简化的同位素平衡方程，我们估计到第四天内源性合成仅占血浆总花生四烯酸的约23%。我们得出结论，如果要达到母乳喂养婴儿的生化状态，喂配方奶粉的足月儿可能需要从饮食中补充一些现成的AA。
