LONG-TERM FEEDING OF FORMULAS HIGH IN LINOLENIC ACID AND MARINE OIL TO VERY-LOW-BIRTH-WEIGHT INFANTS - PHOSPHOLIPID FATTY-ACIDS

LONG-TERM FEEDING OF FORMULAS HIGH IN LINOLENIC ACID AND MARINE OIL TO VERY-LOW-BIRTH-WEIGHT INFANTS - PHOSPHOLIPID FATTY-ACIDS
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DOI:
10.1203/00006450-199111000-00003
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发表时间:
1991-11-01
期刊:
影响因子:
3.6
通讯作者:
TOLLEY, EA
TOLLEY, EA
中科院分区:
医学3区
文献类型:
--
作者:
CARLSON, SE;COOKE, RJ;TOLLEY, EA

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母乳喂养婴儿的红细胞(RBC)磷脂比配方奶粉喂养婴儿的红细胞磷脂含有更多的花生四烯酸(AA)和二十二碳六烯酸(DHA)。在含有0.6 - 2.0% α-亚麻酸(LLA,18:3 n-3)的婴儿配方奶粉中添加低水平的海洋植物油可防止配方奶粉喂养的婴儿的DHA下降;然而,喂养试验时间较短(4 - 6周),与当前配方奶粉(3.0 - 5.0% LLA)相比,LLA浓度较低,配方奶粉不稳定。有必要进行稳定配方的试验,以确定出院后膳食DHA是否能维持磷脂DHA,事实上,是否有必要增加LLA的摄入量。本文报告了急性(4周)和延长(至受孕后79周)喂养这些配方奶粉对RBC和血浆磷脂AA和DHA的影响。对照配方与市售配方相同。实验配方的不同之处仅在于添加了少量的海洋石油。红细胞中的DHA和血浆磷脂酰乙醇胺(PE)下降,在四周的喂养,但不如果海洋石油提供DHA(0.2%或0.4%)和血浆磷脂AA(g/100 g)随着时间和海洋石油喂养下降。延长喂养海洋石油占一半的DHA在红细胞和血浆磷脂酰乙醇胺平衡,然而,红细胞(克/100克)和血浆AA(克/100克;毫克/升血浆)逐步下降,直到婴儿后期,并进一步抑制海洋石油。我们得出的结论是:1)当仅消耗n-6和n-3脂肪酸前体时,早产儿的RBC和血浆磷脂中的AA和DHA会下降; 2)海洋油可以维持RBC磷脂酰乙醇胺DHA的脐带浓度,但进一步降低AA。
Red blood cell (RBC) phospholipids of infants fed human milk compared with formula have more arachidonic acid (AA) and docosahexanoic acid (DHA). The addition of low levels of marine oil to infant formula with 0.6 to 2.0% alpha-linolenic acid (LLA, 18:3n-3) prevented declines in DHA in formula-fed infants; however, the feeding trials were short (4 to 6 wk), LLA concentrations were low compared with current formulas (3.0 to 5.0% LLA), and the formulas were unstable. Trials with stable formulas were necessary to determine if dietary DHA could maintain phospholipid DHA after discharge from the hospital and, in fact, if it was necessary with higher intakes of LLA. The results of acute (4 wk) and extended (to 79 wk postconception) feeding of such formulas on RBC and plasma phospholipid AA and DHA are reported here. Control formulas were identical to commercially available formulas. Experimental formulas differed only in the addition of small amounts of marine oil. DHA in RBC and plasma phosphatidylethanolamine (PE) declined during four weeks of feeding but not if marine oil provided DHA (0.2% or 0.4%) and plasma phospholipid AA (g/100 g) decreased with time and marine oil feeding. Extended feeding with marine oil accounted for half the DHA in RBC and plasma phosphatidylethanolamine at equilibrium; however, RBC (g/100 g) and plasma AA (g/100 g; mg/L plasma) decreased progressively until late infancy and were depressed further by marine oil. We conclude that 1) AA and DHA decline in RBC and plasma phospholipids of preterm infants when only their n-6 and n-3 fatty acid precursors are consumed; and 2) marine oil can maintain cord concentrations of RBC phosphatidylethanolamine DHA but further reduces AA.