Abstract
Infant formulas supplemented with docosahexaenoic acid (DHA) and arachidonic acid (ARA) are now available in the United States; however, little is known about the factors that affect biosynthesis. Baboon neonates were assigned to one of four treatments: term, breast-fed; term, formula-fed; preterm (155 of 182 days gestation), formula-fed; and preterm, formula+DHA/ARA-fed. Standard formula had no DHA/ARA; supplemented formula had 0.61%wt DHA (0.3% of calories) and 1.21%wt ARA (0.6% of calories), and baboon breast milk contained 0.68 +/- 0.22%wt DHA and 0.62 +/- 0.12%wt ARA. At 14 days adjusted age, neonates received a combined oral dose of [U-13C]alpha-linolenic acid (LNA*) and [U-13C]linoleic acid (LA*), and tissues were analyzed 14 days after dose. Brain accretion of linolenic acid-derived DHA was approximately 3-fold greater for the formula groups than for the breast-fed group, and dietary DHA partially attenuated excess DHA synthesis among preterms. A similar, significant pattern was found in other organs. Brain linoleic acid-derived ARA accretion was significantly greater in the unsupplemented term group but not in the preterm groups compared with the breast-fed group. These data show that formula potentiates the biosynthesis/accretion of DHA/ARA in term and preterm neonates compared with breast-fed neonates and that the inclusion of DHA/ARA in preterm formula partially restores DHA/ARA biosynthesis to lower, breast-fed levels. Current formula DHA concentrations are inadequate to normalize long-chain polyunsaturated fatty acids synthesis to that of breast-fed levels.
Highlights
Infant formulas supplemented with docosahexaenoic acid (DHA) and arachidonic acid (ARA) are available in the United States; little is known about the factors that affect biosynthesis
Autopsy data suggest that term formulafed infants deplete adipose tissue DHA stores by 6 months of age compared with breast-fed infants, who generally maintain DHA levels [15, 16]; factors concerning long-chain polyunsaturated fatty acid (LCP) biosynthesis are relevant for all human infants
We reported on the influence of prematurity and LCP supplementation on total fatty acid (FA) of brain and related tissues of preterm baboon neonates at 4 weeks adjusted age [33]
Summary
The design of this study was described in detail in a previous publication [33]. Important details will be outlined here. If the dose FA is elongated from endogenous nonlabeled sources (i.e., LNA to DHA and LA to ARA), this value must be corrected by the number of moles of C in the analyte divided by the number of moles of C in the dose FA, to be expressed in terms of the moles of precursor that have entered the product pool This value is termed the molar dose equivalent (D*) [38] and is calculated as follows: D*. Correlations among tracer concentrations in plasma, RBC, and tissue pools were calculated from individual data from each animal without regard to treatment group to determine the degree to which pools accessible in human infants correlate with tissues. Regression equations were calculated in Excel 2000 for Windows (Microsoft, Seattle, WA)
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