ABSTRACT. Very low birth weight infants demonstrate significant reductions in red blood cell membrane docosahexaenoic acid (DHA, 22:6n-3) following delivery unless fed human milk. The purpose of the present study was to determine if a dietary source of DHA (MaxEPA, R. P. Scherer Corporation, Troy, MI) could prevent the decline in red blood cell phospholipid DHA in very low birth weight infants whose enteral feeding consisted of a preterm formula without DHA. Longitudinal data were obtained on membrane phospholipid DHA in both unsupplemented and MaxEPA-supplemented infants by a combination of thinlayer and gas chromatography. These infants (n = 39) ranged in age from 10 to 53 days at enrollment (0 time). At enrollment, phospholipid DHA and arachidonic acid (20:4n-6) were inversely correlated with age in days. During the study, mean red blood cell phospholipid DHA declined without supplementary DHA as determined by biweekly measurement, but infants supplemented with MaxEPA maintained the same weight percent of phospholipid (phosphatidylethanolanine, phosphatidylcholine, and phosphatidylserine) DHA as at enrollment. and retinal membranes (3). Dietary manipulations which limit accumulation of DHA to 25-50% of controls in these membranes were associated with a 33% reduction in discrimination learning in rats (4), significant reductions in electroretinogram a-wave amplitudes (5), and a 25% loss of visual acuity in the rhesus monkey (5, 6). Furthermore, changes in electroretinograms observed after early deprivation persist following subsequent biochemical normalization of retinal membrane DHA in both species (5,7). Accumulation of DHA in the central nervous system begins at about the 26th wk of gestation in the human fetus (8) with the weight percent of phospholipid DHA approaching adult levels by term (9). Studies in developing rats suggest that differences in red blood cell phospholipid DHA are indicative of qualitative differences in accumulation in the central nervous system. Studies done in very low birth weight preterm infants showed that red blood cell PE DHA was high at birth, but the weight percent declined in the period before infants were nourished completely by orogastric feedings (1). Subsequently, an additional decline in PE DHA occurred in infants fed formula, whereas DHA increased in infants fed mother's milk (I).Infant formula contains linolenic acid (1 8:3n-3) a precursor of DHA. Linoleic (18:2n-6) and linolenic acid are not interconvertible and compete for elongation and desaturation by the same enzyme system. Thus conversion of 20:3n-6 to 20:4n-6 and 20:4n-3 to 20:5n-3 is catalyzed by A5-desaturase and the elongation products of 20:4n-6 and 20:5n-3 (22:4n-6 and 22:5n-3, respectively) are converted to 22:5n-6 and 22:6n-3 by A4-desaturase.Humans appear to have low A4-desaturase activity as indicated by the following observations: 1) diets enriched in 18:3n-3 increase phospholipid 20:5n-3 the A5-desaturase product, but not 22:6n-3, its A4-desaturase product (10); 2) red blood cell membrane phospholipid...
The fatty acid, docosahexaenoic acid (DHA, 22:6n-3), is a major constituent of red blood cell phosphatidylethanolamine and phosphatidylserine at birth but declines in all phospholipid classes following preterm delivery unless the diet contains DHA. A bolus of fish oil prevented declines in DHA of red cell phospholipids (phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine) during 4 to 6 wk of feeding, with red blood cell DHA indistinguishable from that of infants fed human milk. The amount of DHA fed was almost an order of magnitude greater than usually provided by human milk, however, suggesting poor absorption of fish oil by preterm infants. The purpose of these studies was to determine if uptake of fish oil DHA could be improved by dispersion in preterm formula. Since plasma phospholipids rapidly reflect changes in dietary fatty acid composition, DHA uptake was assessed by fatty acid analysis of plasma phosphatidylethanolamine and phosphatidylcholine. All groups receiving fish oil (both bolus and dispersed) demonstrated a rise in plasma phospholipid phosphatidylethanolamine DHA. Infants receiving 11 mg/kg/day DHA from dispersed fish oil, however, appeared to absorb as much or more as those receiving 71 mg/kg/day DHA in a bolus. The lower intake of DHA provided only 0.2% of total dietary fatty acids (human milk typically provides 0.1 to 0.3%). This study, in conjunction with an earlier report, demonstrates the feasibility of 1) long-term maintenance of red cell membrane DHA by its inclusion in infant formula and 2) DHA maintenance by "physiological" intakes of DHA; i.e. the amount provided by human milk.(ABSTRACT TRUNCATED AT 250 WORDS)
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