Increase in plasma phospholipid docosahexaenoic and eicosapentaenoic acids as a reflection of their intake and mode of administration.
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)[1]References
- Increase in plasma phospholipid docosahexaenoic and eicosapentaenoic acids as a reflection of their intake and mode of administration. Liu, C.C., Carlson, S.E., Rhodes, P.G., Rao, V.S., Meydrech, E.F. Pediatr. Res. (1987) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
