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Effect of Different Levels of Docosahexaenoic Acid Supply on Fatty Acid Status and Linoleic and α-Linolenic Acid Conversion in Preterm Infants

Sauerwald, Ulrike C.*; Fink, Maria M.*; Demmelmair, Hans*; Schoenaich, Patrick v.; Rauh-Pfeiffer, Astrid A.M.*; Koletzko, Berthold*

Journal of Pediatric Gastroenterology & Nutrition: March 2012 - Volume 54 - Issue 3 - p 353–363
doi: 10.1097/MPG.0b013e31823c3bfd
Original Articles: Hepatology and Nutrition

Objectives: Long-chain polyunsaturated fatty acid (LC-PUFA) enrichment of preterm infant formulas is recommended to meet high demands. Dietary LC-PUFA may inhibit endogenous LC-PUFA synthesis, thus limiting their benefit. We investigated effects of different docosahexaenoic acid (DHA) intakes on plasma and erythrocyte fatty acids and endogenous LC-PUFA synthesis in preterm infants.

Methods: Forty-two preterm infants (birth weight 1000–2200 g) were randomized double-blind to preterm formulas with γ-linolenic acid (0.4%) and arachidonic acid (AA, 0.1%) but different DHA contents (A: 0.04%, B: 0.33%, C: 0.52%); 24 received human milk (HM: 0.51% AA, 0.38% DHA, nonrandomized). Blood was sampled on study days 0, 14, and 28. Uniformly 13C-labeled linoleic acid (2 mg/kg) and α-linolenic acid (1 mg/kg) were applied orally on day 26 and blood samples collected 48 hours later.

Results: On day 28, group A had the lowest and group C the highest plasma phospholipid concentrations of eicosapentaenoic acid and DHA. Erythrocyte phospholipid DHA was lowest in group A, but comparable in groups B, C, and HM. Plasma and erythrocyte AA were lower in formula groups than in HM. DHA intake had no effect on DHA synthesis. LC-PUFA synthesis was lower in HM infants.

Conclusions: DHA supply dose dependently increased plasma DHA. Formula DHA levels of 0.33% matched plasma DHA status of infants fed HM. LC-PUFA synthesis was lower in infants fed HM than formulas with different DHA and low AA contents. With the LC-PUFA supplementation used, DHA in formulas did not inhibit AA or DHA synthesis.

*Kinderklinik and Kinderpoliklinik, Dr. von Hauner Children′s Hospital, University of Munich Medical Centre, München

Department of Paediatrics, Zentralklinikum Augsburg, Germany.

Address correspondence and reprint request to Berthold Koletzko, Professor of Paediatrics, Division of Metabolic and Nutritional Medicine, Kinderklinik and Kinderpoliklinik, Dr von Hauner Children's Hospital, University of Munich Medical Centre, Lindwurmstr 4, 80337 München, Germany (e-mail: office.koletzko@med.uni-muenchen.de).

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website (www.jpgn.org).

Received 2 March, 2011

Accepted 24 August, 2011

www.clinicaltrials.gov registration number: NCT01300130.

The present study was supported in part by the Bundesministerium für Forschung und Bildung, Berlin, Germany (07 ERG 08/1), Deutsche Forschungsgemeinschaft, Bonn, Germany (KO 912/5-1 and 5-2), and Nestlé Nutrition, Vevey, Switzerland. Formulas for this trial were supplied by Nestlé Nutrition, Frankfurt, Germany.

The authors report no conflicts of interest.

Copyright 2012 by ESPGHAN and NASPGHAN