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 C-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.
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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 C-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 phospholipidDHA 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.
Authors: Salma A Abdelmagid; Shannon E Clarke; Daiva E Nielsen; Alaa Badawi; Ahmed El-Sohemy; David M Mutch; David W L Ma Journal: PLoS One Date: 2015-02-12 Impact factor: 3.240
Authors: Emma Amissah; Luling Lin; Gregory D Gamble; Caroline A Crowther; Frank H Bloomfield; Jane E Harding Journal: Sci Rep Date: 2019-10-11 Impact factor: 4.379