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Plasma phospholipids indicate impaired fatty acid homeostasis in preterm infants
Wolfgang Bernhard1, Marco Raith, Vera Koch
1Department of Neonatology, Faculty of Medicine, Eberhard-Karls-University, Calwer Straße 7, 72076, Tübingen, Germany, wolfgang.bernhard@med.uni-tuebingen.de.
Insights
Preterm infant nutrition alters plasma phospholipids, decreasing essential docosahexaenoic acid (DHA) and arachidonic acid (ARA) fractions. Current feeding practices may not meet fetal needs, potentially impacting neurodevelopment.
Area of Science:
- Neonatal nutrition and development
- Lipid metabolism and homeostasis
- Neuroscience and neurodevelopment
Background:
- Docosahexaenoic acid (DHA) and arachidonic acid (ARA) are crucial for fetal brain development, accumulating in phospholipids.
- Post-preterm delivery, placental transfer is replaced by enteral/parenteral nutrition, often high in linoleic acid (LA).
- Plasma phosphatidylcholine (PC) and phosphatidylethanolamine (PE) species reflect DHA/ARA enrichment and hepatic stores, respectively.
Purpose of the Study:
- To profile PC and PE species in preterm infant plasma.
- To compare these profiles with cord and maternal blood.
- To evaluate if current feeding practices align with fetal needs for essential fatty acids.
Main Methods:
- Analysis of PC and PE molecular species in plasma from preterm infants (N=171), cord blood (N=194), and maternal serum (N=121).
- Lipid extraction followed by tandem mass spectrometry.
- Samples collected from 23-35 weeks postmenstrual age (PMA) for infants and 24-41 weeks PMA for cord/maternal blood.
Main Results:
- Preterm infants showed higher phospholipid concentrations than cord blood (PMA-corrected), primarily due to increased LA-containing PC and PE.
- Postnatal increases in LA led to decreased fractions of DHA- and ARA-containing phospholipids.
- While DHA levels slowly recovered, they remained at 50% of cord blood levels; ARA fractions continued to decrease.
Conclusions:
- Postnatal increases in LA-PC and LA-PE in preterm infants reduce DHA-PC and ARA-PC fractions.
- Altered hepatic fatty acid homeostasis is indicated by PE composition changes.
- Inadequate LA, ARA, and DHA supply likely impairs developing brain availability, potentially contributing to neurodevelopmental deficits.
Background:
During fetal development, docosahexaenoic (DHA) and arachidonic acid (ARA) are particularly enriched in brain phospholipids. After preterm delivery, fetal enrichment of DHA and ARA via placental transfer is replaced by enteral and parenteral nutrition, which is rich in linoleic acid (LA) instead. Specific DHA and ARA enrichment of lipoproteins is reflected by plasma phosphatidylcholine (PC) species, whereas plasma phosphatidylethanolamine (PE) composition reflects hepatic stores.
Objective:
We profiled PC and PE species in preterm infant plasma, compared with cord and maternal blood, to assess whether current feeding practice meets fetal conditions in these patients.
Design:
Preterm infant plasma (N = 171, 23-35 w postmenstrual age (PMA), postnatal day 1-103), cord plasma (N = 194) and maternal serum (N = 121) (both 24-41 w PMA) were collected. After lipid extraction, PC and PE molecular species were analyzed using tandem mass spectrometry.
Results:
Phospholipid concentrations were higher in preterm infant than in cord plasma after correction for PMA. This was mainly due to postnatal increases in LA-containing PC and PE, resulting in decreased fractions of their DHA- and ARA-containing counterparts. These changes in preterm infant plasma phospholipids occurred during the time of transition to full enteral feeds (day 0-10 after delivery). Thereafter, the fraction of ARA-containing phospholipids further decreased, whereas that of DHA slowly reincreased but remained at a level 50% of that of PMA-matched cord blood.
Conclusions:
The postnatal increase in LA-PC in preterm infant plasma results in decreased fractions of DHA-PC and ARA-PC. These changes are also reflected by PE molecular composition as an indicator of altered hepatic fatty acid homeostasis. They are presumably caused by inadequately high LA, and low ARA and DHA supply, at a stage of development when ARA-PC and DHA-PC should be high, probably reducing the availability of DHA and ARA to the developing brain and contributing to impaired neurodevelopment of preterm infants.
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