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Postnatal adaptations of phosphatidylcholine metabolism in extremely preterm infants: implications for choline and
Kevin C W Goss1,2, Victoria M Goss2, J Paul Townsend2
1Child Health, Academic Unit of Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Insights
Extremely preterm infants have immature livers that actively synthesize phosphatidylcholine (PC) via the CDP-choline pathway. Low PEMT activity suggests a need for increased choline and PUFA supplementation in parenteral nutrition.
Area of Science:
- Neonatal physiology and metabolism
- Lipidomics and molecular pathways
- Nutritional biochemistry
Background:
- Pregnancy involves maternal liver delivery of polyunsaturated fatty acids (PUFAs) to the fetus.
- Extremely preterm infants face challenges transitioning to PUFA-poor diets post-birth, often relying on total parenteral nutrition.
- Immature liver function in preterm neonates impacts essential nutrient metabolism.
Purpose of the Study:
- To characterize phosphatidylcholine (PC) and choline metabolism in preterm infants.
- To demonstrate the molecular specificity of PC synthesis by the immature preterm liver in vivo.
- To assess postnatal adaptations in plasma PC composition.
Main Methods:
- Lipidomic analysis using mass spectrometry (MS) in 31 preterm infants (<28 weeks' gestational age).
- Quantification of postnatal adaptations in plasma PC molecular composition.
- Assessment of cytidine diphosphocholine (CDP-choline) and phosphatidylethanolamine-N-methyltransferase (PEMT) pathway activities using deuterated methyl-D9-choline chloride incorporation.
Main Results:
- Plasma PC concentrations significantly increased postnatally (481 µM to 1046 µM within 5 days).
- The CDP-choline pathway actively synthesized PC, enriched in oleic and linoleic acids.
- Liver PEMT activity was found to be very low, indicating minimal endogenous choline synthesis.
Conclusions:
- The preterm infant liver is metabolically active in lipoprotein metabolism shortly after birth.
- Low PEMT activity highlights the critical need for increased choline and PUFA supplementation in preterm parenteral nutrition.
- Findings support enhanced nutritional support for extremely preterm infants to optimize lipid metabolism.
Background:
Lipid metabolism in pregnancy delivers PUFAs from maternal liver to the developing fetus. The transition at birth to diets less enriched in PUFA is especially challenging for immature, extremely preterm infants who are typically supported by total parenteral nutrition.
Objective:
The aim was to characterize phosphatidylcholine (PC) and choline metabolism in preterm infants and demonstrate the molecular specificity of PC synthesis by the immature preterm liver in vivo.
Methods:
This MS-based lipidomic study quantified the postnatal adaptations to plasma PC molecular composition in 31 preterm infants <28 weeks' gestational age. Activities of the cytidine diphosphocholine (CDP-choline) and phosphatidylethanolamine-N-methyltransferase (PEMT) pathways for PC synthesis were assessed from incorporations of deuterated methyl-D9-choline chloride.
Results:
The concentration of plasma PC in these infants increased postnatally from median values of 481 (IQR: 387-798) µM at enrollment to 1046 (IQR: 616-1220) µM 5 d later (P < 0.001). Direct incorporation of methyl-D9-choline demonstrated that this transition was driven by an active CDP-choline pathway that synthesized PC enriched in species containing oleic and linoleic acids. A second infusion of methyl-D9-choline chloride at day 5 clearly indicated continued activity of this pathway. Oxidation of D9-choline through D9-betaine resulted in the transfer of 1 deuterated methyl group to S-adenosylmethionine. A very low subsequent transfer of this labeled methyl group to D3-PC indicated that liver PEMT activity was essentially inactive in these infants.
Conclusions:
This study demonstrated that the preterm infant liver soon after birth, and by extension the fetal liver, was metabolically active in lipoprotein metabolism. The low PEMT activity, which is the only pathway for endogenous choline synthesis and is responsible for hormonally regulated export of PUFAs from adult liver, strongly supports increased supplementation of preterm parenteral nutrition with both choline and PUFAs.
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