Postnatal adaptations of phosphatidylcholine metabolism in extremely preterm infants: implications for choline and PUFA metabolism.


Journal

The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027

Informations de publication

Date de publication:
10 12 2020
Historique:
received: 16 03 2020
accepted: 01 07 2020
pubmed: 12 8 2020
medline: 7 1 2021
entrez: 12 8 2020
Statut: ppublish

Résumé

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. 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. 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. 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. 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.

Sections du résumé

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.

Identifiants

pubmed: 32778895
pii: S0002-9165(22)00923-6
doi: 10.1093/ajcn/nqaa207
pmc: PMC7727469
doi:

Substances chimiques

Fatty Acids, Unsaturated 0
Phosphatidylcholines 0
Choline N91BDP6H0X

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1438-1447

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © The Author(s) on behalf of the American Society for Nutrition 2020.

Références

Arch Dis Child Fetal Neonatal Ed. 2011 Nov;96(6):F443-7
pubmed: 21393312
J Nutr. 1995 Dec;125(12):3049-54
pubmed: 7500183
Arch Physiol Biochem. 2002 Dec;110(5):393-9
pubmed: 12530624
BMJ. 2012 Dec 04;345:e7976
pubmed: 23212881
Biochim Biophys Acta. 1997 Sep 4;1348(1-2):142-50
pubmed: 9370326
Nutr Rev. 2009 Nov;67(11):615-23
pubmed: 19906248
Eur J Nutr. 2015 Aug;54(5):733-41
pubmed: 25148882
J Lipid Res. 2018 Jun;59(6):1034-1045
pubmed: 29716960
Am J Respir Crit Care Med. 2004 Jul 1;170(1):54-8
pubmed: 15044202
Am J Clin Nutr. 2013 Dec;98(6):1459-67
pubmed: 24132975
Am J Clin Nutr. 1996 Oct;64(4):572-6
pubmed: 8839502
Annu Rev Nutr. 2010 Aug 21;30:315-39
pubmed: 20415585
Biochem J. 1999 Jan 1;337 ( Pt 1):23-7
pubmed: 9854020
J Perinat Med. 2007;35 Suppl 1:S5-11
pubmed: 17302540
Biochim Biophys Acta. 2014 Jun;1838(6):1477-87
pubmed: 24184426
J Biol Chem. 2002 May 10;277(19):17217-25
pubmed: 11864970
Can J Biochem Physiol. 1959 Aug;37(8):911-7
pubmed: 13671378
Biochim Biophys Acta. 1997 May 17;1346(1):1-9
pubmed: 9187296
Nature. 2014 May 22;509(7501):503-6
pubmed: 24828044
Annu Rev Nutr. 2006;26:229-50
pubmed: 16848706
Am J Physiol. 1992 Nov;263(5 Pt 1):E988-1001
pubmed: 1443132
J Res Med Sci. 2014 Nov;19(11):1038-40
pubmed: 25657747
Arch Dis Child. 1993 Sep;69(3 Spec No):281-3
pubmed: 8215565
Am J Clin Nutr. 2012 May;95(5):1060-71
pubmed: 22418088
Prog Lipid Res. 2007 May-Jul;46(3-4):200-24
pubmed: 17540449
Am J Clin Nutr. 2011 Dec;94(6 Suppl):1908S-1913S
pubmed: 21562082
Eur J Nutr. 2020 Mar;59(2):729-739
pubmed: 30859363
J Lipid Res. 2011 Feb;52(2):399-407
pubmed: 21068006
Am J Physiol. 1999 Jun;276(6):E1146-70
pubmed: 10362629
J Biol Chem. 2001 Mar 16;276(11):8492-9
pubmed: 11121419
J Mol Neurosci. 2001 Apr-Jun;16(2-3):201-4; discussion 215-21
pubmed: 11478375
Lipids. 2003 Apr;38(4):303-15
pubmed: 12848275
J Biol Chem. 1958 Mar;231(1):53-64
pubmed: 13538947
Br J Obstet Gynaecol. 1982 Mar;89(3):211-5
pubmed: 7066258

Auteurs

Kevin C W Goss (KCW)

Child Health, Academic Unit of Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
NIHR Southampton Respiratory Biomedical Research Unit, University Hospitals Southampton, Southampton, United Kingdom.

Victoria M Goss (VM)

NIHR Southampton Respiratory Biomedical Research Unit, University Hospitals Southampton, Southampton, United Kingdom.

J Paul Townsend (JP)

NIHR Southampton Respiratory Biomedical Research Unit, University Hospitals Southampton, Southampton, United Kingdom.

Grielof Koster (G)

NIHR Southampton Respiratory Biomedical Research Unit, University Hospitals Southampton, Southampton, United Kingdom.

Howard W Clark (HW)

Child Health, Academic Unit of Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
NIHR Southampton Respiratory Biomedical Research Unit, University Hospitals Southampton, Southampton, United Kingdom.

Anthony D Postle (AD)

Child Health, Academic Unit of Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
NIHR Southampton Respiratory Biomedical Research Unit, University Hospitals Southampton, Southampton, United Kingdom.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH