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Metabolites
Special Issues
One-Carbon Metabolism in Pregnant Women, Fetuses, and Infants
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One-Carbon Metabolism in Pregnant Women, Fetuses, and Infants

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 691

Special Issue Editors

Dr. Yoshinori Kubo

E-Mail Website
Guest Editor
Division of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu 520-2192, Japan
Interests: one-carbon metabolism; maternal nutrition; nutritional epidemiology; molecular epidemiology; developmental origins of the health and disease hypothesis (DOHaD); mass spectrometry; vitamins; trace elements
Prof. Dr. Hikaru Hori

E-Mail Website
Guest Editor
Department of Psychiatry, Faculty of Medicine, Fukuoka University, Fukuoka 814-0180, Japan
Interests: cytokines; neurogenesis; proteomics; psychiatric disease; psychopharma-cology; cognitive function; BDNF; HPLC

Special Issue Information

Dear Colleagues,

The one-carbon metabolism (OCM) comprises a folate cycle, a choline metabolic pathway linked to a methionine cycle, and the homocysteine in the latter being connected to the trans-sulphuration pathway. The OCM is mainly involved in the transfer of the one-carbon units required for S-adenosylmethionine (SAM)-dependent methyl transfer reactions, nucleic acid synthesis, and amino acid metabolism, all of which support numerous physiological processes.

Many epidemiological studies have shown that adverse environments during the periconceptional, fetal, and early postnatal periods increase the risk of developing non-communicable diseases, leading to the concept of the developmental origins of health and disease (DOHaD). In the DOHaD theory, abnormal epigenetic modifications during developmental stages are considered new risk factors for non-communicable diseases. The OCM plays a crucial role in epigenetic modifications that regulate gene expression. The methyl group transfer from SAM, which is synthesized through the OCM, to histone or DNA causes epigenetic modifications. Understanding the OCM during pregnancy and the early postnatal period, when drastic epigenetic remodeling occurs, is vital for DOHaD research.

Therefore, for this Special Issue of Metabolites, we welcome submissions of original research articles and reviews covering (but not limited to) the following topics:

  • Studies related to the OCM (folate cycle, choline metabolic pathway, methionine cycle, and trans-sulphuration pathway) in pregnant women or early postnatal infants;
  • Alterations in OCM metabolites, metabolic fluxes, and networks during pregnancy;
  • Association between OCM status and disease;
  • Effects of diet or nutrients on OCM status;
  • Association between maternal OCM status and epigenetic modifications in offspring.

Dr. Yoshinori Kubo
Prof. Dr. Hikaru Hori
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • folate cycle (5-methyltetrahydrofolate, folic acid, vitamin B12, serine, glycine)
  • methionine cycle (homocysteine, methionine, S-adenosylmethionine, S-adenosylhomocysteine)
  • choline metabolic pathway (betaine, choline)
  • trans-sulfuration pathway (cysteine, taurine, vitamin B6)
  • epigenetics
  • developmental origins of health and disease (DOHaD)

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Published Papers (2 papers)

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Research

28 pages, 1006 KiB  
Article
Early Gestational Hepatic Lipidomic Profiles Are Modulated by One-Carbon Metabolite Supplementation and Nutrient Restriction in Beef Heifers and Fetuses
by Kazi Sarjana Safain, Matthew S. Crouse, Jessica G. Syring, Yssi L. Entzie, Layla E. King, Alison K. Ward, Lawrence P. Reynolds, Pawel P. Borowicz, Carl R. Dahlen, Kendall C. Swanson and Joel S. Caton
Metabolites 2025, 15(5), 302; https://doi.org/10.3390/metabo15050302 - 1 May 2025
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Abstract
Background: Maternal nutrition during early gestation induces metabolic adaptations that support maternal health and fetal development. This study evaluated the effects of maternal one-carbon metabolite (OCM: methionine, choline, folate, and vitamin B12) supplementation and restricted rates of maternal gain on the [...] Read more.
Background: Maternal nutrition during early gestation induces metabolic adaptations that support maternal health and fetal development. This study evaluated the effects of maternal one-carbon metabolite (OCM: methionine, choline, folate, and vitamin B12) supplementation and restricted rates of maternal gain on the hepatic lipid profiles of dams and fetuses at day 63 of gestation. Methods: Thirty-one crossbred Angus heifers were inseminated and assigned to a 2 × 2 factorial design with two factors: maternal dietary intake (control [CON]; 0.60 kg/day average daily gain [ADG] vs. restricted [RES]; −0.23 kg/day ADG) and OCM supplementation (supplemented [+OCM] vs. not supplemented [−OCM]). The four resulting groups (CON − OCM, CON + OCM, RES − OCM, RES + OCM) were maintained for 63 days post-breeding. Maternal and fetal liver samples were collected, and lipidomic profiling was performed using ultra-performance liquid chromatography–tandem mass-spectrometry. Results: In maternal liver, 485 lipid metabolites were detected, with 243 differing significantly in maternal gain. RES heifers showed increased levels (p ≤ 0.05) of acylcarnitines, plasmalogens, lysoplasmalogens, glycosphingolipids, and sphingomyelins. Additionally, RES combined with OCM supplementation led to the accumulation of secondary bile acids and a depletion of monoacylglycerols (p ≤ 0.05) in maternal liver. In fetal liver, 487 lipid metabolites were detected, but treatment effects were minimal. Conclusions: Maternal rate of gain significantly influenced hepatic lipid metabolism in the maternal liver, while fetal liver lipid profiles remained relatively unaffected. These findings underscore the significant role of dietary intake/rate of gain compared with OCM supplementation in modulating hepatic lipid metabolism and highlight the maternal liver’s metabolic adaptations during early pregnancy. Full article
(This article belongs to the Special Issue One-Carbon Metabolism in Pregnant Women, Fetuses, and Infants)
18 pages, 954 KiB  
Article
Alcohol Exposure May Increase Prenatal Choline Needs Through Redirection of Choline into Lipid Synthesis Rather than Methyl Donation
by Hannah G. Petry, Nipun Saini, Susan M. Smith and Sandra M. Mooney
Metabolites 2025, 15(5), 289; https://doi.org/10.3390/metabo15050289 - 24 Apr 2025
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Abstract
Background: Prenatal alcohol exposure (PAE) can reduce fetal growth and cause neurodevelopmental disability. Prenatal choline supplements attenuate PAE-induced behavioral and growth deficits; however, the underlying mechanisms are unknown. Alcohol alters nutrient metabolism and potentially increases nutrient needs. Here, we investigate how alcohol [...] Read more.
Background: Prenatal alcohol exposure (PAE) can reduce fetal growth and cause neurodevelopmental disability. Prenatal choline supplements attenuate PAE-induced behavioral and growth deficits; however, the underlying mechanisms are unknown. Alcohol alters nutrient metabolism and potentially increases nutrient needs. Here, we investigate how alcohol affects choline metabolism in the maternal–fetal dyad and the role of supplemental choline. Methods: Pregnant C57BL/6J mice were assigned to one of four groups: alcohol-exposed (3 g/kg alcohol/day) or control +/− 100 mg/kg choline daily from embryonic day (E)8.5–17.5. We performed an exploratory hypothesis-generating analysis of targeted metabolomics on choline-related metabolites in the maternal liver, plasma, placenta, and fetal brain at E17.5 and Spearman correlation analyses to determine their association with gestational and fetal growth outcomes. Results: Although choline levels were largely unaffected by alcohol or choline, alcohol increased many lipid products in the CDP–choline pathway; this was not normalized by choline. Alcohol increased placental CDP–ethanolamine and reduced the maternal hepatic SAM/SAH ratio as well as dimethylglycine and the serine/glycine ratio across the dyad, suggesting a functional insufficiency in methyl donor pools. These outcomes were rescued by supplemental choline. Correlation analyses among choline metabolites and fetal growth outcomes suggest that maternal plasma methionine, serine, and the serine/glycine ratio may be predictive of maternal–fetal choline status. Conclusions: The increased hepatic lipid synthesis that characterizes chronic alcohol exposure may draw choline into phospholipid biosynthesis at the expense of its use as a methyl donor. We propose that PAE increases choline needs, and that its supplementation is necessary to fulfill these competing demands for lipid and methyl use. Full article
(This article belongs to the Special Issue One-Carbon Metabolism in Pregnant Women, Fetuses, and Infants)
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