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Pregnancy and Child Obesity (Poster Theater Flash Session 1)

(PTFS01-05-25) Fetal Liver Weight Is Negatively Associated With Maternal Plasma Lipid Metabolites in a Mouse Model of Prenatal Alcohol Exposure and Choline Supplementation

Saturday, May 31, 2025
12:16 PM – 12:20 PM ET
Location: South Hall B (The Hub) - Poster Theater / Poster Board Number PT-6
Emerging Leaders in Nutrition Science Poster Competition

    Presenting Author(s)

  • Hannah Petry, BS

    PhD Student
    The University of North Carolina at Chapel Hill
    Kannapolis, North Carolina, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • SS

    Susan M. Smith, Ph.D.

    Institute Deputy Director for Science, Professor of Nutrition
    Nutrition Research Institute, University of North Carolina-Chapel Hill
    Kannapolis, North Carolina, United States

  • SM

    Sandra Mooney, Ph.D.

    Associate Professor of Nutrition
    Nutrition Research Institute
    Kannapolis, North Carolina, United States

Objectives: The fetus relies on circulating maternal nutrients for normal development. Prenatal alcohol exposure (PAE) can interfere with the regulation of many nutrients and this likely contributes to its associated growth deficits. Choline is essential for fetal development and its supplementation mitigates the effect of PAE on brain structure and function. Currently, there is little information about whether choline is protective against effects of PAE on other fetal organs. Here we examined whether PAE disrupts fetal liver growth, if choline is protective against this, and what maternal plasma biomarkers predict fetal liver development.

Methods: Pregnant C57BL/6J mice were exposed to 3 g/kg alcohol (ALC) or maltodextrin (CON) and treated +/- 100 mg/kg choline chloride (CHO) daily for embryonic days (E) 8.5 – 17.5. On E 17.5 dams were euthanized; maternal plasma was collected for untargeted metabolomics analyses and fetal livers were weighed. Liver weights were assessed using two-way ANOVA, and ortho-partial least squares discriminant analyses were used to determine the top 30 plasma metabolites that predict liver weight. Spearman correlation analysis identified associations between metabolites and fetal liver weight.

Results: ALC reduced fetal liver weight by 17% and CHO increased it by 7%, suggesting partial rescue. CHO also increased CON liver weight by 4%. The top 30 maternal plasma metabolites that predict fetal liver weight were related to the metabolism of lipids (n=16, 8 of which are diacylglycerols), amino acids (6), carbohydrates (2), and unidentified/other (6). Most (29/30) metabolites were increased by ALC and either reduced or unchanged by CHO, and all of these negatively associated with liver weight. The one metabolite showing the opposite pattern was imidazole propionate, a microbial-derived metabolite of histidine.

Conclusions: CHO partially improves fetal liver weight that’s impaired by ALC. We identified mostly negative associations between maternal plasma metabolites and fetal liver weight. Eight of the lipid metabolites were diacylglycerols, and we previously found that 7 of these were also negatively associated with fetal brain weights and 4 with fetal body weights, suggesting that they may be useful biomarkers of fetal outcomes.

Funding Sources: UNC Nutrition Research Institute