ArticleThe Journal of nutrition2025
Alcohol Reprograms Placental Glucose and Lipid Metabolism, Which Correlate with Reduced Fetal Brain but not Body Weight in a Mouse Model of Prenatal Alcohol Exposure.
Article in The Journal of nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Review
- Prematurity and Multidimensional Risk Patterns in Adolescent and Adult Pregnancies: A Principal Component Analysis in an Eastern European Cohort.Children (Basel, Switzerland) · 2025Article
- Nonconceptus Mechanisms of Prenatal Alcohol Exposure That Disrupt Embryo-Fetal Development: An Integrative View.Alcohol research : current reviews · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
backgroundPrenatal alcohol exposure (PAE) impairs fetal growth and brain development. Dysregulated placental function contributes to these deficits. Whether PAE also disrupts its metabolic functions to impede fetal development is unclear.
objectivesWe performed untargeted metabolomics to gain mechanistic insights on how PAE impacts placental metabolism and fetal nutrient availability.
methodsPregnant C57BL/6J mice were gavaged with alcohol (ALC, 3 g/kg) or isocaloric maltodextrin (CON) daily on embryonic days (E) E8.5 through E17.5. We performed untargeted metabolomics on placentas harvested at E17.5.
resultsAlcohol reduced placental glucose and glycolytic intermediates and increased tricarboxylic acid (TCA) cycle intermediates, suggesting a shift from glucose to lipids to meet its high energetic demands. This was complemented by elevations in intermediates of the pentose phosphate and glucosamine pathways, indicating a diversion of glucose into nonoxidative fates. Alcohol also decreased aspartate and asparagine, consistent with the limited glucose availability and increased fetal demand for nitrogen acceptors to support its increased gluconeogenesis and urea production. Alcohol also caused a selective increase in purine metabolites despite the limited availability of donor sources glucose, serine, glycine, glutamine, and asparagine. Uridine nucleotides were also elevated and may represent an adaptive change to meet the increased need for thiamin pyrophosphate in the oxidative decarboxylations of the TCA cycle and pentose phosphate pathways. Decreases in multiple oxylipins having antivasoconstriction actions could be a mechanism by which alcohol alters the placental vasculature and promotes vasoconstriction. Importantly, the selective and strong correlation of these dysregulated metabolites with reduced fetal brain weight, but not body weight, affirms the importance of the placenta-brain axis and placental metabolism on brain development.
conclusionsAlcohol causes metabolic dysregulation and reprogramming of the late-term placenta. These changes limit fetal nutrient availability and contribute to the reduced brain development and cognitive impairments that partly typify PAE.
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