ArticleAlcoholism, clinical and experimental research2018
Dietary Iron Fortification Normalizes Fetal Hematology, Hepcidin, and Iron Distribution in a Rat Model of Prenatal Alcohol Exposure.
Article in Alcoholism, clinical and experimental research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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14 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Effects of prenatal alcohol exposure on cognitive and behavioral development: Findings from a hierarchical meta-analysis of data from six prospective longitudinal U.S. cohorts.Alcoholism, clinical and experimental research · 2021Pooled it
- The impact of micronutrient supplementation in alcohol-exposed pregnancies on reaction time responses of preschoolers in Ukraine.Alcohol (Fayetteville, N.Y.) · 2022Trial
- Maternal nutritional imbalance during pregnancy and the development of fetal-origin cardiovascular diseases.Frontiers in nutrition · 2026Review
- Nonconceptus Mechanisms of Prenatal Alcohol Exposure That Disrupt Embryo-Fetal Development: An Integrative View.Alcohol research : current reviews · 2025Review
- Alcohol exposure suppresses ribosome biogenesis and causes nucleolar stress in cranial neural crest cells.PloS one · 2024Article
- Fetal anemia and elevated hepcidin in a mouse model of fetal alcohol spectrum disorder.Pediatric research · 2023Article
- Microbiota and nutrition as risk and resiliency factors following prenatal alcohol exposure.Frontiers in neuroscience · 2023Review
- Mediating and Moderating Effects of Iron Homeostasis Alterations on Fetal Alcohol-Related Growth and Neurobehavioral Deficits.Nutrients · 2022Article
- Fetal Alcohol Spectrum Disorder and Iron Homeostasis.Nutrients · 2022Review
- Gestational weight gain and dietary energy, iron, and choline intake predict severity of fetal alcohol growth restriction in a prospective birth cohort.The American journal of clinical nutrition · 2022Article
- Brain Iron and Mental Health Symptoms in Youth with and without Prenatal Alcohol Exposure.Nutrients · 2022Article
- Gestational Iron Supplementation Improves Fetal Outcomes in a Rat Model of Prenatal Alcohol Exposure.Nutrients · 2022Article
- Maternal iron nutriture modulates placental development in a rat model of fetal alcohol spectrum disorder.Alcohol (Fayetteville, N.Y.) · 2020Article
- Alcohol's Dysregulation of Maternal-Fetal IL-6 and p-STAT3 Is a Function of Maternal Iron Status.Alcoholism, clinical and experimental research · 2019Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPrenatal alcohol exposure (PAE) causes neurodevelopmental disability. Clinical and animal studies show gestational iron deficiency (ID) exacerbates PAE's behavioral and growth deficits. In rat, PAE manifests an inability to establish iron homeostasis, increasing hepcidin (maternal and fetal), and fetal liver iron while decreasing brain iron and promoting anemia. Here, we hypothesize dietary iron fortification during pregnancy may mitigate alcohol's disruption of fetal iron homeostasis.
methodsPregnant Long-Evans rats, fed iron-sufficient (100 ppm iron) or iron-fortified (IF; 500 ppm iron) diets, received either 5 g/kg alcohol (PAE) or isocaloric maltodextrin daily on gestational days (GD) 13.5 through 19.5. Maternal and fetal outcomes were evaluated on GD20.5.
resultsPAE reduced mean fetal weight (p < 0.001) regardless of maternal iron status, suggesting iron fortification did not improve fetal growth. Both PAE (p < 0.01) and IF (p = 0.035) increased fetal liver iron. In fetal brain, PAE (p = 0.015) affected total (p < 0.001) and nonheme iron (p < 0.001) such that iron fortification normalized (p = 0.99) the alcohol-mediated reductions in brain iron and nonheme iron. Iron fortification also improved fetal hematologic indices in PAE including hemoglobin, hematocrit, and mean cell volume (ps<0.001). Iron fortification also normalized hepcidin expression in alcohol-exposed maternal and fetal liver. Neither diet nor PAE affected transferrin (Tf) and ferritin (FTN) content in fetal liver, nor Tf or transferrin receptor in fetal brain. However, IF-PAE fetal brains trended to less FTN content (p = 0.074), suggesting greater availability of nonstorage iron. In PAE, hepcidin levels were linearly related to increased liver iron stores and decreased red blood cell count and brain iron.
conclusionsMaternal oral iron fortification mitigated PAE's disruption of fetal iron homeostasis and improved brain iron content, hematologic indices, and hepcidin production in this rat PAE model. Clinical studies show maternal ID substantially enhances fetal vulnerability to PAE, and our work supports increased maternal dietary iron intake may improve fetal iron status in alcohol-exposed pregnancies.
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