ArticleThe Journal of nutrition2016
Prenatal Alcohol Exposure Alters Fetal Iron Distribution and Elevates Hepatic Hepcidin in a Rat Model of Fetal Alcohol Spectrum Disorders.
Article in The Journal of nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Alcohol Exposure May Increase Prenatal Choline Needs Through Redirection of Choline into Lipid Synthesis Rather than Methyl Donation.Metabolites · 2025Article
- Nonconceptus Mechanisms of Prenatal Alcohol Exposure That Disrupt Embryo-Fetal Development: An Integrative View.Alcohol research : current reviews · 2025Review
- Effects of prenatal iron deficiency on neurological development and related disorders in offspring.Frontiers in nutrition · 2025Review
- Contribution of ferritin and zinc to adverse infant outcomes among pregnancies with prenatal alcohol exposure in South Africa.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- Clinical Diagnosis and Management of Fetal Alcohol Spectrum Disorder and Sensory Processing Disorder in Children.Children (Basel, Switzerland) · 2024Review
- Effect of docosahexaenoic acid and olive oil supplementation on pup weight in alcohol-exposed pregnant rats.Frontiers in pediatrics · 2024Article
- Fetal anemia and elevated hepcidin in a mouse model of fetal alcohol spectrum disorder.Pediatric research · 2023Article
- Article
- Microbiota and nutrition as risk and resiliency factors following prenatal alcohol exposure.Frontiers in neuroscience · 2023Review
- Untargeted Metabolome Analysis of Alcohol-Exposed Pregnancies Reveals Metabolite Differences That Are Associated with Infant Birth Outcomes.Nutrients · 2022Article
- 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
- Effects of nutrition and gestational alcohol consumption on fetal growth and development.Nutrition reviews · 2022Review
- Gestational Iron Supplementation Improves Fetal Outcomes in a Rat Model of Prenatal Alcohol Exposure.Nutrients · 2022Article
- Multifactorial Genetic and Environmental Hedgehog Pathway Disruption Sensitizes Embryos to Alcohol-Induced Craniofacial Defects.Alcoholism, clinical and experimental research · 2020Article
- An interaction between fetal sex and placental weight and efficiency predicts intrauterine growth in response to maternal protein insufficiency and gestational exposure window in a mouse model of FASD.Biology of sex differences · 2020Article
- 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
Corrections and comments
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Authors and funding
4 authors at 1 institution in 3 countries.
Funding
Abstract
backgroundPrenatal alcohol exposure (PAE) causes neurodevelopmental disabilities, and gestational iron deficiency (ID) selectively worsens learning and neuroanatomical and growth impairments in PAE. It is unknown why ID worsens outcomes in alcohol-exposed offspring.
objectiveWe hypothesized that PAE alters maternal-fetal iron distribution or its regulation.
methodsNulliparous, 10-wk-old, Long-Evans rats were mated and then fed iron-sufficient (100 mg Fe/kg) or iron-deficient (≤4 mg Fe/kg) diets. On gestational days 13.5-19.5, dams received either 5.0 g ethanol/kg body weight (PAE) or isocaloric maltodextrin by oral gavage. On gestational day 20.5, maternal and fetal clinical blood counts, tissue mineral and iron transport protein concentrations, and hepatic hepcidin mRNA expression were determined.
resultsIn fetal brain and liver (P < 0.001) and in maternal liver (P < 0.005), ID decreased iron (total and nonheme) and ferritin content by nearly 200%. PAE reduced fetal bodyweight (P < 0.001) and interacted with ID (P < 0.001) to reduce it by an additional 20%. Independent of maternal iron status, PAE increased fetal liver iron (30-60%, P < 0.001) and decreased brain iron content (total and nonheme, 15-20%, P ≤ 0.050). ID-PAE brains had lower ferritin, transferrin, and transferrin receptor content (P ≤ 0.002) than ID-maltodextrin brains. PAE reduced fetal hematocrit, hemoglobin, and red blood cell numbers (P < 0.003) independently of iron status. Unexpectedly, and also independent of iron status, PAE increased maternal and fetal hepatic hepcidin mRNA expression >300% (P < 0.001).
conclusionsPAE altered fetal iron distribution independent of maternal iron status in rats. The elevated iron content of fetal liver suggests that PAE may have limited iron availability for fetal erythropoiesis and brain development. Altered fetal iron distribution may partly explain why maternal ID substantially worsens growth and behavioral outcomes in PAE.
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