ArticlePloS one2010
Paternal genetic contribution influences fetal vulnerability to maternal alcohol consumption in a rat model of fetal alcohol spectrum disorder.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Transgenerational Abnormalities Induced by Paternal Preconceptual Alcohol Drinking: Findings from Humans and Animal Models.Current neuropharmacology · 2022Review
- Thyroid Function in Pregnant Women With Moderate to Severe Alcohol Consumption Is Related to Infant Developmental Outcomes.Frontiers in endocrinology · 2018Article
- Modeling Fetal Alcohol Spectrum Disorder: Validating an Ex Vivo Primary Hippocampal Cell Culture System.Alcoholism, clinical and experimental research · 2016Article
- Thyroxine administration prevents matrilineal intergenerational consequences of in utero ethanol exposure in rats.Hormones and behavior · 2016Article
- Hypothesis: genetic and epigenetic risk factors interact to modulate vulnerability and resilience to FASD.Frontiers in genetics · 2014Article
- Low-dose thyroxine attenuates autism-associated adverse effects of fetal alcohol in male offspring's social behavior and hippocampal gene expression.Alcoholism, clinical and experimental research · 2013Article
- Association of maternal and nutrient supply line factors with DNA methylation at the imprinted IGF2/H19 locus in multiple tissues of newborn twins.Epigenetics · 2013Article
- Excess folate during adolescence suppresses thyroid function with permanent deficits in motivation and spatial memory.Genes, brain, and behavior · 2012Article
- Strain-specific vulnerability to alcohol exposure in utero via hippocampal parent-of-origin expression of deiodinase-III.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Candidate placental biomarkers for intrauterine alcohol exposure.Alcoholism, clinical and experimental research · 2011Article
- Focus on: epigenetics and fetal alcohol spectrum disorders.Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFetal alcohol exposure causes in the offspring a collection of permanent physiological and neuropsychological deficits collectively termed Fetal Alcohol Spectrum Disorder (FASD). The timing and amount of exposure cannot fully explain the substantial variability among affected individuals, pointing to genetic influences that mediate fetal vulnerability. However, the aspects of vulnerability that depend on the mother, the father, or both, are not known. METHODOLOGY/PRINCIPAL
findingsUsing the outbred Sprague-Dawley (SD) and inbred Brown Norway (BN) rat strains as well as their reciprocal crosses, we administered ethanol (E), pair-fed (PF), or control (C) diets to the pregnant dams. The dams' plasma levels of free thyroxine (fT4), triiodothyronine (T3), free T3 (fT3), and thyroid stimulating hormone (TSH) were measured to elucidate potential differences in maternal thyroid hormonal environment, which affects specific aspects of FASD. We then compared alcohol-exposed, pair fed, and control offspring of each fetal strain on gestational day 21 (G21) to identify maternal and paternal genetic effects on bodyweight and placental weight of male and female fetuses.
conclusionsSD and BN dams exhibited different baseline hypothalamic-pituitary-thyroid function. Moreover, the thyroid function of SD dams was more severely affected by alcohol consumption while that of BN dams was relatively resistant. This novel finding suggests that genetic differences in maternal thyroid function are one source of maternal genetic effects on fetal vulnerability to FASD. The fetal vulnerability to decreased bodyweight after alcohol exposure depended on the genetic contribution of both parents, not only maternal contribution as previously thought. In contrast, the effect of maternal alcohol consumption on placental weight was consistent and not strain-dependent. Interestingly, placental weight in fetuses with different paternal genetic contributions exhibited opposite responses to caloric restriction (pair feeding). In summary, these novel findings demonstrate both maternal and paternal genetic contributions to in utero vulnerability to alcohol, refining our understanding of the genetically-based heterogeneity seen in human FASD.
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