ArticlePloS one2015
Fetal Alcohol Exposure Reduces Dopamine Receptor D2 and Increases Pituitary Weight and Prolactin Production via Epigenetic Mechanisms.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Association of prenatal alcohol exposure with offspring DNA methylation in mammals: a systematic review of the evidence.Clinical epigenetics · 2022Pooled it
- Early Deficient Lactation Differentially Affects Neonatal Thymic Cortical Development and Humoral Immune Responses in Rats.International journal of molecular sciences · 2026Article
- Increased social reward behavior in adolescent male and female rats exposed prenatally to alcohol is associated with altered dopamine receptor expression.Psychoneuroendocrinology · 2026Article
- Epigenetic Regulation of Inflammation by Dopamine in Primary Human Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic regulation of inflammation by dopamine in primary human macrophages.Frontiers in immunology · 2026Article
- DNA Methylation in Alcohol Use Disorder.International journal of molecular sciences · 2023Review
- Total Barley Maiya Alkaloids Prevent Increased Prolactin Levels Caused by Antipsychotic Drugs and Reduce Dopamine Receptor D2Frontiers in pharmacology · 2022Article
- Targeting Epigenetic Mechanisms to Treat Alcohol Use Disorders (AUD).Current pharmaceutical design · 2021Article
- The effect of heavy prenatal alcohol exposure on adolescent body mass index and waist-to-height ratio at 12-13 years.International journal of obesity (2005) · 2021Article
- Epigenetic Impacts of Early Life Stress in Fetal Alcohol Spectrum Disorders Shape the Neurodevelopmental Continuum.Frontiers in molecular neuroscience · 2021Article
- Prenatal Stress Leads to the Altered Maturation of Corticostriatal Synaptic Plasticity and Related Behavioral Impairments Through Epigenetic Modifications of Dopamine D2 Receptor in Mice.Molecular neurobiology · 2021Article
- Transgenerational inheritance of fetal alcohol exposure adverse effects on immune gene interferon-ϒ.Clinical epigenetics · 2020Article
- PRL/microRNA-183/IRS1 Pathway Regulates Milk Fat Metabolism in Cow Mammary Epithelial Cells.Genes · 2020Article
- Altered amygdala DNA methylation mechanisms after adolescent alcohol exposure contribute to adult anxiety and alcohol drinking.Neuropharmacology · 2019Article
- Prenatal alcohol exposure increases the susceptibility to develop aggressive prolactinomas in the pituitary gland.Scientific reports · 2018Article
- The Impact of Traditional Food and Lifestyle Behavior on Epigenetic Burden of Chronic Disease.Global challenges (Hoboken, NJ) · 2017Review
- A combined opiate agonist and antagonist treatment reduces prolactin secreting pituitary tumor growth.Journal of cell communication and signaling · 2017Article
- Gestational Alcohol Exposure Altered DNA Methylation Status in the Developing Fetus.International journal of molecular sciences · 2017Review
- Expression Profiling of DNA Methylation and Transcriptional Repression Associated Genes in Lens Epithelium Cells of Age-Related Cataract.Cellular and molecular neurobiology · 2017Article
- Pathophysiology of the Effects of Alcohol Abuse on the Endocrine System.Alcohol research : current reviews · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Recent evidence indicated that alcohol exposure during the fetal period increases the susceptibility to tumor development in mammary and prostate tissues. Whether fetal alcohol exposure increases the susceptibility to prolactin-producing tumor (prolactinoma) development in the pituitary was studied by employing the animal model of estradiol-induced prolactinomas in Fischer 344 female rats. We employed an animal model of fetal alcohol exposure that simulates binge alcohol drinking during the first two trimesters of human pregnancy and involves feeding pregnant rats with a liquid diet containing 6.7% alcohol during gestational day 7 to day 21. Control rats were pair-fed with isocaloric liquid diet or fed ad libitum with rat chow diet. Adult alcohol exposed and control female offspring rats were used in this study on the day of estrus or after estrogen treatment. Results show that fetal alcohol-exposed rats had increased levels of pituitary weight, pituitary prolactin (PRL) protein and mRNA, and plasma PRL. However, these rats show decreased pituitary levels of dopamine D2 receptor (D2R) mRNA and protein and increased pituitary levels of D2R promoter methylation. Also, they show elevated pituitary mRNA levels of DNA methylating genes (DNMT1, DNMT3b, MeCP2) and histone modifying genes (HDAC2, HDAC4, G9a). When fetal alcohol exposed rats were treated neonatally with a DNA methylation inhibitor 5-Aza deoxycytidine and/or a HDAC inhibitor trichostatin-A their pituitary D2R mRNA, pituitary weights and plasma PRL levels were normalized. These data suggest that fetal alcohol exposure programs the pituitary to increase the susceptibility to the development of prolactinomas possibly by enhancing the methylation of the D2R gene promoter and repressing the synthesis and control of D2R on PRL-producing cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.