ArticleToxicology and applied pharmacology2015
Developmental bisphenol A (BPA) exposure leads to sex-specific modification of hepatic gene expression and epigenome at birth that may exacerbate high-fat diet-induced hepatic steatosis.
Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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81 citing papers in PubMed, 172 citations in OpenAlex.
- Prenatal Bisphenol A Exposure and Sex-Differentiated Childhood BMI Over Time: A Longitudinal Korean Cohort Study.Pediatric obesity · 2026Article
- Transcriptomic and epigenetic alterations in aging-related genes in the medaka liver due to ancestral BPA exposure.Journal of the Endocrine Society · 2026Article
- Serpina3c protects against metabolic dysfunction-associated steatotic liver disease in offspring induced by prenatal prednisone exposure.Signal transduction and targeted therapy · 2026Article
- Article
- Ancestral bisphenol A exposure led to non-alcoholic fatty liver disease and sex-specific alterations in proline and bile metabolism pathways in the liver.Environmental toxicology and chemistry · 2025Article
- Review
- Stable Transmission of DNA Methylation Epimutations from Germlines to the Liver and Their Association with Fatty Liver Disease in Medaka.Research square · 2025Article
- Bisphenols exposure and non-alcoholic fatty liver disease: from environmental trigger to molecular pathogenesis.Frontiers in endocrinology · 2025Review
- Early-Life Exposure to Bisphenol A Damaged Pancreas That May Increase Offspring Sensitivity to High-Fat Diets.Journal of toxicology · 2025Article
- Medaka liver developed Human NAFLD-NASH transcriptional signatures in response to ancestral bisphenol A exposure.Research square · 2024Article
- Sex-specific expression of the human NAFLD-NASH transcriptional signatures in the liver of medaka with a history of ancestral bisphenol A exposure.bioRxiv : the preprint server for biology · 2024Article
- Bombesin-like receptor 3 expression induced by bisphenol A is likely associated with reduced cell proliferation by inhibiting DNA synthesis and inducing inflammation in liver cells.Molecular biology reports · 2024Article
- The Role of Endocrine Disruptors Bisphenols and Phthalates in Obesity: Current Evidence, Perspectives and Controversies.International journal of molecular sciences · 2024Review
- Article
- Bisphenol A (BPA) and Cardiovascular or Cardiometabolic Diseases.Journal of xenobiotics · 2023Review
- Epidemiologic Advances Generated by the Human Health Exposure Analysis Resource Program.Current epidemiology reports · 2023Article
- An Overview of the Health Effects of Bisphenol A from a One Health Perspective.Animals : an open access journal from MDPI · 2023Review
- The effects of trans fat diet intake on metabolic parameters and pancreatic tissue in offspring of prenatal bisphenol A exposed rats.Scientific reports · 2023Article
- Epigenetic Histone Methylation of PPARγ and CPT1A Signaling Contributes to Betahistine Preventing Olanzapine-Induced Dyslipidemia.International journal of molecular sciences · 2023Article
- Sex, Nutrition, and NAFLD: Relevance of Environmental Pollution.Nutrients · 2023Review
21 more citing papers are in PubMed but not listed here.
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7 authors at 1 institution in 1 country.
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Abstract
Developmental bisphenol A (BPA) exposure increases adulthood hepatic steatosis with reduced mitochondrial function. To investigate the potential epigenetic mechanisms behind developmental BPA-induced hepatic steatosis, pregnant Sprague-Dawley rats were dosed with vehicle (oil) or BPA (100μg/kg/day) from gestational day 6 until postnatal day (PND) 21. After weaning, offspring were either challenged with a high-fat (HF; 45% fat) or remained on a control (C) diet until PND110. From PND60 to 90, both BPA and HF diet increased the fat/lean ratio in males only, and the combination of BPA and HF diet appeared to cause the highest ratio. On PND110, Oil-HF, BPA-C, and BPA-HF males had higher hepatic lipid accumulation than Oil-C, with microvesicular steatosis being marked in the BPA-HF group. Furthermore, on PND1, BPA increased and modified hepatic triglyceride (TG) and free fatty acid (FFA) compositions in males only. In PND1 males, BPA increased hepatic expression of FFA uptake gene Fat/Cd36, and decreased the expression of TG synthesis- and β-oxidation-related genes (Dgat, Agpat6, Cebpα, Cebpβ, Pck1, Acox1, Cpt1a, Cybb). BPA altered DNA methylation and histone marks (H3Ac, H4Ac, H3Me2K4, H3Me3K36), and decreased the binding of several transcription factors (Pol II, C/EBPβ, SREBP1) within the male Cpt1a gene, the key β-oxidation enzyme. In PND1 females, BPA only increased the expression of genes involved in FFA uptake and TG synthesis (Lpl, Fasn, and Dgat). These data suggest that developmental BPA exposure alters and reprograms hepatic β-oxidation capacity in males, potentially through the epigenetic regulation of genes, and further alters the response to a HF diet.
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