ArticleAlcoholism, clinical and experimental research2013
Binge ethanol-induced HDAC3 down-regulates Cpt1α expression leading to hepatic steatosis and injury.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- [Histone deacetylases and alcohol-related liver disease].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Epigenetic signatures and cellular stress response pathways in metabolic dysfunction-associated steatotic liver disease: a personalized medicine perspective.Frontiers in physiology · 2026Review
- Alcohol addiction and Alzheimer's disease: a molecular collision course.Translational psychiatry · 2025Review
- Review
- Mechanism and Therapeutic Opportunities of Histone Modifications in Chronic Liver Disease.Frontiers in pharmacology · 2021Review
- Epigenetic mechanisms underlying pathobiology of alcohol use disorder.Current pathobiology reports · 2020Article
- Tributyrin Inhibits Ethanol-Induced Epigenetic Repression of CPT-1A and Attenuates Hepatic Steatosis and Injury.Cellular and molecular gastroenterology and hepatology · 2020Article
- Targeting Epigenetic Mechanisms to Alleviate Alcoholic Steatosis.Cellular and molecular gastroenterology and hepatology · 2020Article
- Binge Alcohol Is More Injurious to Liver in Female than in Male Rats: Histopathological, Pharmacologic, and Epigenetic Profiles.The Journal of pharmacology and experimental therapeutics · 2019Article
- Epigenetic Mechanisms in Hepatic Stellate Cell Activation During Liver Fibrosis and Carcinogenesis.International journal of molecular sciences · 2019Review
- In Vivo Metabolic Tracing Demonstrates the Site-Specific Contribution of Hepatic Ethanol Metabolism to Histone Acetylation.Alcoholism, clinical and experimental research · 2018Article
- Article
- Alcohol Feeding in Mice Promotes Colonic Hyperpermeability and Changes in Colonic Organoid Stem Cell Fate.Alcoholism, clinical and experimental research · 2017Article
- Age-related alterations in histone deacetylase expression in Purkinje neurons of ethanol-fed rats.Brain research · 2017Article
- Alcohol-induced miR-155 and HDAC11 inhibit negative regulators of the TLR4 pathway and lead to increased LPS responsiveness of Kupffer cells in alcoholic liver disease.Journal of leukocyte biology · 2017Article
- Epigenetics and Liver Fibrosis.Cellular and molecular gastroenterology and hepatology · 2017Review
- Dysregulation of hepatic cAMP levels via altered Pde4b expression plays a critical role in alcohol-induced steatosis.The Journal of pathology · 2016Article
- Article
- In Vivo Acute on Chronic Ethanol Effects in Liver: A Mouse Model Exhibiting Exacerbated Injury, Altered Metabolic and Epigenetic Responses.Biomolecules · 2015Article
- Epigenetic histone modifications in a clinically relevant rat model of chronic ethanol-binge-mediated liver injury.Hepatology international · 2014Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRecently, we have demonstrated that acute alcohol exposure due to binge drinking leads to hepatic steatosis with the deregulation of hepatic histone deacetylase (HDAC) expression. Various class I, II, and IV HDACs were down-regulated, whereas expression of HDAC3 was solely up-regulated. Hence, in the present work, we specifically examined the mechanistic role of HDAC3 in the development of hepatic steatosis occurring in response to binge alcohol administration.
methodsC57BL/6 mice were gavaged 3 times with ethanol (EtOH) at a dose of 4.5 g/kg. HDAC inhibitor, Trichostatin A (TSA) was simultaneously injected intraperitoneally at a dose of 1 mg/kg. Hepatic steatosis, injury, expression of HDAC3 and carnitine palmitoyltransferase 1α (CPT1α) were evaluated. HDAC3 and histone H3 acetylation levels at the Cpt1α promoter were analyzed by chromatin immunoprecipitation (ChIP).
resultsThe binge EtOH-mediated increase in HDAC3 was prevented by simultaneous administration of HDAC inhibitor, TSA, which markedly attenuated hepatic steatosis and injury. Importantly, HDAC3 inhibition was able to normalize the down-regulation of Cpt1α expression. Causal role of HDAC3 in the transcriptional repression of Cpt1α was demonstrated by increased HDAC3 binding at the thyroid receptor element site in the Cpt1α distal promoter region. Further, a resultant decrease in the transcriptionally permissive histone H3 lysine 9 acetylation in the proximal promoter region near the transcriptional start site was observed. Notably, TSA treatment reduced HDAC3 binding and increased H3K9 acetylation at Cpt1α promoter leading to increased Cpt1α expression. These molecular events resulted in attenuation of binge alcohol-induced hepatic steatosis.
conclusionsThese findings provide insights into potential epigenetic mechanisms underlying transcriptional regulation of Cpt1α in the hepatic steatosis occurring in response to binge EtOH administration.
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