ArticleAlcoholism, clinical and experimental research2017
Chronic Alcohol Exposure Differentially Alters One-Carbon Metabolism in Rat Liver and Brain.
Article in Alcoholism, clinical and experimental research, 2017. 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, 46 citations in OpenAlex.
- Unraveling the Time-Dependent Effects of Ethanol on Liver Disease: Insights From a Mice Model.Biotechnology and applied biochemistry · 2026Article
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- Ethanol exposure promotes tumor cell migration and angiogenesis in a mouse model of glioblastoma.Alcohol (Fayetteville, N.Y.) · 2025Article
- Effects of four-week lasting aerobic treadmill training on hepatic injury biomarkers, oxidative stress parameters, metabolic enzymes activities and histological characteristics in liver tissue of hyperhomocysteinemic rats.Molecular and cellular biochemistry · 2025Article
- Effect of Lead Exposure and Lifestyle Factors on Methylation Index Markers Among Pb-Exposed Workers.Biological trace element research · 2025Article
- Epigenetic drugs and psychedelics as emerging therapies for alcohol use disorder: insights from preclinical studies.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- DNA Methylation in Alcohol Use Disorder.International journal of molecular sciences · 2023Review
- A ketogenic diet alters mTOR activity, systemic metabolism and potentially prevents collagen degradation associated with chronic alcohol consumption in mice.Metabolomics : Official journal of the Metabolomic Society · 2023Article
- Mitigating the detrimental developmental impact of early fetal alcohol exposure using a maternal methyl donor-enriched diet.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Is DNA methylation in the brain a mechanism of alcohol use disorder?Frontiers in behavioral neuroscience · 2023Review
- Advances in DNA, histone, and RNA methylation mechanisms in the pathophysiology of alcohol use disorder.Advances in drug and alcohol research · 2023Review
- Impact of excessive alcohol abuse on age prediction using the VISAGE enhanced tool for epigenetic age estimation in blood.International journal of legal medicine · 2021Article
- Targeting Epigenetic Mechanisms to Treat Alcohol Use Disorders (AUD).Current pharmaceutical design · 2021Article
- Persistence of cerebellar ataxia during chronic ethanol exposure is associated with epigenetic up-regulation of Fmr1 gene expression in rat cerebellum.Alcoholism, clinical and experimental research · 2021Article
- Toxic and Teratogenic Effects of Prenatal Alcohol Exposure on Fetal Development, Adolescence, and Adulthood.International journal of molecular sciences · 2021Review
- Review
- Epigenetic landscape of stress surfeit disorders: Key role for DNA methylation dynamics.International review of neurobiology · 2021Article
- Glutathione Protects the Developing Heart from Defects and Global DNA Hypomethylation Induced by Prenatal Alcohol Exposure.Alcoholism, clinical and experimental research · 2021Article
- Methionine metabolism in chronic liver diseases: an update on molecular mechanism and therapeutic implication.Signal transduction and targeted therapy · 2020Review
- Epigenetic mechanisms underlying pathobiology of alcohol use disorder.Current pathobiology reports · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEpigenetic mechanisms such as DNA methylation play an important role in regulating the pathophysiology of alcoholism. Chronic alcohol exposure leads to behavioral changes as well as decreased expression of genes associated with synaptic plasticity. In the liver, it has been documented that chronic alcohol exposure impairs methionine synthase (Ms) activity leading to a decrease in S-adenosyl methionine/S-adenosyl homocysteine (SAM/SAH) ratio which results in DNA hypomethylation; however, it is not known whether similar alterations of SAM and SAH levels are also produced in brain.
methodsMale adult Sprague Dawley rats were fed chronically with Lieber-DeCarli ethanol (EtOH) (9% v/v) or control diet. The EtOH-diet-fed rats were withdrawn for 0 and 24 hours. The cerebellum and liver tissues were dissected and used to investigate changes in one-carbon metabolism, SAM, and SAH levels.
resultsWe found that chronic EtOH exposure decreased SAM levels, SAM/SAH ratio, Ms, methylene tetrahydrofolate reductase, and betaine homocysteine methyltransferase (Bhmt) expression and increased methionine adenosyltransferase-2b (Mat2b) but not Mat2a expression in the liver. In contrast, chronic EtOH exposure decreased SAH levels, increased SAM/SAH ratio and the expression of Mat2a and S-adenosyl homocysteine hydrolase, while the levels of SAM or Bhmt expression in cerebellum remained unaltered. However, in both liver and cerebellum, chronic EtOH exposure decreased the expression of Ms and increased Mat2b expression. All chronic EtOH-induced changes of one-carbon metabolism in cerebellum, but not liver, returned to near-normal levels during EtOH withdrawal.
conclusionsThese results indicate a decreased "methylation index" in liver and an increased "methylation index" in cerebellum. The opposing changes of the "methylation index" suggest altered DNA methylation in liver and cerebellum, thus implicating one-carbon metabolism in the pathophysiology of alcoholism.
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