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- W1999504039 endingPage "606" @default.
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- W1999504039 abstract "Alcoholic liver disease (ALD) is typically associated with folate deficiency, which is the result of reduced dietary folate intake, intestinal malabsorption, reduced liver uptake and storage, and increased urinary folate excretion. Folate deficiency favors the progression of liver disease through mechanisms that include its effects on methionine metabolism with consequences for DNA synthesis and stability and the epigenetic regulation of gene expression involved in pathways of liver injury. This paper reviews the pathogenesis of ALD with particular focus on ethanol-induced alterations in methionine metabolism, which may act in synergy with folate deficiency to decrease antioxidant defense as well as DNA stability while regulating epigenetic mechanisms of relevant gene expressions. We also review the current evidence available on potential treatments of ALD based on correcting abnormalities in methionine metabolism and the methylation regulation of relevant gene expressions." @default.
- W1999504039 created "2016-06-24" @default.
- W1999504039 creator A5035509372 @default.
- W1999504039 creator A5059222898 @default.
- W1999504039 date "2012-11-08" @default.
- W1999504039 modified "2023-10-15" @default.
- W1999504039 title "Folate, alcohol, and liver disease" @default.
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- W1999504039 doi "https://doi.org/10.1002/mnfr.201200077" @default.
- W1999504039 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3736728" @default.
- W1999504039 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23136133" @default.
- W1999504039 hasPublicationYear "2012" @default.
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