ReviewWorld journal of gastroenterology2007
Role of transmethylation reactions in alcoholic liver disease.
Review in World journal of gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed.
- Deletion of phosphatidylethanolamine methyltransferase promotes the spontaneous development of hepatic steatosis, inflammation, and fibrosis in young mice.Clinical science (London, England : 1979) · 2026Article
- Betaine Dietary Supplementation: Healthy Aspects in Human and Animal Nutrition.Antioxidants (Basel, Switzerland) · 2025Review
- Betaine regulates the gut-liver axis: a therapeutic approach for chronic liver diseases.Frontiers in nutrition · 2025Review
- Alcohol- and Low-Iron Induced Changes in Antioxidant and Energy Metabolism Associated with Protein Lys Acetylation.International journal of molecular sciences · 2024Article
- Lipidomic Analysis of Liver Lipid Droplets after Chronic Alcohol Consumption with and without Betaine Supplementation.Biology · 2023Article
- Alcohol: basic and translational research; 15th annual Charles Lieber &1st Samuel French satellite symposium.Experimental and molecular pathology · 2022Review
- Acute ethanol-induced liver injury is prevented by betaine administration.Frontiers in physiology · 2022Article
- Beneficial Effects of Betaine: A Comprehensive Review.Biology · 2021Review
- Genome-wide 5-hydroxymethylcytosine (5hmC) emerges at early stage of in vitro differentiation of a putative hepatocyte progenitor.Scientific reports · 2020Article
- Glutathione deficiency-elicited reprogramming of hepatic metabolism protects against alcohol-induced steatosis.Free radical biology & medicine · 2019Article
- Role of Nutrition in Alcoholic Liver Disease: Summary of the Symposium at the ESBRA 2017 Congress.Biomolecules · 2018Article
- Article
- Emerging Role of One-Carbon Metabolism and DNA Methylation Enrichment on δ-Containing GABAA Receptor Expression in the Cerebellum of Subjects with Alcohol Use Disorders (AUD).The international journal of neuropsychopharmacology · 2017Article
- Prolonged feeding with guanidinoacetate, a methyl group consumer, exacerbates ethanol-induced liver injury.World journal of gastroenterology · 2016Article
- Validated HPLC-Fl method for the analysis of S-adenosylmethionine and S-adenosylhomocysteine biomarkers in human blood.Journal of fluorescence · 2013Article
- Betaine treatment attenuates chronic ethanol-induced hepatic steatosis and alterations to the mitochondrial respiratory chain proteome.International journal of hepatology · 2012Article
- The redox basis of epigenetic modifications: from mechanisms to functional consequences.Antioxidants & redox signaling · 2011Review
- Temporal study of acetaminophen (APAP) and S-adenosyl-L-methionine (SAMe) effects on subcellular hepatic SAMe levels and methionine adenosyltransferase (MAT) expression and activity.Toxicology and applied pharmacology · 2010Article
- Impaired methylation as a novel mechanism for proteasome suppression in liver cells.Biochemical and biophysical research communications · 2010Article
- TNFalpha-dependent hepatic steatosis and liver degeneration caused by mutation of zebrafish S-adenosylhomocysteine hydrolase.Development (Cambridge, England) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alcoholic liver disease is a major health care problem worldwide. Findings from many laboratories, including ours, have demonstrated that ethanol feeding impairs several of the many steps involved in methionine metabolism. Ethanol consumption predominantly results in a decrease in the hepatocyte level of S-adenosylmethionine and the increases in two toxic metabolites, homocysteine and S-adenosylhomocysteine. These changes, in turn, result in serious functional consequences which include decreases in essential methylation reactions via inhibition of various methyltransferases. Of particular interest to our laboratory is the inhibition of three important enzymes, phosphatidylethanolamine methyltransferase, isoprenylcysteine carboxyl methyltransferase and protein L-isoaspartate methyltransferase. Decreased activity of these enzymes results in increased fat deposition, increased apoptosis and increased accumulation of damaged proteins-all of which are hallmark features of alcoholic liver injury. Of all the therapeutic modalities available, betaine has been shown to be the safest, least expensive and most effective in attenuating ethanol-induced liver injury. Betaine, by virtue of aiding in the remethylation of homocysteine, removes both toxic metabolites (homocysteine and S-adenosylhomocysteine), restores S-adenosylmethionine level, and reverses steatosis, apoptosis and damaged proteins accumulation. In conclusion, betaine appears to be a promising therapeutic agent in relieving the methylation and other defects associated with alcoholic abuse.
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