Effects of Ethanol on Amino Acid and Protein Metabolism

Adibi, Siamak A.; Baraona, Enrique; Lieber, Charles S.

doi:10.1007/978-1-4615-3320-7_5

Cited by 4 publications

(1 citation statement)

References 214 publications

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“…Three of the genes the CpGs map to, which have already been reported to be associated to alcohol consumption in previous EWAS efforts 9,11,15,42 , are part of the aminotransferase family ( SLC7A11, PSAT1, and SLC43A1 ). Alcohol is known to disrupt protein metabolism and amino acid transport 43,44 and SLC7A11 ’s role in the liver– brain-axis in alcohol-related disease and potential as a future drug target has been described 11 . One of our strongest CpG associations (cg26774981) mapped to the SRPK2 gene, a kinase that controls alternative splicing.…”

Section: Discussionmentioning

confidence: 99%

Blood-based DNA methylation study of alcohol consumption

Bernabeu,

Chybowska,

Kresovich

et al. 2024

Preprint

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Alcohol consumption is an important risk factor for multiple diseases. It is typically assessed via self-report, which is open to measurement error and bias. Instead, molecular data such as blood-based DNA methylation (DNAm) could be used to derive a more objective measure of alcohol consumption by incorporating information from cytosine-phosphate-guanine (CpG) sites known to be linked to the trait. Here, we explore the epigenetic architecture of self-reported weekly units of alcohol consumption in the Generation Scotland study. We first create a blood-based epigenetic score (EpiScore) of alcohol consumption using elastic net penalised linear regression. We explore the effect of pre-filtering for CpG features ahead of elastic net, as well as differential patterns by sex and by units consumed in the last week relative to an average week. The final EpiScore was trained on 16,717 individuals and tested in four external cohorts: the Lothian Birth Cohorts (LBC) of 1921 and 1936, the Sister Study, and the Avon Longitudinal Study of Parents and Children (total N across studies > 10,000). The maximum Pearson correlation between the EpiScore and self-reported alcohol consumption within cohort ranged from 0.41 to 0.53. In LBC1936, higher EpiScore levels had significant associations with poorer global brain imaging metrics, whereas self-reported alcohol consumption did not. Finally, we identified two novel CpG loci via a Bayesian penalized regression epigenome-wide association study (EWAS) of alcohol consumption. Together, these findings show how DNAm can objectively characterize patterns of alcohol consumption that associate with brain health, unlike self-reported estimates.

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Section: Discussionmentioning

confidence: 99%

Blood-based DNA methylation study of alcohol consumption

Bernabeu,

Chybowska,

Kresovich

et al. 2024

Preprint

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Leucine metabolism during chronic ethanol consumption

1993

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Chronic Ethanol Consumption Affects Glutathione Status in Rat Liver , ,

Kim

Chun

et al. 1998

The Journal of Nutrition

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There is no consensus yet on the role of oxidative stress in the nutritional outcome of chronic ethanol feeding and the status of cellular antioxidative defense systems against ethanol toxicity. In this study, chronic alcohol consumption in humans was reproduced in Sprague-Dawley rats to investigate the effect of ethanol ingestion on the regulation of oxidative stress in liver with a special focus on glutathione. Adult male rats were given 36% of total energy as alcohol in the Lieber-DeCarli liquid diet for 6 wk. The control group was pair-fed the diet containing isocaloric dextrin-maltose instead of ethanol. Chronic ethanol ingestion enhanced expression of cytochrome P450 II E1 in the liver, but did not significantly alter either the level of hepatic thiobarbituric acid reactive substances or the carbonyl group content of proteins. The hepatic concentrations of total and reduced glutathione and the activities of catalase, glutathione reductase and glutathione S-transferase were significantly higher in the ethanol group than in the control group. The activities of glutathione peroxidase and glucose-6-phosphate dehydrogenase were significantly lower in the ethanol group than in controls. Chronic ethanol consumption by well-nourished rats for 6 wk increased enzyme activities related to the recycling and utilization of glutathione in the liver. Such an enhancement in the activities of the hepatic antioxidative defense system may be one of the protective mechanisms of the body against oxidative tissue damage caused by ethanol-induced free radicals.

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Effects of Ethanol on Amino Acid and Protein Metabolism

Cited by 4 publications

References 214 publications

Blood-based DNA methylation study of alcohol consumption

Blood-based DNA methylation study of alcohol consumption

Leucine metabolism during chronic ethanol consumption

Chronic Ethanol Consumption Affects Glutathione Status in Rat Liver , ,

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