Development, Prevention, and Treatment of Alcohol-Induced Organ Injury: The Role of Nutrition

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Abstract

Alcohol and nutrition have the potential to interact at multiple levels. For example, heavy alcohol consumption can interfere with normal nutrition, resulting in overall malnutrition or in deficiencies of important micronutrients, such as zinc, by reducing their absorption or increasing their loss. Interactions between alcohol consumption and nutrition also can affect epigenetic regulation of gene expression by influencing multiple regulatory mechanisms, including methylation and acetylation of histone proteins and DNA. These effects may contribute to alcohol-related organ or tissue injury. The impact of alcohol–nutrition interactions has been assessed for several organs and tissues, including the intestine, where heavy alcohol use can increase intestinal permeability, and the liver, where the degree of malnutrition can be associated with the severity of liver injury and liver disease. Alcohol–nutrition interactions also play a role in alcohol-related lung injury, brain injury, and immune dysfunction. Therefore, treatment involving nutrient supplementation (e.g., with zinc or S-adenosylmethionine) may help prevent or attenuate some types of alcohol-induced organ damage.

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Resolvins and protectins in inflammation resolution.

Charles Serhan, Nicos Petasis (2011)

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Metagenomic Analyses of Alcohol Induced Pathogenic Alterations in the Intestinal Microbiome and the Effect of Lactobacillus rhamnosus GG Treatment

Lara Bull-Otterson, Wenke Feng, Irina Kirpich … (2013)

Enteric dysbiosis plays an essential role in the pathogenesis of alcoholic liver disease (ALD). Detailed characterization of the alterations in the gut microbiome is needed for understanding their pathogenic role in ALD and developing effective therapeutic approaches using probiotic supplementation. Mice were fed liquid Lieber-DeCarli diet without or with alcohol (5% v/v) for 6 weeks. A subset of mice were administered the probiotic Lactobacillus rhamnosus GG (LGG) from 6 to 8 weeks. Indicators of intestinal permeability, hepatic steatosis, inflammation and injury were evaluated. Metagenomic analysis of the gut microbiome was performed by analyzing the fecal DNA by amplification of the V3–V5 regions of the 16S rRNA gene and large-scale parallel pyrosequencing on the 454 FLX Titanium platform. Chronic ethanol feeding caused a decline in the abundance of both Bacteriodetes and Firmicutes phyla, with a proportional increase in the gram negative Proteobacteria and gram positive Actinobacteria phyla; the bacterial genera that showed the biggest expansion were the gram negative alkaline tolerant Alcaligenes and gram positive Corynebacterium. Commensurate with the qualitative and quantitative alterations in the microbiome, ethanol caused an increase in plasma endotoxin, fecal pH, hepatic inflammation and injury. Notably, the ethanol-induced pathogenic changes in the microbiome and the liver were prevented by LGG supplementation. Overall, significant alterations in the gut microbiome over time occur in response to chronic alcohol exposure and correspond to increases in intestinal barrier dysfunction and development of ALD. Moreover, the altered bacterial communities of the gut may serve as significant therapeutic target for the prevention/treatment of chronic alcohol intake induced intestinal barrier dysfunction and liver disease.

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Increased intestinal permeability to macromolecules and endotoxemia in patients with chronic alcohol abuse in different stages of alcohol-induced liver disease.

Alexandr Parlesak, Christian Schäfer, Tatjana Schütz … (2000)

No information is yet available about the influence of alcohol abuse on the translocation of larger molecules (Mr>1200) through the intestinal mucosa in man. The present study aimed to determine the intestinal permeability to macromolecules in patients with chronic alcohol abuse and mild to more advanced stages of liver disease, and to measure the concentration of endotoxins in the plasma, as these compounds derive from the intestinal flora and are suspected to contribute to the development of alcoholic liver disease (ALD). The permeability to polyethylene glycol Mr 400, Mr 1500, Mr 4000, and Mr 10,000 and endotoxin plasma concentrations were measured in 54 patients with alcoholic liver disease, 19 of them with cirrhosis, and in 30 non-alcoholic healthy controls. Permeability to polyethylene glycol Mr 400 was found to be unchanged in patients with ALD in comparison to healthy controls, whereas polyethylene glycol Mr 1500 and Mr 4000 were recovered in about twice as high concentrations in the urine of ALD patients (p<0.01). Polyethylene glycol Mr 10,000 was detected significantly less frequently in urine from healthy controls (0/30) than in urine of patients with alcoholic liver disease (20/54, p<0.01). Endotoxin concentrations in the plasma of alcoholics were increased more than 5-fold compared to healthy controls (p<0.01). The results of this study indicate that alcohol abuse impairs the function of the intestinal barrier, which might enhance the translocation of bacterial toxins, thereby contributing to inflammatory processes in alcoholic liver disease.

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Author and article information

Journal

Journal ID (nlm-ta): Alcohol Res

Journal ID (iso-abbrev): Alcohol Res

Title: Alcohol Research : Current Reviews

Publisher: National Institute on Alcohol Abuse and Alcoholism

ISSN (Print): 2168-3492

ISSN (Electronic): 2169-4796

Publication date (Print): 2017

Volume: 38

Issue: 2

Pages: 289-302

Affiliations

Shirish Barve, Ph.D., is a Professor in the Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and a Professor in the Department of Pharmacology and Toxicology; Shao-Yu Chen, Ph.D., is a Professor in the Department of Pharmacology and Toxicology; Irina Kirpich, Ph.D., and Walter H. Watson, Ph.D., both are Assistant Professors in the Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and in the Department of Pharmacology and Toxicology; all at the University of Louisville School of Medicine, Louisville, Kentucky. Craig McClain, M.D., is a Professor in the Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and a Professor in the Department of Pharmacology and Toxicology at the University of Louisville School of Medicine, Louisville, Kentucky, and a Staff Physician at the Robley Rex Veterans Medical Center, Louisville, Kentucky

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Publisher ID: arcr-38-2-289

PMC ID: 5513692

PubMed ID: 28988580

SO-VID: 45d804a3-40ba-4f35-a71b-cc6c7594b390

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Unless otherwise noted in the text, all material appearing in this journal is in the public domain and may be reproduced without permission. Citation of the source is appreciated.

Development, Prevention, and Treatment of Alcohol-Induced Organ Injury: The Role of Nutrition

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Karger: Nutrition and Dietetics

Most cited references 50

Resolvins and protectins in inflammation resolution.

Metagenomic Analyses of Alcohol Induced Pathogenic Alterations in the Intestinal Microbiome and the Effect of Lactobacillus rhamnosus GG Treatment

Increased intestinal permeability to macromolecules and endotoxemia in patients with chronic alcohol abuse in different stages of alcohol-induced liver disease.

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