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

Date Published: , 2017

Publisher: National Institute on Alcohol Abuse and Alcoholism

Author(s): Shirish Barve, Shao-Yu Chen, Irina Kirpich, Walter H. Watson, Craig McClain.

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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.

Partial Text

In virtually every cell type, epigenetic mechanisms—that is, modifications to the genetic material that do not alter the DNA sequence—play a critical role in both the physiologic and pathologic regulation of gene expression. These mechanisms, which involve chromatin remodeling initiated by posttranslational modifications of histones and changes in DNA methylation status, can activate or deactivate gene transcription. The proteins that are involved in posttranslational histone modifications and DNA methylation changes require a variety of cofactors, including acetyl coenzyme A, S-adenosylmethionine (SAM), nicotinamide adenine dinucleotide, and zinc (Moghe et al. 2011). A person’s nutritional status can significantly influence the availability of these cofactors and, consequently, epigenetic mechanisms, gene expression, and disease pathogenesis. Chronic alcohol consumption is known to affect nutritional status at many levels, including nutrient intake, absorption, utilization, and excretion, causing nutritional disturbances and deficiencies in these cofactors. Research has determined that alcohol-induced nutrient fluctuations can impact transcriptional activity and expression of genes by modulating epigenetic parameters, including histone modifications and DNA methylation (Moghe et al. 2011; Zakhari 2013). Hence, in people with AUD, the combined effects of alcohol metabolism and compromised nutrition are likely to influence epigenetic mechanisms, gene expression, and disease pathogenesis involving intestinal barrier dysfunction, immune suppression, and organ injury.

Alterations in nutrition and nutrient metabolism are common in chronic alcoholics and may contribute to alcohol-induced organ injury. Conversely, nutritional supplementation may prevent the development or attenuate the progression of alcohol-induced organ injury. Nutritional supplements may alleviate a nutrient deficiency or act as pharmacologic agents. Such nutrients also may have epigenetic effects. Nutritional supplementation as a therapy is especially attractive because there are currently no Food and Drug Administration–approved therapies for most forms of alcohol-induced organ injury and nutrient supplements are readily available.

 

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