Abstract
Ethanol consumption is responsible for chronic diseases worldwide, particularly in developed Western countries, as well as in parts of Asia. Ethanol can be metabolized by two distinct pathways: oxidative and nonoxidative alcohol metabolism, leading to the production of acetaldehyde, acetate, reactive oxygen species (ROS), and fatty acid ethyl esters (FAEE), to name a few. Elevated levels of ROS and the NADH/NAD ratio, resulting from heavy alcohol consumption, are also associated with epigenetic changes of DNA, and histone mechanisms leading to their modification and reduced methylation. Upregulation and high expression of various genes in alcoholic individuals are the main effects resulting from epigenetic changes. For example, P90RSK, osteopontin, TGF-β, and PNPLA3 are some of the genes that are overexpressed in liver fibrogenesis, whereas PPAR-α and SREBP-1c are transcriptional factors involved in the metabolism of lipids, and affected by heavy alcohol consumption. This chapter describes the metabolism of ethanol, and the epigenetic changes of its metabolites in health and disease.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
