Journal
BIOMEDICINES
Volume 9, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines9091256
Keywords
epigenome; nonalcoholic fatty liver disease (NAFLD); metabolic associated fatty liver disease (MAFLD); nutrition; DNA methylation; histone modifications; gene expression; hepatic steatosis
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Nonalcoholic fatty liver disease (NAFLD) is a condition characterized by the accumulation of fat in liver cells, increasingly becoming the leading cause of metabolic disorders linked with genetics, lifestyle, diet, and microbiota. Epigenetic processes play a key role in gene expression and NAFLD pathogenesis. Research suggests innovative epigenetic-based strategies for early prevention and treatment of NAFLD.
Nonalcoholic fatty liver disease (NAFLD) refers to the pathologic buildup of extra fat in the form of triglycerides in liver cells without excessive alcohol intake. NAFLD became the most common cause of chronic liver disease that is tightly associated with key aspects of metabolic disorders, including insulin resistance, obesity, diabetes, and metabolic syndrome. It is generally accepted that multiple mechanisms and pathways are involved in the pathogenesis of NAFLD. Heredity, sedentary lifestyle, westernized high sugar saturated fat diet, metabolic derangements, and gut microbiota, all may interact on a on genetically susceptible individual to cause the disease initiation and progression. While there is an unquestionable role for gene-diet interaction in the etiopathogenesis of NAFLD, it is increasingly apparent that epigenetic processes can orchestrate many aspects of this interaction and provide additional mechanistic insight. Exciting research demonstrated that epigenetic alterations in chromatin can influence gene expression chiefly at the transcriptional level in response to unbalanced diet, and therefore predispose an individual to NAFLD. Thus, further discoveries into molecular epigenetic mechanisms underlying the link between nutrition and aberrant hepatic gene expression can yield new insights into the pathogenesis of NAFLD, and allow innovative epigenetic-based strategies for its early prevention and targeted therapies. Herein, we outline the current knowledge of the interactive role of a high-fat high-calories diet and gene expression through DNA methylation and histone modifications on the pathogenesis of NAFLD. We also provide perspectives on the advancement of the epigenomics in the field and possible shortcomings and limitations ahead.
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