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Nonalcoholic fatty liver disease (NAFLD) is initially characterized by triglyceride deposits within the hepatocytes. Nutritional status is the major factor in the etiology of NAFLD. Although the epidemiologic relationship between plasma/serum betaine and NAFLD is not well documented, evidence from animal experiments and clinical trials has suggested that betaine supplementation effectively alleviates hepatic steatosis. However, The underlying biological mechanisms are not fully understood. The role of genetic and epigenetic dysregulation has increasingly been recognized in the pathogenesis of NAFLD, as aberrant DNA methylation is directly related to alterations in gene expression. Betaine has been observed to reverse the dysregulated expression of genes in triglyceride metabolism. As a methyl donor, betaine is required for SAM synthesis and is essential for DNA methylation, indicating a plausible epigenetic mechanism whereby betaine regulates hepatic triglyceride metabolism. Evidence that betaine affects DNA methylation in NAFLD is limited, however, betaine has been shown to alleviate hepatic steatosis by modifying the DNA methylation level in the genome and specific gene promoter in high-fat fed mice. Further research is required to determine the effect of betaine on NAFLD prevention and treatment in humans and to elucidate the epigenetic profile of betaine and its associated effects on steatosis.

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