In order to maintain normal function and homeostasis, appropriate gene expression is critical in individual cells. Aberrant gene expression can induce disordered conditions. Regulation of gene expression is not fully known yet but current evidence indicates that epigenetics, a phenomenon that affects gene expression without changes in DNA base pairs (1), is an important mechanism in gene expression control. A body of evidence has accumulated in recent years pointing out that DNA methylation, a major epigenetic phenomenon, is critical for embryonic development, aging and the process of certain diseases such as cancer. Epidemiologic and animal studies have demonstrated increased carcinogenesis associated with diets containing low methyl donor nutrients such as methionine, choline and folate (2, 3), evoking the idea that altered methylation of DNA due to diminished methyl availability in one-carbon metabolism is a plausible candidate mechanism through which diet facilitates carcinogenesis. Moreover, in an animal model, diets containing different levels of methyl donors (4) or bioactive food compounds (5) altered the expression of a specific gene for embryonic development by modifying DNA methylation. More studies regarding the relationship between nutrients and DNA methylation will shed light on the nature of gene regulation as well as nutritional chemoprevention. In contrast to mutation, which implies irreversibly altered base sequence, DNA methylation is reversible and can be modified by nutrients. This characteristic initiated the research for nutritional prevention of diseases by modulating DNA methylation. In this chapter we briefly describe the role of DNA methylation in embryonic development, aging and carcinogenesis, and thereafter we aim to address the topic of specific roles of nutrients on DNA methylation as well as what pertain to the associated physiologic and pathologic processes.
Nutrients and DNA methylation
CORROCHER, Roberto;FRISO, Simonetta
2009-01-01
Abstract
In order to maintain normal function and homeostasis, appropriate gene expression is critical in individual cells. Aberrant gene expression can induce disordered conditions. Regulation of gene expression is not fully known yet but current evidence indicates that epigenetics, a phenomenon that affects gene expression without changes in DNA base pairs (1), is an important mechanism in gene expression control. A body of evidence has accumulated in recent years pointing out that DNA methylation, a major epigenetic phenomenon, is critical for embryonic development, aging and the process of certain diseases such as cancer. Epidemiologic and animal studies have demonstrated increased carcinogenesis associated with diets containing low methyl donor nutrients such as methionine, choline and folate (2, 3), evoking the idea that altered methylation of DNA due to diminished methyl availability in one-carbon metabolism is a plausible candidate mechanism through which diet facilitates carcinogenesis. Moreover, in an animal model, diets containing different levels of methyl donors (4) or bioactive food compounds (5) altered the expression of a specific gene for embryonic development by modifying DNA methylation. More studies regarding the relationship between nutrients and DNA methylation will shed light on the nature of gene regulation as well as nutritional chemoprevention. In contrast to mutation, which implies irreversibly altered base sequence, DNA methylation is reversible and can be modified by nutrients. This characteristic initiated the research for nutritional prevention of diseases by modulating DNA methylation. In this chapter we briefly describe the role of DNA methylation in embryonic development, aging and carcinogenesis, and thereafter we aim to address the topic of specific roles of nutrients on DNA methylation as well as what pertain to the associated physiologic and pathologic processes.
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