Oxidative stress and DNA methylation regulation in the metabolic syndrome.
DNA methylation is implicated in tissue-specific gene expression and genomic imprinting. It is modulated by environmental factors, especially nutrition. Modified DNA methylation patterns may contribute to health problems and susceptibility to complex diseases. Current advances have suggested that the metabolic syndrome (MS) is a programmable disease, which is characterized by epigenetic modifications of vital genes when exposed to oxidative stress. Therefore, the main objective of this paper is to critically review the central context of MS while presenting the most recent knowledge related to epigenetic alterations that are promoted by oxidative stress. Potential pro-oxidant mechanisms that orchestrate changes in methylation profiling and are related to obesity, diabetes and hypertension are discussed. It is anticipated that the identification and understanding of the role of DNA methylation marks could be used to uncover early predictors and define drugs or diet-related treatments able to delay or reverse epigenetic changes, thereby combating MS burden.
Faculty of Medicine, Research Centre, Université de Montréal, CHU-Sainte-Justine, Montreal, QC, Canada, H3T 1C5.
Sabrina
S
Yara
Jean-Claude
JC
Lavoie
Emile
E
Levy
D019175:DNA Methylation; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology; D044127:Epigenesis, Genetic; D006801:Humans; D006973:Hypertension / Q000209:etiology; D024821:Metabolic Syndrome / Q000201:enzymology / Q000209:etiology / Q000235:genetics* / Q000378:metabolism*; D009747:Nutritional Physiological Phenomena; D009765:Obesity / Q000209:etiology; D018384:Oxidative Stress
DNA methylation; antioxidant defense; fetal programming; inflammation; metabolic syndrome; nutrition; oxidative stress