Abstract
In obese compared with lean individuals, lower methylation of tumor necrosis factor α in peripheral blood leukocytes, pyruvate dehydrogenase kinase 4 in muscle, and leptin in whole blood were reported. Furthermore, increased methylation of proopiomelanocortin occurs in whole blood, PPARγ coactivator 1α (PGC1α) in muscle, as well as CLOCK and aryl hydrocarbon receptor nuclear translocator-like genes in peripheral blood leukocytes. Obesity-associated differentially methylated sites in peripheral blood cells were also detected in genome-wide studies, showing, for example, an association with alpha-ketoglutarate-dependent dioxygenase (FTO) methylation. In type 2 diabetes, DNA hypermethylation of the PGC1α promoter and concomitant transcriptional repression is also observed in pancreatic islets. It is interesting that several epigenetic marks are modifiable, not only by changing the exposure in utero, but also by lifestyle changes in adult life, which implies that there is the potential for interventions to be introduced in postnatal life to modify or rescue unfavorable epigenomic profiles.
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