The molecular regulatory mechanism controlling POMC expression with fetal alcohol exposure is not clearly understood. Aberrant epigenetic changes in response to environmental exposure in the uterus during fetal development are considered a potential mechanism [16], [17]. Epigenetic alterations including DNA methylation, histone code modifications and micro RNAs play an important role in regulating gene expression. Epigenetic regulation of POMC gene expression in obesity associated metabolic syndrome, lung cancer and Cushing's syndromes have been reported [18]–[20]. We recently showed increased promoter DNA methylation in the POMC is due to altered DNA methyl transferase (DNMT) and histone deacetylase (HDAC) activity in POMC-producing cells in the arcuate nucleus of the hypothalamus in fetal alcohol exposed rats [17], [21]. It has been reported that methylated promoters recruit methyl CpG binding domain (MBD) containing proteins to silence gene expression [22]. MeCP2 is a founding member in this family of proteins, possessing a MBD motif which can recognize and bind methylated DNA thus recruiting additional transcriptional repressors such as HDACs to maintain repressive chromatin function [23]. In this study we tested the hypothesis that fetal alcohol
