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Folate Modulation of Adipocyte Promoter Methylation and Lipolysis
Author(s) -
Gouffon Julia S,
Johnstone Megan,
Zemel Michael B
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.597.6
Epigenetic modifications serve as a means of intermediate gene expression control and nutritional inputs may modify methylation patterns in regulatory regions of genes. Therefore, we predict that specific nutrient availability will affect adipocyte development and metabolism. Accordingly, we sought to determine if the methylation level of CpG islands can be influenced in adipocytes and if so, how this might affect gene signaling in mature adipocytes. Methylated regions of adipocyte genomic DNA were obtained using a methylation‐specific antibody and hybridized against a Nimblegen whole genome CpG island array. We found methylated regions in or near transcription start sites for acetyl CoA carboxylase A, acetyl CoA Carboxylase B, adiponectin receptor 2, cytochrome C oxidase, DNA methyltransferase 3A, folate receptors 1 and 2, hormone sensitive lipase(HSL), resistin, retinoid X receptor beta and vitamin D receptor. To determine the functional significance of these observations, we treated adipocytes with 0–0.9 mM folate, the methyl donor S‐adenosylmethionine (SAM) or a methylation inhibitor, 5‐aza‐2‐deoxycitidine (2DC) and found folate to dose‐dependently increased lipolysis 18–45% (p<0.02); however, it is not clear if this is a methylation effect as SAM and 2DC exerted only minimal effects. Thus, folate stimulates adipocyte lipolysis, but this effect may not be methylation dependent.