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Background  Offspring of pregnancy complicated with gestational diabetes (GDM) are at high risk for metabolic diseases. The mechanisms behind the association of intrauterine exposure to GDM and high risk of health problems in later life remain largely unknown. The aim of this study was to clarify the alteration in methylation levels at differentially methylated regions (DMRs) of  GNAS  and  IGF2  in fetuses of GDM women and to explore the possible mechanisms linking maternal GDM with high risk of metabolic diseases in later life of GDM offspring.    Methods  Lymphocytes were isolated from umbilical cord blood of infants born to 87 women with GDM and 81 women with normal pregnancy. Genomic DNA was extracted and DNA methylation levels of  GNAS  and  IGF2  DMRs were determined by Massarray quantitative methylation analysis.    Results  The methylation levels were detected in 7 CpG sites of  GNAS  DMRs and 6 sites of  IGF2  DMRs. Methylation levels were significantly higher at sites 4, 5 and 7 of  GNAS  DMR in GDM compared to normal pregnancy (P = 0.007, 0.008 and 0.008, respectively). The methylation level at site 4 of  GNAS  was significantly correlated with the presence of GDM (P = 0.003), the methylation levels at site 5 and 7 were significantly correlated with the presence of GDM (P = 0.002 for both) and gestational age (P = 0.027 for both). There was no significant difference in any sites of  IGF2  DMR (P > 0.05 for all).    Conclusions  We concluded maternal GDM-induced hypermethylation at  GNAS  DMR and this condition may be among the mechanisms associating maternal GDM with increased risk of metabolic diseases in later life of offspring.

Increased methylation at differentially methylated region of GNASin infants born to gestational diabetes