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Background  Fetal exposure to maternal diabetes increases the risk of type 2 diabetes (T2DM), possibly mediated by epigenetic mechanisms. Low blood  TXNIP  DNA methylation has been associated with elevated glucose levels and risk of T2DM, and increased skeletal muscle  TXNIP  gene expression was reported in subjects with impaired glucose metabolism or T2DM. Subcutaneous adipose tissue (SAT) and skeletal muscle play a key role in the control of whole body glucose metabolism and insulin action. The extent to which  TXNIP  DNA methylation levels are decreased and/or gene expression levels increased in SAT or skeletal muscle of a developmentally programmed at-risk population is unknown.    Objective and methods  The objective of this study was to investigate  TXNIP  DNA methylation and gene expression in SAT and skeletal muscle, and DNA methylation in blood, from adult offspring of women with gestational diabetes (O-GDM, n = 82) or type 1 diabetes (O-T1DM, n = 67) in pregnancy compared with offspring of women from the background population (O-BP, n = 57).    Results  SAT  TXNIP  DNA methylation was increased (p = 0.032) and gene expression decreased (p = 0.001) in O-GDM, but these differences were attenuated after adjustment for confounders. Neither blood/muscle  TXNIP  DNA methylation nor muscle gene expression differed between groups.    Conclusion  We found no evidence of decreased  TXNIP  DNA methylation or increased gene expression in metabolic target tissues of offspring exposed to maternal diabetes. Further studies are needed to confirm and understand the paradoxical SAT  TXNIP  DNA methylation and gene expression changes in O-GDM subjects.

DNA methylation and gene expression of TXNIP in adult offspring of women with diabetes in pregnancy