Data from: Impact on offspring methylation patterns of maternal gestational diabetes mellitus and intrauterine growth restraint suggest common genes and pathways linked to subsequent type 2 diabetes risk

Size at birth, postnatal weight gain, and adult risk for type 2 diabetes
may reflect environmental exposures during developmental plasticity and
may be mediated by epigenetics. Both low birth weight (BW), as a marker of
fetal growth restraint, and high birth weight (BW), especially after
gestational diabetes mellitus (GDM), have been linked to increased risk of
adult type 2 diabetes. We assessed DNA methylation patterns using a bead
chip in cord blood samples from infants of mothers with GDM (group 1) and
infants with prenatal growth restraint indicated by rapid postnatal
catch-up growth (group 2), compared with infants with normal postnatal
growth (group 3). Seventy-five CpG loci were differentially methylated in
groups 1 and 2 compared with the controls (group 3), representing 72
genes, many relevant to growth and diabetes. In replication studies using
similar methodology, many of these differentially methylated regions were
associated with levels of maternal glucose exposure below that defined by
GDM [the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study] or were
identified as changes observed after randomized periconceptional
nutritional supplementation in a Gambian cohort characterized by maternal
deprivation. These studies provide support for the concept that similar
epigenetic modifications may underpin different prenatal exposures and
potentially increase long-term risk for diseases such as type 2 diabetes.