The significance of the maternal thyroid function for epigenetic programming of glucose metabolism in the offspring

Background The placenta, which has a low permeability for thyroid hormones (TH), is considered to be the interface between mother and fetus. The inhibition of maternal TH production leads to severe hypothyroidism in the offspring, since the fetal thyroid gland cannot produce TH hormones on its own until 20 weeks of gestation. Several studies have reported the strong link between thyroid dysfunctions, obesity and metabolic disorders like diabetes mellitus. Furthermore, a number of epigenetic markers have been identified that regulate glucose tolerance and insulin sensitivity.