Since aberrant methylation at IGF2 and subsequently the expression of IGF2 affects postnatal growth and contribute to the development of diabetes, hypertension and other metabolic disorders in late life, our findings implies that preeclampsia-induced decrease in fetal DNA methylation at IGF2 DMR might be among the mechanisms associating maternal preeclampsia and metabolic disorders in late life of the offspring. This evidence concerns the gene IGF2 and metabolic disease.