Objective Gestational Diabetes Mellitus (GDM) , develops in 3%-5% of pregnant women.Furthermore, GDM is assciated with increased perinatal morbidit and mortality, and increasing epidemiological evidence inferred that long-term consequences for the offsping born to a GDM pregnancy resulting in endothelial/vascular dysfunction associated with obesity, hypertension, type 2 diabetes mellitus (T2D), and metabolic syndrome.However, the exact mechanisms underling the fetal programming are not clear.Epigenetic regulation have been repeatedly proved as molecular mechanisms that could explain how an adverse fetal environment can be associated with chronic adult diseases, but only a few studies have addressed this hypothesis directly.We supposed these diseases may be linked to abnormal placental development and function, and sought to identify the molecular and morphological changes in GDM mice.Design We established a mouse model of GDM and observed the placental development in GDM mice in day 18.5.Besides, we added methy-donor diet for GDM mice.We tested the morphology of GDM placenta in different stages.