: Nowadays, the continuous rise of maternal obesity is followed by increased gestational diabetes mellitus incidence. GDM is associated with adverse fetal and neonatal outcome that often presents with macrosomia, birth trauma, neonatal hypoglycemia, and respiratory distress syndrome. Inclusion of GDM into 'the great obstetrical syndromes' emphasizes the role of the placenta in interactions of the maternal and fetal unit. The placenta acts as a natural selective barrier between maternal and fetal blood circulations. Placenta is sensitive to the hyperglycemic milieu and responses with adaptive changes of the structure and function. Alteration of the placental development and subsequent vascular dysfunction are presented in 6 out of 7 women with all ranges of diabetic severity. Most placentas from GDM pregnancies present typical histological findings such as villous immaturity, villous fibrinoid necrosis, chorangiosis, and increased angiogenesis. The type of dysfunction depends on how early in pregnancy glycaemia disorders occurred. Generally, if impaired glucose metabolism is diagnosed in the early pregnancy, mainly structural dysfunctions are observed. GDM that is detected in late gestation affects placental function to a greater extent. Moreover many studies suggest that diabetic placental changes are associated with inflammation and oxidative stress that can lead to the chronic fetal hypoxia. This article aims to review particular changes of the development, anatomy and function of the placenta in the environment of abnormal glucose metabolism which can establish the maternal-placental-fetal interface dysfunction as a potential source of adverse pregnancy outcomes. A detailed sequence of events that leads from hyperglycemia to placental dysfunction and subsequent pregnancy complications may become an important issue for further studies.