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Maternal diabetes constitutes an unavorable environment or embryonic and etoplacental development. Despite current treatments, pregnant women with pregestational diabetes are at increased risk or congenital malormations, materno-etal complications, placental abnormalities and intrauterine malprogramming. The complications during pregnancy concern the mother (gravidic hypertension and/or preeclampsia, cesarean section) and the etus (macrosomia or intrauterine growth restriction, shoulder dystocia, hypoglycemia and respiratory distress). The etoplacental impairment and intrauterine programming o diseases in the ospring's later lie induced by gestational diabetes are similar to those induced by type 1 and type 2 diabetes mellitus. Despite the existence o several developmental and morphological dierences in the placenta rom rodents and women, there are similarities in the alterations induced by maternal diabetes in the placenta rom diabetic patients and diabetic experimental models. From both human and rodent diabetic experimental models, it has been suggested that the placenta is a compromised target that largely suers the impact o maternal diabetes. Depending on the maternal metabolic and proinflammatory derangements, macrosomia is explained by an excessive availability o nutrients and an increase in etal insulin release, a phenotype related to the programming o glucose intolerance. The degree o etal damage and placental dysunction and the availability and utilisation o etal substrates can lead to the induction o macrosomia or intrauterine growth restriction. In maternal diabetes, both the maternal environment and the genetic background are important in the complex and multiactorial processes that induce damage to the embryo, the placenta, the etus and the ospring. Nevertheless, urther research is needed to better understand the mechanisms that govern the early embryo development, the induction o congenital anomalies and etal overgrowth in maternal diabetes.