ABSTRACT
This chapter discusses the intense interplay between the mother and fetus and the role of the placenta as mediator. Maternal changes may lead to placental changes, which are essential for determining the fetal phenotype in maternal diabesity, while intrinsic placental changes may determine the maternal phenotype and/or the fetal phenotype. Diabetes and obesity share several features such as insulin resistance, dyslipidemia, and inflammation. The term "diabesity" was coined to reflect these commonalities. It is unclear whether any of these placental changes are causally linked with the fetal and neonatal phenotype of pregnancies in diabesity. A growing body of evidence shows that the major difference in the neonatal phenotype between normal and diabetic/obese pregnancies is the fetal body composition independent of birth weight. The placenta as a fetal tissue receives fetal signals and adapts its development and function according to fetal needs. This explains why the placenta is often hypervascularized in maternal diabetes.
