An increasing number of women of reproductive age are obese which affects the continuum of pregnancy and is associated with an increased incidence of adverse maternal and fetal outcomes, including preeclampsia, preterm birth, stillbirth, congenital anomalies, and macrosomia. Maternal obesity is associated with an increased incidence of metabolic and cardiovascular disease later in life in the mother and in the offspring who are developmentally programed by the obese pregnancy environment. The placenta transduces and mediates the effect of the adverse maternal environment to the fetus. The obese maternal environment is characterized by hyperlipidemia and an exaggerated state of inflammation and oxidative stress compared with normal pregnancy. Heightened inflammation and oxidative/nitrative stress are found in the placenta in association with placental dysfunction. We have described reduced mitochondrial respiration and ATP generation in trophoblast isolated from placentas of obese compared with lean women, again suggesting compromised placental function. In utero development exhibits sexual dimorphism with the male fetus at greater risk of poor outcome. We have shown dimorphism in inflammation-mediated regulation of trophoblast mitochondrial respiration. There is also increasing evidence that the obese in utero environment may cause epigenetic changes in placenta leading to altered function.
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