Fig. 5.

Maternal adiponectin informs the placenta about maternal nutrition status. High maternal adiponectin in low nutrient status mothers inhibits insulin signaling in the placenta and reduces nutrient transport capacity. The combination of high adiponectin and low insulin limits placental uptake and protects the mother from additional depletion, resulting in a smaller but potentially viable offspring. In the obese mother with low adiponectin and high insulin there is no inhibition of transport, leading to larger placentas, greater transport capacity and the excess supply of nutrients to the fetus, enhancing fetal growth and resulting in large-for-gestational age babies. These studies demonstrate that the placenta is responding to maternal nutrient status and altering delivery of nutrients to the fetus to match maternal stores. Correcting adiponectin in obese mice to normal levels prevents these changes in placental function, fetal overgrowth and developmental programming of cardiometabolic disease, suggesting that targeting the placenta is a therapeutic alternative that should be further investigated.