The Role of Leptin in Fetal Growth Restriction in Obese Pregnancies

Abstract

Fetal growth restriction (FGR) is associated with many complications, both for the mother and the neonate.1 Many FGR cases occur in mothers who have limited resources and are unable to provide enough nutrients to meet the metabolic needs of their fetus.2 However, there are many cases of obese mothers with FGR pregnancies. The etiology of fetal growth restriction in obese pregnancies is unclear, but leptin may be the key in understanding how this occurs. Leptin is a hormone that is produced by adipocytes and is proportional to the amount of fat an individual has.3 Additionally, leptin is produced by the placenta, which helps regulate transport of nutrients to the fetus and maintains a healthy placenta.4 Leptin’s role in obese pregnancies that result in FGR is not well understood, but leptin may contribute to FGR through the following mechanisms: poor angiogenesis of the placenta; contributing to the development of pathological placental leptin resistance; decreasing SNAT activity; increased inhibition of leptin function with hyperinsulinemia. These mechanisms will be discussed in this thesis, along with possible therapeutic approaches to mitigate the negative effects of hyperleptinemia.