The Role of the Fetal-Placental Unit in the Development of GDM
During pregnancy, as gestational age progresses, the size of the placenta increases. There is a rise in the levels of pregnancy-associated hormones like estrogen, progesterone, cortisol and placental lactogen in the maternal circulation [8, 9] accompanied by an increasing insulin resistance.
This usually begins between 20 and 24 weeks of gestation. As the mother goes through parturition and
delivers the fetus, the placental hormone production stops, and so does the illness of GDM, which strongly suggests that these hormones cause GDM [10] . Human placental lactogen raises approximately 10- fold in the second half of the pregnancy. It stimulates lipolysis, which leads to an increase in free fatty acids in order to provide a different fuel to the mother and to conserve
glucose and amino acids for the fetus. In turn, the increase in free fatty acid levels directly interferes with the insulin-directed entry of glucose into cells. Therefore, human placental lactogen is considered as a potent antagonist of insulin action during pregnancy.