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.