Pathophysiology
Insulin resistance during pregnancy stems from a variety of factors, including alterations in growth hormone and cortisol secretion (insulin antagonists), human placental lactogen secretion (which is produced by the placenta and affects fatty acids and glucose metabolism, promotes lipolysis, and decreases glucose uptake), and insulinase secretion (which is produced by the placenta and facilitates metabolism of insulin). In addition, estrogen and progesterone also contribute to a disruption of the glucose insulin balance. Increased maternal adipose deposition, decreased exercise, and increased caloric intake also contribute to this state of relative glucose intolerance.