If the maternal pancreatic insulin response is inadequate, maternal and, then, fetal hyperglycemia results. This typically manifests as recurrent postprandial hyperglycemic episodes. These postprandial episodes are the most significant source of the accelerated growth exhibited by the fetus.
Surging maternal and fetal glucose levels are accompanied by episodic fetal hyperinsulinemia. Fetal hyperinsulinemia promotes excess nutrient storage, resulting in macrosomia. The energy expenditure associated with the conversion of excess glucose into fat causes depletion in fetal oxygen levels.
In the pregnant woman, each meal sets in motion a complex series of hormonal actions, including a rise in blood glucose and the secondary secretion of pancreatic insulin, glucagon, somatomedins, and adrenal catecholamines. These adjustments ensure that an ample, but not excessive, supply of glucose is available to the mother and fetus.
Gestational diabetes mellitus is defined as glucose intolerance of variable degree with onset or first recognition during pregnancy. A study by Stuebe et al found this condition to be associated with persistent metabolic dysfunction in women at 3 years after delivery, separate from other clinical risk factors.
Abnormal maternal glucose regulation occurs in 3-10% of pregnancies, and gestational diabetes mellitus (GDM), which is defined as glucose intolerance of variable degree with onset or first recognition during pregnancy, accounts for 90% of cases of diabetes mellitus (DM) in pregnancy. However, the rising prevalence of diabetes mellitus—21 million people (7% of the population) have some form of diagnosed diabetes; another 6 million people may be undiagnosed —particularly type 2 among women of childbearing age in the United States, has resulted in increasing numbers of pregnant women with preexisting diabetes. Currently, type 2 diabetes mellitus accounts for 8% of cases of diabetes mellitus in pregnancy, and preexisting diabetes mellitus now affects 1% of all pregnancies.