Diabetes in Pregnancy: Considerations for the Management of Delivery

Abstract

Throughout normal pregnancy, metabolic adaptations occur so that a constant fuel supply may be provided for the life and development of the fetus. These adaptations begin quite early when, in response to rising levels of estrogen and progesterone in the mother, the fetal β-cells become hyperplastic and secrete more insulin, which, in turn, results in greater utilization of glucose, increased glycogen storage, and a reduction in the output of glucose from the liver; in other words, an anabolic state is created. The simplest evidence of this change is a reduction in the maternal fasting blood glucose level. Maternal or exogenous insulin does not cross the placenta, and the fetus secretes insulin from its own β-cells from the eighth week of gestation (1). Glucose is transferred across the placenta by facilitated diffusion, while amino acids (alanine being the most important because it stimulates the fetal p-cells) are actively transported by the placenta to the fetus. Consequently, the activity of fetal β-cells is determined by the maternal blood glucose and amino acid levels. “Giant” islets are a common finding at autopsy in infants of diabetic mothers in whom diabetic control has been inadequate.