The Effect of Prematurity and Intrauterine Growth Restriction on Glucose Metabolism in the Newborn

After completing this article, readers should be able to: 1. List the three components required for the transition to independent glucose homeostasis in the newborn. 2. Explain why preterm infants are at increased risk for neonatal hypoglycemia. 3. Compare the capacity for gluconeogenesis in the term and preterm infant and in the infant who has intrauterine growth restriction. 4. Describe the effects of enteral feedings on glucose homeostasis in the newborn. At birth, the transplacental supply of nutrients, especially glucose, to the newborn is interrupted abruptly. This sets into motion a complex cascade of metabolic and endocrine events that allow a healthy term newborn to adjust to his or her new environment. This cascade is triggered by a surge in the concentrations of glucagon and catecholamines and cessation of insulin secretion. Glucagon and catecholamines increase glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis. The complex enzyme machinery responsible for these processes is mature in term healthy newborns. In contrast, the metabolic and endocrine processes allowing the transition to the extrauterine environment are not developed fully in preterm infants and those who have suffered intrauterine growth restriction (IUGR), placing these newborns at significant risk of hypoglycemia. This review focuses on the regulation of glucose metabolism during the fetal period and the metabolic and endocrine changes that occur at birth and in the postnatal period, with special reference to preterm infants and infants who have experienced IUGR. Carbohydrate is transported to the fetus as glucose, which is taken up from the maternal plasma by glucose transporters. GLUT1 and GLUT3 are the primary glucose transporters involved in the transplacental movement of glucose and are present on both the microvillus and basal membranes of the syncytial barrier. Glucose is transported to the fetus by facilitative diffusion according to concentration-dependent kinetics, with placental glucose transport capacity increasing with gestational age. The …