Introduction

The mammalian fetus, in utero, is entirely dependent upon the mother for a continuous supply of glucose and other nutrients. Data from a number of studies in humans and animals have shown that under physiological circumstances there is no measurable production of glucose by the fetus, and that the entire glucose pool in the fetal compartment is derived from the mother. The transition from the intrauterine environment to an independent extrauterine life is associated with a number of metabolic and hormonal responses, which allow the vast majority of neonates to adapt to the extrauterine environment without any problem. Among the key events involved in this adaptation is the initiation of systemic glucose production, both from glycogenolysis and gluconeogenesis, in the period immediately after birth. Failure to adapt, as a consequence of alterations in maternal metabolism such as in diabetes in pregnancy, or as a consequence of metabolic problems in the neonate, may result in perturbations in glucose homeostasis leading to low blood glucose concentrations or hypoglycemia. It should be underscored that, during the initial period after birth, there is a decline in plasma glucose concentration from the cord blood levels in all infants, followed by an increase to a steady-state concentration. Although in the majority of infants this decrease in blood glucose concentration may be transient and inconsequential, in others it may be profound or persistent and lead to clinically serious problems involving significant neurological injury.