Abstract
Glucose is the primary substrate for cerebral metabolism and function. When there is a recurrent and prolonged imbalance in glucose homeostasis, the result is cerebral energy failure, which can lead to neurologic injury in the neonate. However, for neonates with transient hypoglycemia, the relationship between low plasma concentrations, cerebral injury, and neurodevelopmental outcomes remains uncertain. This article reviews glucose metabolism in the fetus and neonate, the neuroprotective responses to hypoglycemia, and the continued diagnostic and therapeutic dilemmas that clinicians face in the management of neonatal hypoglycemia.
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