Abstract
Neonatal hypoglycemia is a common condition. A transient reduction in blood glucose values is part of a transitional metabolic adaptation following birth, which resolves within the first 48 to 72 h of life. In addition, several factors may interfere with glucose homeostasis, especially in case of limited metabolic stores or increased energy expenditure. Although the effect of mild transient asymptomatic hypoglycemia on brain development remains unclear, a correlation between severe and prolonged hypoglycemia and cerebral damage has been proven. A selective vulnerability of some brain regions to hypoglycemia including the second and the third superficial layers of the cerebral cortex, the dentate gyrus, the subiculum, the CA1 regions in the hippocampus, and the caudate-putamen nuclei has been observed. Several mechanisms contribute to neuronal damage during hypoglycemia. Neuronal depolarization induced by hypoglycemia leads to an elevated release of glutamate and aspartate, thus promoting excitotoxicity, and to an increased release of zinc to the extracellular space, causing the extensive activation of poly ADP-ribose polymerase-1 which promotes neuronal death. In this review we discuss the cerebral glucose homeostasis, the mechanisms of brain injury following neonatal hypoglycemia and the possible treatment strategies to reduce its occurrence.
Highlights
Hypoglycemia is a common condition in the neonatal population [1]
As the maintenance of a constant and adequate supply of sugar for the brain is a priority, it is obvious that the ability to detect changes in blood glucose levels by sensitive neurons situated behind the BBB is not useful to glucose homeostasis because it only foresees changes in brain glucose
Mitochondria have been implicated as a source of reactive oxygen species (ROS) in many disorders, and mitochondria taken from a hypoglycemic brain exhibit an increased capacity to generate ROS in response to glutamate excitotoxicity
Summary
Laura Costanza De Angelis 1,2*, Giorgia Brigati 1, Giulia Polleri 1, Mariya Malova 1,2, Alessandro Parodi 1,2, Diego Minghetti 1, Andrea Rossi 3,4, Paolo Massirio 1,2, Cristina Traggiai 1, Mohamad Maghnie 2,5 and Luca Antonio Ramenghi 1,2. A transient reduction in blood glucose values is part of a transitional metabolic adaptation following birth, which resolves within the first 48 to 72 h of life. The effect of mild transient asymptomatic hypoglycemia on brain development remains unclear, a correlation between severe and prolonged hypoglycemia and cerebral damage has been proven. In this review we discuss the cerebral glucose homeostasis, the mechanisms of brain injury following neonatal hypoglycemia and the possible treatment strategies to reduce its occurrence.
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