Introduction to Neonatal Hypoglycemia
- Neonatal hypoglycemia is common, especially affecting infants who are large-for-gestational age (LGA), small-for-gestational age (SGA), infants of diabetic mothers, and preterm infants.
- Transient blood glucose drops occur normally after birth, usually resolving within 72 hours.
- Prolonged severe hypoglycemia is linked to neurological impairment; the consequences of transient mild hypoglycemia remain uncertain.
Transition of Glucose Homeostasis at Birth
- Fetal glucose metabolism relies on maternal glucose via placental diffusion.
- After birth, the neonate undergoes hormonal and metabolic changes to maintain glucose levels:
- Increased glucagon, cortisol, and catecholamines
- Reduced insulin secretion
- Activation of glycogenolysis, gluconeogenesis, lipolysis, and proteolysis.
Brain Energetics and Glucose Sensing Neurons
- Brain metabolism primarily uses glucose, critical for energy and neurotransmitter synthesis.
- Specialized neurons detect blood glucose variations and help maintain cerebral glucose homeostasis.
- Glucose transport to the brain is mediated by GLUT1 and GLUT3 transporters across the blood-brain barrier (BBB).
Pathophysiology of Hypoglycemic Brain Damage
- Hypoglycemia-induced brain injury involves multiple mechanisms:
- Excitotoxicity: Glutamate release causing neuronal cell death.
- Oxidative stress: ROS causing oxidative neuronal damage.
- Zinc toxicity: Pathological zinc release affecting mitochondrial function and energy metabolism.
- PARP-1 activation: Excessive consumption of NAD+, disrupting glucose utilization.
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