Abnormal glucose levels damage the central nervous system, especially in case of rapid fluctuations. Even a single episode of glucose reperfusion can result in overt impairment of neurons. Oxidative stress plays an important role in this process, sharing properties with the pathophysiologic changes of glucose neurotoxicity. Glucose transporters (GLUTs) located in the brain are involved in direct glucose uptake by neurons. Instead of being insulin-sensitive, these transporters are regulated by glucose levels in the extracellular fluid, increasing their expression while glucose levels fall, to absorb more glucose. Therefore, we hypothesized that mismatch between altered GLUTs and sudden glucose level changes is responsible for neuronal damage during glucose fluctuations. Modulating hypoglycemia by increasing blood glucose slowly may improve the neurological outcomes of hypoglycemia.
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