Abstract
Introduction: Glucose is the cerebral energy fuel; this relationship is fully established in most reviews due to neuronal tissue's avid and almost exclusive glucose consumption. In this sphere, hypoglycemia is translated by default into a set of neurological symptoms resulting from the neuroglycopenic state. When the drop in these glycemic levels is pronounced, it triggers alterations in the sensory state, being able to reach a coma with irreversible damage if sustained over time.
Purpose of the review: The objective is to present a case of severe hypoglycemia without neuroglycopenic symptoms.
Recent findings: The absence of neurological symptoms is due to the consumption of lactate – traditionally an anaerobic product – as an alternative energy metabolic pathway to glucose consumption. Hypoglycemia can be compensated at the neurological level with lactate launching systems in neuronal tissue, replacing glucose as the brain's energy substrate.
Conclusions: Hypoglycemia without adrenergic or neuroglycopenic symptoms is an issue linked to cancer patients, and lactate is proposed as fuel for nervous tissue in addition to glucose. On the other hand, the lactate-hypoperfusion association is another entity that must be reviewed and reanalyzed for everything that lactate implies within the body's metabolic pathophysiological pathway.
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