Decreased GLUT 3 expression compromises glucose transport and alters bioenergetic parameters in neurons

In the central nervous system, approximately 70 to 80% of metabolic energy is required by neurons. The ATP obtained from the metabolism of glucose is essential in processes such as membrane potentials, glutamate-glutamine cycle, cytoplasmic dynamics of Ca²⁺ and functioning of synaptic receptors. Glucose enters neurons via glucose transporters (GLUTs) located in the plasma membrane and is then metabolized in two main pathways: (i) glycolysis and (ii) mitochondrial (tricarbocylic acid cycle/oxidative phosphorylation). Alterations in the expression or functioning mechanisms of GLUTs can be modulated in tumor neurons, leading such cells to present an increase in glucose uptake and in its anaerobic metabolism; thus, irregular expression of GLUTs with different affinities could provide greater energy intake and potentiate tumor growth. Currently, the definition of a biological model for studies related to neuronal energy metabolism is still a challenge; moreover, it is questionable whether neuronal cell lines with tumor phenotype maintain the same cell patterns as primary neuronal cultures or immortalized, non-carcinogenic cell lines.