| Literature DB >> 28150866 |
L Felipe Barros1, Alejandro San Martín1, Ivan Ruminot1, Pamela Y Sandoval1, Ignacio Fernández-Moncada1,2, Felipe Baeza-Lehnert1,2, Robinson Arce-Molina1,2, Yasna Contreras-Baeza1, Francisca Cortés-Molina1, Alex Galaz1, Karin Alegría1.
Abstract
Recent articles have drawn renewed attention to the housekeeping glucose transporter GLUT1 and its possible involvement in neurodegenerative diseases. Here we provide an updated analysis of brain glucose transport and the cellular mechanisms involved in its acute modulation during synaptic activity. We discuss how the architecture of the blood-brain barrier and the low concentration of glucose within neurons combine to make endothelial/glial GLUT1 the master controller of neuronal glucose utilization, while the regulatory role of the neuronal glucose transporter GLUT3 emerges as secondary. The near-critical condition of glucose dynamics in the brain suggests that subtle deficits in GLUT1 function or its activity-dependent control by neurons may contribute to neurodegeneration.Entities:
Keywords: Alzheimer disease; GLUT1 deficiency; Slc2a1; astrocyte; endothelium; glucose transporter
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Year: 2017 PMID: 28150866 DOI: 10.1002/jnr.23998
Source DB: PubMed Journal: J Neurosci Res ISSN: 0360-4012 Impact factor: 4.164