Near‐critical GLUT1 and Neurodegeneration. Issue 11 (2nd February 2017)

• Record Type: Journal Article
• Authors: Barros, L. Felipe; San Martín, Alejandro; Ruminot, Ivan; Sandoval, Pamela Y.; Fernández‐Moncada, Ignacio; Baeza‐Lehnert, Felipe; Arce‐Molina, Robinson; Contreras‐Baeza, Yasna; Cortés‐Molina, Francisca; Galaz, Alex; Alegría, Karin
• Other Names: Schousboe Arne guestEditor.; Yu Albert C. H. guestEditor.; McKenna Mary C. guestEditor.
• Is Part Of: Journal of neuroscience research. Volume 95:Issue 11(2017)
• Page Start: 2267
• Page End: 2274
• Publication Date: 2017-02-02
• Subjects: glucose transporter -- Slc2a1 -- endothelium -- astrocyte -- Alzheimer disease -- GLUT1 deficiency; Neurobiology -- Periodicals; 612
• DOI: 10.1002/jnr.23998
• Languages: English
• ISSNs: 0360-4012

Abstract

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. © 2017 Wiley Periodicals, Inc. Abstract : Glucose flows from blood into endothelial cells, astrocytes, and neurons, its passage through membranes being mediated by GLUT1 and GLUT3. The degree of flux control exerted by these transporters depends on their relative resistance to flux, which also determines the tolerance of neurons to transport deficits. One of nine possible configurations of brain glucose dynamics is depicted here in which neurons are highly exposed to deficits in astrocytic GLUT1, but not in endothelial GLUT1 or in neuronal GLUT3.