title: Why glucose transport in the brain matters for PET.
abstract: Neuronal activity is fueled by glucose metabolism, a phenomenon exploited in basic research and clinical diagnosis using fluorodeoxyglucose positron emission tomography (FDG-PET). According to the current view, glucose transport into the brain is not rate-limiting; thus, it cannot exert control over metabolism. This article challenges such a view by showing that basal transport hovers near its maximum, making metabolic activation unable to increase flux on its own. In the light of recent evidence on the identity of the cell type that preferentially breaks down glucose, we suggest that FDG-PET reports the synergistic activation of glucose transport and metabolism in astrocytes, rather than in neurons.
authors.affiliation: Centro de Estudios Científicos CECS, Arturo Prat 514, Casilla 1469, Valdivia, Chile. fbarros@cecs.cl
authors.forename: L Felipe
authors.initials: LF
authors.lastname: Barros
authors.forename: Omar H
authors.initials: OH
authors.lastname: Porras
authors.forename: Carla X
authors.initials: CX
authors.lastname: Bittner
mesh_terms: D000818:Animals; D001692:Biological Transport / Q000502:physiology*; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism*; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism; D049268:Positron-Emission Tomography
chemical_list: D019788:Fluorodeoxyglucose F18; D005947:Glucose