TY  - JOUR
AU  - Backes, Heiko
AU  - Walberer, Maureen
AU  - Ladwig, Anne
AU  - Rueger, Maria A.
AU  - Neumaier, Bernd
AU  - Endepols, Heike
AU  - Hoehn, Mathias
AU  - Fink, Gereon R.
AU  - Schroeter, Michael
AU  - Graf, Rudolf
TI  - Glucose consumption of inflammatory cells masks metabolic deficits in the brain
JO  - NeuroImage
VL  - 128
SN  - 1053-8119
CY  - Orlando, Fla.
PB  - Academic Press
M1  - FZJ-2016-00582
SP  - 54 - 62
PY  - 2016
AB  - Inflammatory cells such as microglia need energy to exert their functions and to maintain their cellular integrity and membrane potential. Subsequent to cerebral ischemia, inflammatory cells infiltrate tissue with limited blood flow where neurons and astrocytes died due to insufficient supply with oxygen and glucose. Using dual tracer positron emission tomography (PET), we found that concomitant with the presence of inflammatory cells, transport and consumption of glucose increased up to normal levels but returned to pathological levels as soon as inflammatory cells disappeared. Thus, inflammatory cells established sufficient glucose supply to satisfy their energy demands even in regions with insufficient supply for neurons and astrocytes to survive. Our data suggest that neurons and astrocytes died from oxygen deficiency and inflammatory cells metabolized glucose non-oxidatively in regions with residual availability. As a consequence, glucose metabolism of inflammatory cells can mask metabolic deficits in neurodegenerative diseases. We further found that the PET tracer did not bind to inflammatory cells in severely hypoperfused regions and thus only a part of the inflammation was detected. We conclude that glucose consumption of inflammatory cells should be taken into account when analyzing disease-related alterations of local cerebral metabolism.
LB  - PUB:(DE-HGF)16
UR  - <Go to ISI:>//WOS:000370386000006
C6  - pmid:26747749
DO  - DOI:10.1016/j.neuroimage.2015.12.044
UR  - https://juser.fz-juelich.de/record/280871
ER  -