Journal Article FZJ-2016-00582

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Glucose consumption of inflammatory cells masks metabolic deficits in the brain

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2016
Academic Press Orlando, Fla.

NeuroImage 128, 54 - 62 () [10.1016/j.neuroimage.2015.12.044]

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Abstract: 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.

Classification:

Contributing Institute(s):
  1. Kognitive Neurowissenschaften (INM-3)
  2. Nuklearchemie (INM-5)
Research Program(s):
  1. 572 - (Dys-)function and Plasticity (POF3-572) (POF3-572)

Appears in the scientific report 2016
Database coverage:
Medline ; Creative Commons Attribution-NonCommercial-NoDerivs CC BY-NC-ND 4.0 ; OpenAccess ; BIOSIS Previews ; Current Contents - Life Sciences ; IF >= 5 ; JCR ; NCBI Molecular Biology Database ; NationallizenzNationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection
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Dokumenttypen > Aufsätze > Zeitschriftenaufsätze
Institutssammlungen > INM > INM-3
Institutssammlungen > INM > INM-5
Workflowsammlungen > Öffentliche Einträge
Publikationsdatenbank
Open Access

 Datensatz erzeugt am 2016-01-18, letzte Änderung am 2021-01-29


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