Evidence map›Paper›PMID 26747749›Full record

ArticleNeuroImage2016

Glucose consumption of inflammatory cells masks metabolic deficits in the brain.

Heiko Backes, Maureen Walberer, Anne Ladwig, Maria A Rueger, Bernd Neumaier, Heike Endepols, Mathias Hoehn, Gereon R Fink, Michael Schroeter, Rudolf Graf

Open access · hybridAbstract read
In one paragraph

Article in NeuroImage, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 70 citations in OpenAlex.

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  20. Aberrant Energy Metabolism in Alzheimer's Disease.Journal of translational internal medicine · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Heiko BackesMax Planck Institute for Metabolism Research, Cologne, Germany. Electronic address: backes@sf.mpg.de.
Maureen WalbererMax Planck Institute for Metabolism Research, Cologne, Germany; Department of Neurology, University Hospital, Cologne, Germany.
Anne LadwigMax Planck Institute for Metabolism Research, Cologne, Germany; Department of Neurology, University Hospital, Cologne, Germany.
Maria A RuegerMax Planck Institute for Metabolism Research, Cologne, Germany; Department of Neurology, University Hospital, Cologne, Germany.
Bernd NeumaierMax Planck Institute for Metabolism Research, Cologne, Germany; Department of Radiochemistry and Experimental Molecular Imaging, University of Cologne, Germany.
Heike EndepolsDepartment of Radiochemistry and Experimental Molecular Imaging, University of Cologne, Germany.
Mathias HoehnMax Planck Institute for Metabolism Research, Cologne, Germany.
Gereon R FinkDepartment of Neurology, University Hospital, Cologne, Germany; Institute of Neuroscience and Medicine (INM-3), Cognitive Neurology Section, Research Centre Juelich, Germany.
Michael SchroeterMax Planck Institute for Metabolism Research, Cologne, Germany; Department of Neurology, University Hospital, Cologne, Germany.
Rudolf GrafMax Planck Institute for Metabolism Research, Cologne, Germany.
Max Planck Institute for Metabolism Research · DEUniversity Hospital Cologne · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsBrainBrain IschemiaEnergy MetabolismGlucoseImage Processing, Computer-AssistedInflammationMagnetic Resonance ImagingMalePositron-Emission TomographyRatsRats, WistarGlucose[(11)C]PK11195Cerebral ischemiaFDGGlucose metabolismNeuroinflammationPositron emission tomography

Identifiers

PMID26747749
PMCPMC4767221
OpenAlexW2204761283

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.