Evidence map›Paper›PMID 28611773›Full record

ArticleFrontiers in immunology2017

Fatty Acid Oxidation Compensates for Lipopolysaccharide-Induced Warburg Effect in Glucose-Deprived Monocytes.

Nora Raulien, Kathleen Friedrich, Sarah Strobel, Stefan Rubner, Sven Baumann, Martin von Bergen, Antje Körner, Martin Krueger, Manuela Rossol, Ulf Wagner

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 75 citations in OpenAlex.

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  11. Immunometabolism at the Heart of Cardiovascular Disease.JACC. Basic to translational science · 2023
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  14. 1,2-Current issues in molecular biology · 2023
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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.

Nora RaulienDivision of Rheumatology, Department of Internal Medicine, University of Leipzig, Leipzig, Germany.
Kathleen FriedrichDivision of Rheumatology, Department of Internal Medicine, University of Leipzig, Leipzig, Germany.
Sarah StrobelDivision of Rheumatology, Department of Internal Medicine, University of Leipzig, Leipzig, Germany.
Stefan RubnerDivision of Rheumatology, Department of Internal Medicine, University of Leipzig, Leipzig, Germany.
Sven BaumannDepartment of Molecular Systems Biology, Helmholtz Centre for Environmental Research - UFZ, Leipzig, Germany.
Martin von BergenDepartment of Molecular Systems Biology, Helmholtz Centre for Environmental Research - UFZ, Leipzig, Germany.
Antje KörnerHospital for Children and Adolescents, Department of Women and Child Health, University Hospitals, University of Leipzig, Leipzig, Germany.
Martin KruegerInstitute of Anatomy, University of Leipzig, Leipzig, Germany.
Manuela RossolDivision of Rheumatology, Department of Internal Medicine, University of Leipzig, Leipzig, Germany.
Ulf WagnerDivision of Rheumatology, Department of Internal Medicine, University of Leipzig, Leipzig, Germany.
Leipzig University · DEHelmholtz Centre for Environmental Research · DEUniversity Hospital Leipzig · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocytes enter sites of microbial or sterile inflammation as the first line of defense of the immune system and initiate pro-inflammatory effector mechanisms. We show that activation with bacterial lipopolysaccharide (LPS) induces them to undergo a metabolic shift toward aerobic glycolysis, similar to the Warburg effect observed in cancer cells. At sites of inflammation, however, glucose concentrations are often drastically decreased, which prompted us to study monocyte function under conditions of glucose deprivation and abrogated Warburg effect. Experiments using the Seahorse Extracellular Flux Analyzer revealed that limited glucose supply shifts monocyte metabolism toward oxidative phosphorylation, fueled largely by fatty acid oxidation at the expense of lipid droplets. While this metabolic state appears to provide sufficient energy to sustain functional properties like cytokine secretion, migration, and phagocytosis, it cannot prevent a rise in the AMP/ATP ratio and a decreased respiratory burst. The molecular trigger mediating the metabolic shift and the functional consequences is activation of AMP-activated protein kinase (AMPK). Taken together, our results indicate that monocytes are sufficiently metabolically flexible to perform pro-inflammatory functions at sites of inflammation despite glucose deprivation and inhibition of the LPS-induced Warburg effect. AMPK seems to play a pivotal role in orchestrating these processes during glucose deprivation in monocytes.

Indexed as

fatty acid oxidationglucose deprivationinflammationmonocytesWarburg effect

Identifiers

PMID28611773
PMCPMC5447039
OpenAlexW2616963786

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.