Evidence map›Paper›PMID 37225684›Full record

ArticleNature communications2023

Glycolytically impaired Drosophila glial cells fuel neural metabolism via β-oxidation.

Ellen McMullen, Helen Hertenstein, Katrin Strassburger, Leon Deharde, Marko Brankatschk, Stefanie Schirmeier

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 38 citations in OpenAlex.

  1. Neurons run on fat.npj metabolic health and disease · 2026
    Article
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  4. Review
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  6. Article
  7. Review
  8. Regulation of Metabolic Rhythms by Glial Clocks.Journal of biological rhythms · 2026
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Observational
  16. Article
  17. Article
  18. Review
  19. Alzheimer's disease and gut-brain axis:Frontiers in neuroscience · 2025
    Review
  20. Article
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

6 authors at 2 institutions in 2 countries.

Ellen McMullen *Department of Molecular Biology and Genetics, University of South Bohemia, České Budějovice, Czech Republic.
Helen Hertenstein *Zoology and Animal Physiology, Faculty of Biology, Technische Universität Dresden, Dresden, Germany.
Katrin StrassburgerZoology and Animal Physiology, Faculty of Biology, Technische Universität Dresden, Dresden, Germany.
Leon DehardeZoology and Animal Physiology, Faculty of Biology, Technische Universität Dresden, Dresden, Germany.
Marko BrankatschkBiotechnologisches Zentrum, Technische Universität Dresden, Dresden, Germany. marko.brankatschk@tu-dresden.de.ORCID 0000-0001-5274-4552
Stefanie SchirmeierZoology and Animal Physiology, Faculty of Biology, Technische Universität Dresden, Dresden, Germany. stefanie.schirmeier@tu-dresden.de.ORCID 0000-0001-8431-9593
Technische Universität Dresden · DEUniversity of South Bohemia in České Budějovice · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal function is highly energy demanding and thus requires efficient and constant metabolite delivery by glia. Drosophila glia are highly glycolytic and provide lactate to fuel neuronal metabolism. Flies are able to survive for several weeks in the absence of glial glycolysis. Here, we study how Drosophila glial cells maintain sufficient nutrient supply to neurons under conditions of impaired glycolysis. We show that glycolytically impaired glia rely on mitochondrial fatty acid breakdown and ketone body production to nourish neurons, suggesting that ketone bodies serve as an alternate neuronal fuel to prevent neurodegeneration. We show that in times of long-term starvation, glial degradation of absorbed fatty acids is essential to ensure survival of the fly. Further, we show that Drosophila glial cells act as a metabolic sensor and can induce mobilization of peripheral lipid stores to preserve brain metabolic homeostasis. Our study gives evidence of the importance of glial fatty acid degradation for brain function, and survival, under adverse conditions in Drosophila.

Indexed as

DrosophilaNeurogliaAnimalsFatty AcidsKetone BodiesLactic AcidOxidation-ReductionFatty AcidsKetone BodiesLactic Acid

Identifiers

PMID37225684
PMCPMC10209077
OpenAlexW4377982599

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.