Evidence mapPaperPMID 39475607Full record

ArticleScience advances2024

Reducing the mitochondrial oxidative burden alleviates lipid-induced muscle insulin resistance in humans.

Matteo Fiorenza, Johan Onslev, Carlos Henríquez-Olguín, Kaspar W Persson, Sofie A Hesselager, Thomas E Jensen, Jørgen F P Wojtaszewski, Morten Hostrup, Jens Bangsbo

Abstract read
In one paragraph

Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
field-weighted citation impact
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

27 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025
    Review
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

9 authors.

Matteo FiorenzaAugust Krogh Section for Human Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.ORCID 0000-0002-8377-0857
Johan OnslevAugust Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.
Carlos Henríquez-OlguínAugust Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.
Kaspar W PerssonAugust Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.ORCID 0000-0001-9557-3503
Sofie A HesselagerAugust Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.ORCID 0009-0008-4054-1430
Thomas E JensenAugust Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.ORCID 0000-0001-6139-8268
Jørgen F P WojtaszewskiAugust Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.ORCID 0000-0001-8185-3408
Morten HostrupAugust Krogh Section for Human Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.ORCID 0000-0002-6201-2483
Jens BangsboAugust Krogh Section for Human Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen 2100, Denmark.ORCID 0000-0003-1305-9274

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preclinical models suggest mitochondria-derived oxidative stress as an underlying cause of insulin resistance. However, it remains unknown whether this pathophysiological mechanism is conserved in humans. Here, we used an invasive in vivo mechanistic approach to interrogate muscle insulin action while selectively manipulating the mitochondrial redox state in humans. To this end, we conducted insulin clamp studies combining intravenous infusion of a lipid overload with intake of a mitochondria-targeted antioxidant (mitoquinone). Under lipid overload, selective modulation of mitochondrial redox state by mitoquinone enhanced insulin-stimulated glucose uptake in skeletal muscle. Mechanistically, mitoquinone did not affect canonical insulin signaling but augmented insulin-stimulated glucose transporter type 4 (GLUT4) translocation while reducing the mitochondrial oxidative burden under lipid oversupply. Complementary ex vivo studies in human muscle fibers exposed to high intracellular lipid levels revealed that mitoquinone improves features of mitochondrial bioenergetics, including diminished mitochondrial H

Indexed as

Insulin ResistanceMitochondriaMuscle, SkeletalOxidation-ReductionOxidative StressAdultAntioxidantsGlucoseGlucose Transporter Type 4HumansInsulinLipidsMaleMitochondria, MuscleOrganophosphorus CompoundsUbiquinoneAntioxidantsGlucoseGlucose Transporter Type 4InsulinLipidsmitoquinoneOrganophosphorus CompoundsUbiquinone

Identifiers

PMID39475607
PMCPMC11524190

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.