Evidence map›Paper›PMID 29402381›Full record

ArticleeLife2018

Mitochondrial CoQ deficiency is a common driver of mitochondrial oxidants and insulin resistance.

Daniel J Fazakerley, Rima Chaudhuri, Pengyi Yang, Ghassan J Maghzal, Kristen C Thomas, James R Krycer, Sean J Humphrey, Benjamin L Parker, Kelsey H Fisher-Wellman, Christopher C Meoli and 14 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing 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

75 citing papers in PubMed, 159 citations in OpenAlex.

  1. Trial
  2. SRM-Mediated Spermidine Synthesis Links Lipid Overload With AMPK Pathway to Regulate Hepatic Insulin Signaling and Gluconeogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Observational
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Coenzyme QFree radical biology & medicine · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Understanding coenzyme Q.Physiological reviews · 2024
    Review
  19. Review
  20. Review

15 more citing papers are in PubMed but not listed here.

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

24 authors at 6 institutions in 2 countries.

Daniel J FazakerleyCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.ORCID 0000-0001-8241-2903
Rima ChaudhuriCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
Pengyi YangSchool of Mathematics and Statistics, University of Sydney, Camperdown, Australia.
Ghassan J MaghzalVascular Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.
Kristen C ThomasCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
James R KrycerCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
Sean J HumphreyCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
Benjamin L ParkerCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
Kelsey H Fisher-WellmanDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, United States.
Christopher C MeoliCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
Nolan J HoffmanCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
Ciana DiskinCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
James G BurchfieldCharles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.
Mark J CowleyThe Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst, Australia.
Warren KaplanPeter Wills Bioinformatics Centre, Garvan Institute of Medical Research, Darlinghurst, Australia.
Zora ModrusanGenentech Inc., South San Francisco, United States.
Ganesh KolumamGenentech Inc., South San Francisco, United States.
Jean Yh YangSchool of Mathematics and Statistics, University of Sydney, Camperdown, Australia.
Daniel L ChenGarvan Institute of Medical Research, Darlinghurst, Australia.
Dorit Samocha-BonetGarvan Institute of Medical Research, Darlinghurst, Australia.
Jerry R GreenfieldGarvan Institute of Medical Research, Darlinghurst, Australia.
Kyle L HoehnSchool of Biotechnology and Biomedical Sciences, University of New South Wales, Sydney, Australia.
Roland Stocker *Vascular Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.
David E James *Charles Perkins Centre, School of Life and Environmental Sciences, University of Sydney, Camperdown, Australia.ORCID 0000-0001-5946-5257
The University of Sydney · AUGarvan Institute of Medical Research · AUVictor Chang Cardiac Research Institute · AUDolby (United States) · USDuke University · USUNSW Sydney · AU

Funding

Wellcome TrustWellcome Trust 092255/Z/10/Z
6 · The paper itself

Abstract

Insulin resistance in muscle, adipocytes and liver is a gateway to a number of metabolic diseases. Here, we show a selective deficiency in mitochondrial coenzyme Q (CoQ) in insulin-resistant adipose and muscle tissue. This defect was observed in a range of in vitro insulin resistance models and adipose tissue from insulin-resistant humans and was concomitant with lower expression of mevalonate/CoQ biosynthesis pathway proteins in most models. Pharmacologic or genetic manipulations that decreased mitochondrial CoQ triggered mitochondrial oxidants and insulin resistance while CoQ supplementation in either insulin-resistant cell models or mice restored normal insulin sensitivity. Specifically, lowering of mitochondrial CoQ caused insulin resistance in adipocytes as a result of increased superoxide/hydrogen peroxide production via complex II. These data suggest that mitochondrial CoQ is a proximal driver of mitochondrial oxidants and insulin resistance, and that mechanisms that restore mitochondrial CoQ may be effective therapeutic targets for treating insulin resistance.

Indexed as

AtaxiaInsulin ResistanceMuscle WeaknessAdipocytesAdipose TissueAnimalsHumansMiceMitochondriaMitochondrial DiseasesMusclesOxidantsSensitivity and SpecificityUbiquinoneOxidantsUbiquinonecell biologyCoenzyme Qhumanhuman biologyInsulinInsulin resistancemedicineMitochondriamouseOxidantsUbiquinone

Identifiers

PMID29402381
PMCPMC5800848
OpenAlexW2785501834

What Socratic 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 Socratic graph.