Evidence map›Paper›PMID 24944900›Full record

ArticleMolecular metabolism2014

Mitochondrial dysfunction has divergent, cell type-dependent effects on insulin action.

Sheree D Martin, Shona Morrison, Nicky Konstantopoulos, Sean L McGee

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Effects of antipsychotic drugs on energy metabolism.European archives of psychiatry and clinical neuroscience · 2024
    Article
  3. Article
  4. Article
  5. Observational
  6. Article
  7. Article
  8. Review
  9. Adipocyte · 2020
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Mechanisms Underpinning the Polypharmacy Effects of Medications in Psychiatry.The international journal of neuropsychopharmacology · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart.Trends in endocrinology and metabolism: TEM · 2017
    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

4 authors at 2 institutions in 1 country.

Sheree D MartinMetabolic Remodelling Laboratory, Metabolic Research Unit, School of Medicine, Deakin University, Geelong, Australia.
Shona MorrisonMetabolic Remodelling Laboratory, Metabolic Research Unit, School of Medicine, Deakin University, Geelong, Australia.
Nicky KonstantopoulosMetabolic Remodelling Laboratory, Metabolic Research Unit, School of Medicine, Deakin University, Geelong, Australia.
Sean L McGeeMetabolic Remodelling Laboratory, Metabolic Research Unit, School of Medicine, Deakin University, Geelong, Australia ; Cell Signalling and Metabolism Division, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
Deakin University · AUBaker Heart and Diabetes Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The contribution of mitochondrial dysfunction to insulin resistance is a contentious issue in metabolic research. Recent evidence implicates mitochondrial dysfunction as contributing to multiple forms of insulin resistance. However, some models of mitochondrial dysfunction fail to induce insulin resistance, suggesting greater complexity describes mitochondrial regulation of insulin action. We report that mitochondrial dysfunction is not necessary for cellular models of insulin resistance. However, impairment of mitochondrial function is sufficient for insulin resistance in a cell type-dependent manner, with impaired mitochondrial function inducing insulin resistance in adipocytes, but having no effect, or insulin sensitising effects in hepatocytes. The mechanism of mitochondrial impairment was important in determining the impact on insulin action, but was independent of mitochondrial ROS production. These data can account for opposing findings on this issue and highlight the complexity of mitochondrial regulation of cell type-specific insulin action, which is not described by current reductionist paradigms.

Indexed as

AdipocyteAMPK, AMP-activated protein kinaseAS160, Akt substrate of 160 kDaBSA, bovine serum albuminECAR, extracellular acidification rateFoxO1, forkhead box protein O1GLUT4, facilitative glucose transporter isoform 4G.O., glucose oxidaseGP, glucose productionHepatocyteHI-FBS, heat-inactivated foetal bovine serumInsulin actionIRS1, insulin receptor substrate 1LDH, lactate dehydrogenaseMitochondriaMMP, mitochondrial membrane potentialMnTBAP, manganese (III) tetrakis (4-benzoic acid) porphyrin chloridePI3K, phosphatidylinositol 3-kinaseReactive oxygen speciesROS, reactive oxygen speciesSOD, superoxide dismutaseT2D, type 2 diabetesTNFα, tumour necrosis factor alpha

Identifiers

PMID24944900
PMCPMC4060359
OpenAlexW2087944248

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.