Evidence map›Paper›PMID 23974920›Full record

ArticleDiabetes2014

Mitochondrial respiratory capacity and content are normal in young insulin-resistant obese humans.

Kelsey H Fisher-Wellman, Todd M Weber, Brook L Cathey, Patricia M Brophy, Laura A A Gilliam, Constance L Kane, Jill M Maples, Timothy P Gavin, Joseph A Houmard, P Darrell Neufer

Abstract read
In one paragraph

Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
–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

48 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Human studies of mitochondrial biology demonstrate an overall lack of binary sex differences: A multivariate meta-analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Pooled it
  2. Trial
  3. Trial
  4. Metabolic Inflexibility with Obesity and the Effects of Fenofibrate on Skeletal Muscle Fatty Acid Oxidation.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2017
    Trial
  5. Trial
  6. Article
  7. Article
  8. Article
  9. Article
  10. Exercise as a tool to mitigate metabolic disease.American journal of physiology. Cell physiology · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
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  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Kelsey H Fisher-WellmanEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC.
Todd M Weber
Brook L Cathey
Patricia M Brophy
Laura A A Gilliam
Constance L Kane
Jill M Maples
Timothy P Gavin
Joseph A Houmard
P Darrell Neufer

Funding

LIPID METABOLISM IN OBESITY, WEIGHT LOSS AND EXERCISER01DK056112 · NIDDK · EAST CAROLINA UNIVERSITY · PI HOUMARD, JOSEPH A · 2000 to 2016
$4.5M
Linking Mitochondrial Bioenergetics to Muscle Insulin SensitivityR01DK074825 · NIDDK · EAST CAROLINA UNIVERSITY · PI NEUFER, P DARRELL · 2009 to 2013
$1.6M
NIDDK NIH HHS DK-075825NIDDK NIH HHS R01 DK056112NIDDK NIH HHS R01 DK074825
6 · The paper itself

Abstract

Considerable debate exists about whether alterations in mitochondrial respiratory capacity and/or content play a causal role in the development of insulin resistance during obesity. The current study was undertaken to determine whether such alterations are present during the initial stages of insulin resistance in humans. Young (∼23 years) insulin-sensitive lean and insulin-resistant obese men and women were studied. Insulin resistance was confirmed through an intravenous glucose tolerance test. Measures of mitochondrial respiratory capacity and content as well as H(2)O(2) emitting potential and the cellular redox environment were performed in permeabilized myofibers and primary myotubes prepared from vastus lateralis muscle biopsy specimens. No differences in mitochondrial respiratory function or content were observed between lean and obese subjects, despite elevations in H(2)O(2) emission rates and reductions in cellular glutathione. These findings were apparent in permeabilized myofibers as well as in primary myotubes. The results suggest that reductions in mitochondrial respiratory capacity and content are not required for the initial manifestation of peripheral insulin resistance.

Indexed as

AdolescentAdultBlood GlucoseFemaleHumansHydrogen PeroxideInsulinInsulin ResistanceMaleMitochondria, MuscleMuscle Fibers, SkeletalMuscle, SkeletalObesityOxidation-ReductionBlood GlucoseHydrogen PeroxideInsulin

Identifiers

PMID23974920
PMCPMC3868052

What OpenQuestion holds

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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.