Evidence map›Paper›PMID 25605809›Full record

Trial reportDiabetes2015

Defects in mitochondrial efficiency and H2O2 emissions in obese women are restored to a lean phenotype with aerobic exercise training.

Adam R Konopka, Albert Asante, Ian R Lanza, Matthew M Robinson, Matthew L Johnson, Chiara Dalla Man, Claudio Cobelli, Mark H Amols, Brian A Irving, K S Nair

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 6 pooled it
5.8field-weighted citation impact, top 3% 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, 6 syntheses or guidelines pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  5. Lifestyle changes in women with polycystic ovary syndrome.The Cochrane database of systematic reviews · 2019
    Pooled it
  6. Pooled it
  7. Trial
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  10. Trial
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  12. Trial
  13. Trial
  14. Myokines and mitochondrial function in cardiometabolic diseases.Journal of physiology and biochemistry · 2026
    Review
  15. Review
  16. Review
  17. Review
  18. Multidimensional Modeling to Maximize Adaptations to eXercise: the MJournal of applied physiology (Bethesda, Md. : 1985) · 2025
    Article
  19. Article
  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

10 authors at 2 institutions in 2 countries.

Adam R KonopkaDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN.
Albert AsanteDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN.
Ian R LanzaDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN.
Matthew M RobinsonDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN.
Matthew L JohnsonDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN.
Chiara Dalla ManDepartment of Information Engineering, University of Padova, Padova, Italy.
Claudio CobelliDepartment of Information Engineering, University of Padova, Padova, Italy.
Mark H AmolsDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN.
Brian A IrvingDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN.
K S NairDivision of Endocrinology, Diabetes, Metabolism, and Nutrition Research, Mayo Clinic College of Medicine, Rochester, MN nair@mayo.edu.
Mayo Clinic · USUniversity of Padua · IT

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
Mayo Clinic Center for Translational Science ActivitiesKL2RR024151 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$15.3M
DIABETES AND METABOLISMT32DK007352 · NIDDK · MAYO CLINIC ROCHESTER · PI MICHAEL D. JENSEN · 1986 to 2026
$9.4M
TECHNOLOGY NMR SPECTROSCOPYU24DK100469 · NIDDK · MAYO CLINIC ROCHESTER · PI NAIR, K SREEKUMARAN · 2013 to 2017
$9.0M
IN VIVO REGULATION OF PROTEIN TURNOVER BY HORMONESR01DK041973 · NIDDK · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NAIR, K SREEKUMARAN · 1989 to 2014
$7.3M
Mayo Clinic Center for Translational Science ActivitiesKL2TR000136 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$6.6M
In Vivo Regulation of Protein Turnover by HormonesR56DK041973 · NIDDK · MAYO CLINIC ROCHESTER · PI NAIR, K SREEKUMARAN · 2015 to 2015
$159k
NCATS NIH HHS KL2 TR000136NCATS NIH HHS KL2TR000136NCATS NIH HHS UL1 TR000135NCATS NIH HHS UL1TR000135NCRR NIH HHS KL2 RR024151NCRR NIH HHS KL2RR024151NIDDK NIH HHS DK41973NIDDK NIH HHS R01 DK041973NIDDK NIH HHS R56 DK041973NIDDK NIH HHS T32 DK007352NIDDK NIH HHS T32DK007352NIDDK NIH HHS U24 DK100469NIDDK NIH HHS U24DK100469
6 · The paper itself

Abstract

The notion that mitochondria contribute to obesity-induced insulin resistance is highly debated. Therefore, we determined whether obese (BMI 33 kg/m(2)), insulin-resistant women with polycystic ovary syndrome had aberrant skeletal muscle mitochondrial physiology compared with lean, insulin-sensitive women (BMI 23 kg/m(2)). Maximal whole-body and mitochondrial oxygen consumption were not different between obese and lean women. However, obese women exhibited lower mitochondrial coupling and phosphorylation efficiency and elevated mitochondrial H2O2 (mtH2O2) emissions compared with lean women. We further evaluated the impact of 12 weeks of aerobic exercise on obesity-related impairments in insulin sensitivity and mitochondrial energetics in the fasted state and after a high-fat mixed meal. Exercise training reversed obesity-related mitochondrial derangements as evidenced by enhanced mitochondrial bioenergetics efficiency and decreased mtH2O2 production. A concomitant increase in catalase antioxidant activity and decreased DNA oxidative damage indicate improved cellular redox status and a potential mechanism contributing to improved insulin sensitivity. mtH2O2 emissions were refractory to a high-fat meal at baseline, but after exercise, mtH2O2 emissions increased after the meal, which resembles previous findings in lean individuals. We demonstrate that obese women exhibit impaired mitochondrial bioenergetics in the form of decreased efficiency and impaired mtH2O2 emissions, while exercise effectively restores mitochondrial physiology toward that of lean, insulin-sensitive individuals.

Indexed as

EstradiolExerciseFemaleHumansHydrogen PeroxideInsulin ResistanceMitochondriaObesityOxidative StressOxygen ConsumptionProgesteroneThinnessEstradiolHydrogen PeroxideProgesterone

Identifiers

PMID25605809
PMCPMC4439568
OpenAlexW1989373047

What OpenQuestion holds

Textmetadata
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.