Cited by 128Mitochondrial Function and PathologyAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

Reduction in Reactive Oxygen Species Production by Mitochondria From Elderly Subjects With Normal and Impaired Glucose Tolerance

Open access
Ghosh, Sangeeta, Lertwattanarak, Raweewan, Lefort, Natalie, Molina-Carrion, Marjorie, Joya-Galeana, Joaquin, Bowen, Benjamin P., Garduno-Garcia, Jose de Jesus, Abdul-Ghani, Muhammad +5 more·2011·Diabetes

Abstract

OBJECTIVE: Aging increases the risk of developing impaired glucose tolerance (IGT) and type 2 diabetes. It has been proposed that increased reactive oxygen species (ROS) generation by dysfunctional mitochondria could play a role in the pathogenesis of these metabolic abnormalities. We examined whether aging per se (in subjects with normal glucose tolerance [NGT]) impairs mitochondrial function and how this relates to ROS generation, whether older subjects with IGT have a further worsening of mitochondrial function (lower ATP production and elevated ROS generation), and whether exercise reverses age-related changes in mitochondrial function. RESEARCH DESIGN AND METHODS: Mitochondrial ATP and ROS production were measured in muscle from younger individuals with NGT, older individuals with NGT, and older individuals with IGT. Measurements were performed before and after 16 weeks of aerobic exercise. RESULTS: ATP synthesis was lower in older subjects with NGT and older subjects with IGT versus younger subjects. Notably, mitochondria from older subjects (with NGT and IGT) displayed reduced ROS production versus the younger group. ATP and ROS production were similar between older groups. Exercise increased ATP synthesis in the three groups. Mitochondrial ROS production also increased after training. Proteomic analysis revealed downregulation of several electron transport chain proteins with aging, and this was reversed by exercise. CONCLUSIONS: Old mitochondria from subjects with NGT and IGT display mitochondrial dysfunction as manifested by reduced ATP production but not with respect to increased ROS production. When adjusted to age, the development of IGT in elderly individuals does not involve changes in mitochondrial ATP and ROS production. Lastly, exercise reverses the mitochondrial phenotype (proteome and function) of old mitochondria.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.2337/db11-0121

Cites

51 of 51 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Maximal mitochondrial ATP production rates in response to a supply of complex I substrates are lower in older than in younger adults.

    “These findings are consistent with recent data indicating that maximal mitochondrial ATP production rates in response to a supply of complex I substrates are lower in older than in younger adults (35, 39).”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Ghosh, S., Lertwattanarak, R., Lefort, N., Molina-Carrion, M., Joya-Galeana, J., Bowen, B. P., Garduno-Garcia, J. D. J., Abdul-Ghani, M., Richardson, A., DeFronzo, R. A., Mandarino, L., Van Remmen, H., & Musi, N.
Affiliations
  • The University of Texas at San Antonio Health Science Center (US)
  • Arizona State University (US)
  • Diabetes Division, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas
  • Lawrence Berkeley National Laboratory (US)
  • Audie L. Murphy Memorial VA Hospital (US)
  • Sam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, Texas
Corresponding author
Musi, Nicolas
Venue
Diabetes
Published
2011-07-18
Volume
60
Issue
8
Pages
2051-2060
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2101232589
Cited by
128
References
51
Citations by year
2026: 5 · 2025: 4 · 2024: 5 · 2023: 3 · 2022: 7 · 2021: 5 · 2020: 12 · 2019: 9 · 2018: 11 · 2017: 8 · 2016: 12 · 2015: 17 · 2014: 10 · 2013: 11 · 2012: 9
FWCI
3.90
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • OSTI OAI (U.S. Department of Energy Office of Scientific and Technical Information) (submittedVersion)
Funders
  • American Diabetes Association
  • U.S. Department of Veterans Affairs (I01 BX000517)
  • National Institutes of Health
  • National Institute on Aging (AG-030979, K23AG030979, P01AG020591, AG-019316, P01AG019316)
  • National Heart, Lung, and Blood Institute (T32-HL-04776)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R56DK024092, DK80157, R01DK080157, DK 24092, R01DK024092)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
reactive oxygen species, mitochondrial dysfunction, aging, impaired glucose tolerance, type 2 diabetes, skeletal muscle mitochondria, ATP production, aerobic exercise training, mitochondrial proteome, glucose tolerance
MeSH terms
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Adenosine Triphosphate, Adolescent, Adult, Aged, Aging, DNA-Binding Proteins, Heat-Shock Proteins, Humans, Mitochondria, Transcription Factors, Lipid Peroxidation, Exercise, Reactive Oxygen Species, Glucose Intolerance, Gene Expression Profiling, Mitochondrial Proteins, Proteomics, Nuclear Respiratory Factor 1

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review