Cited by 319Mitochondrial Function and PathologyAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

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Targeted Expression of Catalase to Mitochondria Prevents Age-Associated Reductions in Mitochondrial Function and Insulin Resistance

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Lee, Hui-Young, Choi, Cheol Soo, Birkenfeld, Andreas L., Alves, Tiago C., Jornayvaz, Francois R., Jurczak, Michael J., Zhang, Dongyan, Woo, Dong Kyun, Shadel, Gerald S., Ladiges, Warren, Rabinovitch, Peter S., Santos, Janine H., Petersen, Kitt F., Samuel, Varman T., Shulman, Gerald I.·2010·Cell Metabolism

DOI 10.1016/j.cmet.2010.11.004PMC PMC3013349

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Abstract

Aging-associated muscle insulin resistance has been hypothesized to be due to decreased mitochondrial function, secondary to cumulative free radical damage, leading to increased intramyocellular lipid content. To directly test this hypothesis, we examined both in vivo and in vitro mitochondrial function, intramyocellular lipid content, and insulin action in lean healthy mice with targeted overexpression of the human catalase gene to mitochondria (MCAT mice). Here, we show that MCAT mice are protected from age-induced decrease in muscle mitochondrial function (∼30%), energy metabolism (∼7%), and lipid-induced muscle insulin resistance. This protection from age-induced reduction in mitochondrial function was associated with reduced mitochondrial oxidative damage, preserved mitochondrial respiration and muscle ATP synthesis, and AMP-activated protein kinase-induced mitochondrial biogenesis. Taken together, these data suggest that the preserved mitochondrial function maintained by reducing mitochondrial oxidative damage may prevent age-associated whole-body energy imbalance and muscle insulin resistance.

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Authors: Lee, H.-Y., Choi, C. S., Birkenfeld, A. L., Alves, T. C., Jornayvaz, F. R., Jurczak, M. J., Zhang, D., Woo, D. K., Shadel, G. S., Ladiges, W., Rabinovitch, P. S., Santos, J. H., Petersen, K. F., Samuel, V. T., & Shulman, G. I.
Affiliations: Howard Hughes Medical Institute (US)
Gachon University (KR)
Yale University (US)
University of Washington (US)
Rutgers New Jersey Medical School (US)
Corresponding author: Shulman, Gerald I.
ORCID: Lee, Hui-Young
Choi, Cheol Soo
Birkenfeld, Andreas L.
Alves, Tiago C.
Jurczak, Michael J.
Zhang, Dongyan
Woo, Dong Kyun
Shadel, Gerald S.
Ladiges, Warren
Rabinovitch, Peter S.
Santos, Janine H.
Petersen, Kitt F.
Samuel, Varman T.
Shulman, Gerald I.
Venue: Cell Metabolism
Publisher: Elsevier BV
Published: 2010-12
Volume: 12
Issue: 6
Pages: 668-674
ISSN: 1550-4131 (ISSN-L)
DOI: 10.1016/j.cmet.2010.11.004
PMC: PMC3013349
OpenAlex: W2056525347
Cited by: 319
References: 38
Citations by year: 2026: 6 · 2025: 8 · 2024: 17 · 2023: 7 · 2022: 16 · 2021: 15 · 2020: 21 · 2019: 22 · 2018: 20 · 2017: 16 · 2016: 26 · 2015: 28 · 2014: 38 · 2013: 26 · 2012: 33
FWCI: 10.09
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 959 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Cell Metabolism (publishedVersion)
PubMed (publishedVersion)
Archive ouverte UNIGE (University of Geneva) (publishedVersion)
PubMed Central (acceptedVersion)
Site cant be reached (submittedVersion)
Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Funders: U.S. Department of Veterans Affairs
U.S. Public Health Service (P01 AG001751, P01 ES01116, R01 AG23686, R01 DK40936, U24 DK076169)
Deutsche Forschungsgemeinschaft (Bi1292/2-1)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords: catalase, mitochondrial targeting, muscle aging, insulin resistance, mitochondrial function, oxidative damage, intramyocellular lipid, energy metabolism, AMPK, mitochondrial biogenesis, ATP production, free radicals
MeSH terms: Adenosine Triphosphate, Aging, Animals, Catalase, DNA Damage, Energy Metabolism, Humans, Insulin, Insulin Resistance, Male, Mice, Transgenic, Mitochondria, Oxygen Consumption, Reactive Oxygen Species, Oxidative Stress, Muscle, Skeletal, Microscopy, Electron, Transmission, Mice

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Targeted Expression of Catalase to Mitochondria Prevents Age-Associated Reductions in Mitochondrial Function and Insulin Resistance

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