The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Mitochondrial DNA Damage and Dysfunction, and Oxidative Stress Are Associated with Endoplasmic Reticulum Stress, Protein Degradation and Apoptosis in High Fat Diet-Induced Insulin Resistance Mice
Open accessAbstract
BACKGROUND: Recent studies showed a link between a high fat diet (HFD)-induced obesity and lipid accumulation in non-adipose tissues, such as skeletal muscle and liver, and insulin resistance (IR). Although the mechanisms responsible for IR in those tissues are different, oxidative stress and mitochondrial dysfunction have been implicated in the disease process. We tested the hypothesis that HFD induced mitochondrial DNA (mtDNA) damage and that this damage is associated with mitochondrial dysfunction, oxidative stress, and induction of markers of endoplasmic reticulum (ER) stress, protein degradation and apoptosis in skeletal muscle and liver in a mouse model of obesity-induced IR. METHODOLOGY/PRINCIPAL FINDINGS: C57BL/6J male mice were fed either a HFD (60% fat) or normal chow (NC) (10% fat) for 16 weeks. We found that HFD-induced IR correlated with increased mtDNA damage, mitochondrial dysfunction and markers of oxidative stress in skeletal muscle and liver. Also, a HFD causes a change in the expression level of DNA repair enzymes in both nuclei and mitochondria in skeletal muscle and liver. Furthermore, a HFD leads to activation of ER stress, protein degradation and apoptosis in skeletal muscle and liver, and significantly reduced the content of two major proteins involved in insulin signaling, Akt and IRS-1 in skeletal muscle, and Akt in liver. Basal p-Akt level was not significantly influenced by HFD feeding in skeletal muscle and liver. CONCLUSIONS/SIGNIFICANCE: This study provides new evidence that HFD-induced mtDNA damage correlates with mitochondrial dysfunction and increased oxidative stress in skeletal muscle and liver, which is associated with the induction of markers of ER stress, protein degradation and apoptosis.
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Cites
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Mechanisms for Insulin Resistance: Common Threads and Missing Links
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Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling.
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Anderson, E. J., Lustig, M. E., Boyle, K. E., Woodlief, T. L., Kane, D. A., Lin, C.-T., Price, J. W., Kang, L., Rabinovitch, P. S., Szeto, H. H., et al. (2009) · Journal of Clinical Investigation · doi:10.1172/jci37048 · Cited by 1,253
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Insulin resistance is a cellular antioxidant defense mechanism
Hoehn, K. L., Salmon, A. B., Hohnen-Behrens, C., Turner, N., Hoy, A. J., Maghzal, G. J., Stocker, R., Van Remmen, H., Kraegen, E. W., Cooney, G. J., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0902380106 · Cited by 540
High-fat diets cause insulin resistance despite an increase in muscle mitochondria
Hancock, C. R., Han, D.-H., Chen, M., Terada, S., Yasuda, T., Wright, D. C., & Holloszy, J. O. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0802057105 · Cited by 538 · cited 1×
“In agreement with our finding, the DIO study performed by Bonnard et al [7] has shown a significant reduction in mtDNA content in gastrocnemius muscle from IR obese mice, whereas another study has reported that a HFD caused IR despite an increase in muscle mtDNA, proteins and mitochondria [11].”
ResultExcess Lipid Availability Increases Mitochondrial Fatty Acid Oxidative Capacity in Muscle
Turner, N., Bruce, C. R., Beale, S. M., Hoehn, K. L., So, T., Rolph, M. S., & Cooney, G. J. (2007) · Diabetes · doi:10.2337/db07-0093 · Cited by 520
Cited by
Beta Cell Dysfunction and Insulin Resistance
Cerf, M. E. (2013) · Frontiers in Endocrinology · doi:10.3389/fendo.2013.00037 · Cited by 964
PINK1 deficiency impairs mitochondrial homeostasis and promotes lung fibrosis
Bueno, M., Lai, Y.-C., Romero, Y., Brands, J., St. Croix, C. M., Kamga, C., Corey, C., Herazo-Maya, J. D., Sembrat, J., Lee, J. S., et al. (2015) · Journal of Clinical Investigation · doi:10.1172/jci74942 · Cited by 627
Obesity-Associated Oxidative Stress: Strategies Finalized to Improve Redox State
Savini, I., Catani, M., Evangelista, D., Gasperi, V., & Avigliano, L. (2013) · International Journal of Molecular Sciences · doi:10.3390/ijms140510497 · Cited by 503
Nani, A., Murtaza, B., Sayed Khan, A., Khan, N. A., & Hichami, A. (2021) · Molecules · doi:10.3390/molecules26040985 · Cited by 321
Skeletal muscle insulin resistance: role of mitochondria and other ROS sources
Di Meo, S., Iossa, S., & Venditti, P. (2017) · Journal of Endocrinology · doi:10.1530/joe-16-0598 · Cited by 282
Metadata
- Authors
- Yuzefovych, L. V., Musiyenko, S. I., Wilson, G. L., & Rachek, L. I.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-01-16
- Volume
- 8
- Issue
- 1
- Pages
- e54059
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W1973185447
- Cited by
- 303
- References
- 15
- FWCI
- 12.24
- Type
- journal article
- Language
- en
- Open access
- gold
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- Yuzefovych, L. V., Musiyenko, S. I., Wilson, G. L., & Rachek, L. I. (2013). Mitochondrial DNA Damage and Dysfunction, and Oxidative Stress Are Associated with Endoplasmic Reticulum Stress, Protein Degradation and Apoptosis in High Fat Diet-Induced Insulin Resistance Mice. PLoS ONE. https://doi.org/10.1371/journal.pone.0054059
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