Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice
Open accessAbstract
Mitochondrial dysfunction in skeletal muscle has been implicated in the development of type 2 diabetes. However, whether these changes are a cause or a consequence of insulin resistance is not clear. We investigated the structure and function of muscle mitochondria during the development of insulin resistance and progression to diabetes in mice fed a high-fat, high-sucrose diet. Although 1 month of high-fat, high-sucrose diet feeding was sufficient to induce glucose intolerance, mice showed no evidence of mitochondrial dysfunction at this stage. However, an extended diet intervention induced a diabetic state in which we observed altered mitochondrial biogenesis, structure, and function in muscle tissue. We assessed the role of oxidative stress in the development of these mitochondrial abnormalities and found that diet-induced diabetic mice had an increase in ROS production in skeletal muscle. In addition, ROS production was associated with mitochondrial alterations in the muscle of hyperglycemic streptozotocin-treated mice, and normalization of glycemia or antioxidant treatment decreased muscle ROS production and restored mitochondrial integrity. Glucose- or lipid-induced ROS production resulted in mitochondrial alterations in muscle cells in vitro, and these effects were blocked by antioxidant treatment. These data suggest that mitochondrial alterations do not precede the onset of insulin resistance and result from increased ROS production in muscle in diet-induced diabetic mice.
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Skeletal muscle experiences elevated ROS production due to cellular responses to elevated free fatty acids and hyperglycemia in obesity.
“Notably, skeletal muscle experiences an elevated ROS production due to cellular responses to elevated levels of free fatty acids and hyperglycemia in obesity [18, 19].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [18]
n = 3-4 is a sample size commonly used in TEM-based studies investigating mitochondrial morphology and ultrastructure.
“It is important to highlight here that n = 3–4 is a sample size commonly used in TEM-based studies investigating mitochondrial morphology and ultrastructure (Bonnard et al., 2008; Sato et al., 2013; Arruda et al., 2014; Leduc-Gaudet et al., 2015; Saleem et al., 2015; Demeter-Haludka et al., 2018; Loro et al., 2018).”
From Effects of Aging and Caloric Restriction on Fiber Type Composition, Mitochondrial Morphology and Dynamics in Rat Oxidative and Glycolytic Muscles (2019) · cites this paper as Bonnard et al., 2008
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RetractedTargeting skeletal muscle mitochondrial health in obesity
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Recent research advances in metabolism, clinical and experimental
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- Authors
- Bonnard, C., Durand, A., Peyrol, S., Chanseaume, E., Chauvin, M.-A., Morio, B., Vidal, H., & Rieusset, J.
- Affiliations
- Inserm (FR)
- Lyon 1 Université (FR)
- Institut National de la Recherche Agronomique (FR)
- Corresponding author
- Rieusset, Jennifer
- Venue
- Journal of Clinical Investigation
- Published
- 2008-01-10
- Volume
- 118
- Issue
- 2
- Pages
- 789-800
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2176186
- OpenAlex
- W2169593539
- Cited by
- 819
- References
- 38
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 27 · 2023: 33 · 2022: 30 · 2021: 28 · 2020: 45 · 2019: 50 · 2018: 44 · 2017: 50 · 2016: 55 · 2015: 61 · 2014: 67 · 2013: 57 · 2012: 79
- FWCI
- 23.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Agence Nationale de la Recherche (ANR-05)
- Institut National de la Santé et de la Recherche Médicale (ANR-05-PCOD-012)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- mitochondrial dysfunction, skeletal muscle, insulin resistance, oxidative stress, reactive oxygen species, mitochondrial biogenesis, high-fat high-sugar diet, type 2 diabetes, impaired glucose tolerance, streptozotocin-induced diabetes, antioxidant treatment, mitochondrial integrity
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Diet, Dietary Fats, Insulin Resistance, Male, Mice, Inbred C57BL, Mitochondria, Muscle, Sucrose, Reactive Oxygen Species, Oxidative Stress, Muscle, Skeletal, Muscle Fibers, Skeletal, Mitochondrial Diseases, Mice
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