Are Alterations in Skeletal Muscle Mitochondria a Cause or Consequence of Insulin Resistance?
Open accessAbstract
As a major site of glucose uptake following a meal, skeletal muscle has an important role in whole-body glucose metabolism. Evidence in humans and animal models of insulin resistance and type 2 diabetes suggests that alterations in mitochondrial characteristics accompany the development of skeletal muscle insulin resistance. However, it is unclear whether changes in mitochondrial content, respiratory function, or substrate oxidation are central to the development of insulin resistance or occur in response to insulin resistance. Thus, this review will aim to evaluate the apparent conflicting information placing mitochondria as a key organelle in the development of insulin resistance in skeletal muscle.
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Insulin resistance and reductions in glucose tolerance have previously been linked to altered mitochondrial characteristics.
“Insulin resistance and reductions in glucose tolerance have previously been linked to altered mitochondrial characteristics [14,15,54]”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [54]
Dysregulation of mitochondrial function can accelerate lipid deposition and oxidative stress in muscle, thereby exacerbating the decrease in muscle mass.
“Additionally, the dysregulation of mitochondrial function can accelerate lipid deposition and oxidative stress in muscle, thereby exacerbating the decrease in muscle mass [12].”
From A High-Fat Diet Induces Muscle Mitochondrial Dysfunction and Impairs Swimming Capacity in Zebrafish: A New Model of Sarcopenic Obesity (2022) · cites this paper as [12]
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Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction
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Passive heat stress induces mitochondrial adaptations in skeletal muscle
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Exercise does not improve insulin resistance and mitochondrial characteristics together
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Loss of Trim28 in muscle alters mitochondrial signalling but not systemic metabolism
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- Authors
- Genders, A. J., Holloway, G. P., & Bishop, D. J.
- Affiliations
- Victoria University (AU)
- University of Guelph (CA)
- Corresponding author
- Genders, Amanda J.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-09-22
- Volume
- 21
- Issue
- 18
- Pages
- 6948
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7554894
- OpenAlex
- W3088784860
- Cited by
- 51
- References
- 145
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 9 · 2023: 5 · 2022: 13 · 2021: 8 · 2020: 3
- FWCI
- 0.69
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Victoria University Research Repository (Victoria University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Australian Research Council (DP140104165)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- skeletal muscle insulin resistance, mitochondrial dysfunction, type 2 diabetes, glucose uptake, mitochondrial respiratory function, substrate oxidation, mitochondrial content, glucose metabolism
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Mitochondria, Muscle, Muscle, Skeletal
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