Targeting skeletal muscle mitochondrial health in obesity
Open accessAbstract
Metabolic demands of skeletal muscle are substantial and are characterized normally as highly flexible and with a large dynamic range. Skeletal muscle composition (e.g., fiber type and mitochondrial content) and metabolism (e.g., capacity to switch between fatty acid and glucose substrates) are altered in obesity, with some changes proceeding and some following the development of the disease. Nonetheless, there are marked interindividual differences in skeletal muscle composition and metabolism in obesity, some of which have been associated with obesity risk and weight loss capacity. In this review, we discuss related molecular mechanisms and how current and novel treatment strategies may enhance weight loss capacity, particularly in diet-resistant obesity.
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Mitochondrial dysfunction, characterized by reduced mitochondrial size and activity, is prevalent in individuals with obesity and T2DM.
“Mitochondrial dysfunction, characterized by reduced mitochondrial size and activity, is prevalent in individuals with obesity and T2DM and is a known contributor to muscle wasting in ageing and some chronic diseases.”
From The Effects of Glucagon-Like Peptide-1 Receptor Agonists on Mitochondrial Function Within Skeletal Muscle: A Systematic Review (2025) · cites this paper as [30]
The review’s Skeletal muscle and mitochondrial bioenergetics section reports reduced mitochondrial content and impaired mitochondrial function in obesity; its Aerobic exercise section says mitochondria appear smaller in skeletal muscle from people with obesity. The passages do not establish that reduced mitochondrial size and activity are also prevalent in people with T2DM. (LLM, conf=0.82)
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Flagged first, then by citations
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- Authors
- Pileggi, C. A., Hooks, B. G., McPherson, R., Dent, R. R. M., & Harper, M.-E.
- Affiliations
- University of Ottawa (CA)
- Ottawa Heart Institute (CA)
- Corresponding author
- Harper, Mary-Ellen
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2022-07
- Volume
- 136
- Issue
- 14
- Pages
- 1081-1110
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- PMC
- PMC9334731
- OpenAlex
- W4288046809
- Cited by
- 21
- References
- 395
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 4 · 2023: 3 · 2022: 1
- FWCI
- 0.55
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Clinical Science (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (143278_1)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- skeletal muscle, mitochondrial function, obesity, mitochondrial biogenesis, muscle fiber type, substrate metabolism, fatty acid oxidation, glucose utilization, interindividual variability, obesity risk, obesity treatment strategies
- MeSH terms
- Fatty Acids, Humans, Mitochondria, Mitochondria, Muscle, Obesity, Weight Loss, Muscle, Skeletal
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.
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