Expression and function of myostatin in obesity, diabetes, and exercise adaptation
Open accessAbstract
Myostatin is a member of the transforming growth factor-β/bone morphogenetic protein (TGF-β/BMP) superfamily of secreted factors that functions as a potent inhibitor of skeletal muscle growth. Moreover, considerable evidence has accumulated that myostatin also regulates metabolism and that its inhibition can significantly attenuate the progression of obesity and diabetes. Although at least part of these effects on metabolism can be attributable to myostatin's influence over skeletal muscle growth and therefore on the total volume of metabolically active lean body mass, there is mounting evidence that myostatin affects the growth and metabolic state of other tissues, including the adipose and the liver. In addition, recent work has explored the role of myostatin in substrate mobilization, uptake, and/or utilization of muscle independent of its effects on body composition. Finally, the effects of both endurance and resistance exercise on myostatin expression, as well as the potential role of myostatin in the beneficial metabolic adaptations occurring in response to exercise, have also begun to be delineated in greater detail. The purpose of this review was to summarize the work to date on the expression and function of myostatin in obesity, diabetes, and exercise adaptation.
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Inhibition of myostatin upregulates oxidative metabolism in skeletal muscle.
“On the contrary, inhibition of myostatin upregulates oxidative metabolism in SkM [115].”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [115]
The Myostatin and Endurance Exercise Adaptation section (page unavailable) reports that untrained myostatin-null mice have more fast, glycolytic muscle fibers and poorer endurance performance, contrary to a general claim that inhibition upregulates skeletal-muscle oxidative metabolism. It also says their muscle oxidative potential increases with endurance training comparably to wild-type mice, not that myostatin inhibition itself causes the increase. (LLM, conf=0.78)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredMyostatin was the first identified muscle-secreted factor and is known to promote skeletal muscle atrophy.
“Myostatin was the first identified muscle-secreted factor and is known to promote SkM atrophy [115].”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [115]
The Introduction says myostatin is secreted and that its overexpression is associated with dramatic muscle atrophy in mice. It describes myostatin’s identification in 1997 but does not say it was the first muscle-secreted factor identified. Page numbers are not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMyostatin is the only myokine known to be downregulated by acute and chronic endurance- and resistance-type exercise in both rodents and humans.
“It is the only myokine known to be downregulated by acute and chronic endurance- and resistance-type exercise in both rodents and humans [115].”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [115]
The Endurance Exercise Adaptation section reports decreased muscle myostatin expression after acute and chronic endurance exercise, including training in rodents and humans. The Resistance Exercise Adaptation section reports decreases after acute and chronic resistance exercise in humans, but also describes studies finding an increase or no change. The copy does not establish that myostatin is the only myokine with this response or document the full combination of exercise types and durations in both species; page numbers were not available. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMyostatin expression increases in skeletal muscle due to obesity and insulin resistance, and it could favor the loss of skeletal muscle in sarcopenic obesity.
“Myostatin expression increases in skeletal muscle due to obesity and IR. Thus, it could favor the loss of skeletal muscle in SO [14, 61, 62].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [61]
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- Authors
- ALLEN, D. L., HITTEL, D. S., & MCPHERRON, A. C.
- Affiliations
- University of Colorado Boulder (US)
- University of Calgary (CA)
- National Institutes of Health (US)
- Venue
- Medicine & Science in Sports & Exercise
- Published
- 2011-10
- Volume
- 43
- Issue
- 10
- Pages
- 1828-1835
- ISSN
- 0195-9131 (ISSN-L)
- PMC
- PMC3192366
- OpenAlex
- W2008438711
- Cited by
- 207
- References
- 75
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 19 · 2023: 17 · 2022: 24 · 2021: 16 · 2020: 13 · 2019: 14 · 2018: 12 · 2017: 13 · 2016: 7 · 2015: 11 · 2014: 17 · 2013: 9 · 2012: 9
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Medicine & Science in Sports & Exercise (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (ZIADK056020, ZIADK075048)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- myostatin, obesity, diabetes mellitus, exercise adaptation, skeletal muscle growth, adipose tissue, liver, substrate mobilization, lean body mass, endurance exercise, resistance training, metabolic adaptation
- MeSH terms
- Adaptation, Physiological, Adipose Tissue, Animals, Diabetes Mellitus, Type 2, Female, Humans, Liver, Male, Obesity, Exercise, Muscle, Skeletal, Mice, Rats, Myostatin
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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