IL-15 Overexpression Promotes Endurance, Oxidative Energy Metabolism, and Muscle PPARδ, SIRT1, PGC-1α, and PGC-1β Expression in Male Mice
Open accessAbstract
Endurance exercise initiates a pattern of gene expression that promotes fat oxidation, which in turn improves endurance, body composition, and insulin sensitivity. The signals from exercise that initiate these pathways have not been completely characterized. IL-15 is a cytokine that is up-regulated in skeletal muscle after exercise and correlates with leanness and insulin sensitivity. To determine whether IL-15 can induce any of the metabolic adaptations associated with exercise, substrate metabolism, endurance, and molecular expression patterns were examined in male transgenic mice with constitutively elevated muscle and circulating IL-15 levels. IL-15 transgenic mice ran twice as long as littermate control mice in a run-to-exhaustion trial and preferentially used fat for energy metabolism. Fast muscles in IL-15 transgenic mice exhibited high expression of intracellular mediators of oxidative metabolism that are induced by exercise, including sirtuin 1, peroxisome proliferator-activated receptor (PPAR)-δ, PPAR-γ coactivator-1α, and PPAR-γ coactivator-1β. Muscle tissue in IL-15 transgenic mice exhibited myosin heavy chain and troponin I mRNA isoform expression patterns indicative of a more oxidative phenotype than controls. These findings support a role for IL-15 in induction of exercise endurance, oxidative metabolism, and skeletal muscle molecular adaptations induced by physical training.
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IL-15 augments PPARδ and PGC-1α activity, favoring mitochondrial biogenesis and fatty acid oxidation.
“and augments PPARδ and PGC-1α activity, favoring mitochondrial biogenesis and FAO [84,91,126]”
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 [91]
The Discussion reports increased PPARδ and PGC-1α expression in IL-15 transgenic mice and up-regulation of proteins that promote fatty acid oxidation. It does not establish increased mitochondrial biogenesis: the Discussion explicitly says mitochondrial density was not increased and notes that fatty acid metabolism can increase independently of mitochondrial biogenesis. PPARδ and PGC-1α activity is suggested rather than directly demonstrated. (LLM, conf=0.89)
Experimental — accuracy not yet measuredExercise-inducible myokines irisin, IL-6, IL-15, BAIBA, and METRNL, as well as osteokine OCN, directly stimulate oxidative metabolism in autocrine and endocrine ways.
“Exercise-inducible myokines, such as irisin [62,63], IL-6 [76,77], IL-15 [91,126], BAIBA [111], and METRNL [100], as well as the osteokine OCN [71] have been shown to directly stimulate oxidative metabolism in autocrine and endocrine ways, respectively (1).”
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 [91]
The Abstract (page unavailable) reports that exercise increases muscle IL-15 expression and that mice with elevated IL-15 show greater fat use and an oxidative muscle phenotype. The Discussion (page unavailable) suggests IL-15 acts primarily through a paracrine role in muscle and describes endocrine effects as possible; it does not establish direct stimulation through both autocrine and endocrine pathways. This citation supports only the IL-15 portion of the list, not claims about the other factors. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIL-15 is suggested to be an important modulator of body fat mass and actively participates in innate immune response, playing a role in development and function of NK cells and lymphocytes.
“It has been suggested to be an important modulator of body fat mass, which also actively participates in the innate immune response, playing an important role in the development and function of natural killer (NK) cells and lymphocytes (Quinn et al., 2013).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Quinn et al., 2013
The Abstract identifies IL-15 as part of the innate immune system, and the Results report significantly lower visceral fat mass in IL-15-overexpressing mice, although the difference in total body fat was not significant in this cohort. The paper does not state that IL-15 has a role in the development or function of NK cells and lymphocytes. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIL-15 is directly related to muscle metabolism, diet-induced obesity, and insulin sensitivity.
“In addition, IL-15 is directly related to muscle metabolism, or even diet-induced obesity and insulin sensitivity (Quinn et al., 2011, 2013).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Quinn et al., 2013
IL-15 is expressed by skeletal muscle and has an important metabolic role.
“Another IL expressed by SkM with an important metabolic role is IL-15.”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Quinn et al., 2013
Circulating IL-15 concentration is closely related to physical exercise and increases lipid oxidation and gene expression of PPARδ in rodents when treated with the cytokine.
“The concentration of circulating IL-15 was shown to be closely related to physical exercise, in addition to increasing lipid oxidation and gene expression of peroxisome proliferator-activated receptor delta (PPARδ) in rodents when they were treated with the cytokine (Quinn et al., 2013).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Quinn et al., 2013
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- Authors
- Quinn, L. S., Anderson, B. G., Conner, J. D., & Wolden-Hanson, T.
- Affiliations
- University of Washington (US)
- VA Puget Sound Health Care System (US)
- Research Service (L.S.Q., J.D.C., T.W.-H.), VA Puget Sound Health Care System, Seattle, Washington 98108
- Corresponding author
- Quinn, LeBris S.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2013-01-01
- Volume
- 154
- Issue
- 1
- Pages
- 232-245
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC3529369
- OpenAlex
- W1963939681
- Cited by
- 102
- References
- 44
- Citations by year
- 2026: 7 · 2025: 2 · 2024: 8 · 2023: 8 · 2022: 7 · 2021: 8 · 2020: 7 · 2019: 5 · 2018: 14 · 2017: 4 · 2016: 9 · 2015: 7 · 2014: 10 · 2013: 6
- FWCI
- 7.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX001026)
- National Institute on Aging (R01AG024136, P30AG013280)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30-DK 17047, P30DK017047)
- Topics
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- IL-15, endurance exercise, skeletal muscle, oxidative metabolism, fat oxidation, PPARδ, SIRT1, PGC-1α, PGC-1β, transgenic mice, myosin heavy chain isoforms, troponin I isoforms, exercise adaptation, insulin sensitivity, muscle fiber type
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Energy Metabolism, Male, Mice, Transgenic, Transcription Factors, Trans-Activators, Muscle, Skeletal, Myosin Heavy Chains, Troponin I, Interleukin-15, PPAR delta, Mice, Sirtuin 1
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