Interleukin-15 contributes to the regulation of murine adipose tissue and human adipocytes
Abstract
An alarming global rise in the prevalence of obesity and its contribution to the development of chronic diseases is a serious health concern. Recently, obesity has been described as a chronic low-grade inflammatory condition, influenced by both adipose tissue and immune cells suggesting proinflammatory cytokines may play a role in its etiology. Here we examined the effects of interleukin-15 (IL-15) on adipose tissue and its association with obesity. Over expression of IL-15 (IL-15tg) was associated with lean body condition whereas lack of IL-15 (IL-15(-/-)) results in significant increase in weight gain without altering appetite. Interestingly, there were no differences in proinflammatory cytokines such as IL-6 and tumor necrosis factor-alpha (TNF-alpha) in serum between the three strains of mice. In addition, there were significant numbers of natural killer (NK) cells in fat tissues from IL-15tg and B6 compared to IL-15(-/-) mice. IL-15 treatment results in significant weight loss in IL-15(-/-) knockout and diet-induced obese mice independent of food intake. Fat pad cross-sections show decreased pad size with over expression of IL-15 is due to adipocyte shrinkage. IL-15 induces weight loss without altering food consumption by affecting lipid deposition in adipocytes. Treatment of differentiated human adipocytes with recombinant human IL-15 protein resulted in decreased lipid deposition. In addition, obese patients had significantly lower serum IL-15 levels when compared to normal weight individuals. These results clearly suggest that IL-15 may be involved in adipose tissue regulation and linked to obesity.
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IL-15 decreases fat mass by promoting influx of energetic substrates to skeletal muscle, which limits free fatty acid deposits in visceral adipose tissue and adipocytes.
“It decreases fat mass by promoting influx of energetic substrates to SkM, which limits FFA deposits in VAT and in adipocytes [127].”
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- Authors
- Barra, N. G., Reid, S., MacKenzie, R., Werstuck, G., Trigatti, B. L., Richards, C., Holloway, A. C., & Ashkar, A. A.
- Affiliations
- McMaster University (CA)
- Corresponding author
- Holloway, Alison C.
- ORCID
- Venue
- Obesity
- Publisher
- Wiley
- Published
- 2010-08
- Volume
- 18
- Issue
- 8
- Pages
- 1601-1607
- ISSN
- 1930-7381 (ISSN-L)
- 1930-739X
- OpenAlex
- W2064954598
- Cited by
- 116
- References
- 27
- Citations by year
- 2026: 7 · 2025: 2 · 2024: 5 · 2023: 2 · 2022: 5 · 2021: 10 · 2020: 6 · 2019: 5 · 2018: 14 · 2017: 7 · 2016: 10 · 2015: 5 · 2014: 9 · 2013: 12 · 2012: 10
- FWCI
- 3.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Obesity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- McMaster University
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- IL-15, adipose tissue, adipocytes, natural killer cells, weight gain, diet-induced obesity, low-grade inflammation
- MeSH terms
- Adipose Tissue, Animals, Appetite, Energy Intake, Female, Humans, Killer Cells, Natural, Mice, Inbred C57BL, Mice, Obese, Obesity, Recombinant Proteins, Weight Gain, Weight Loss, Cytokines, Adipocytes, Mice, Knockout, Inflammation Mediators, Interleukin-15, Lipid Metabolism, Mice
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