Decreased Fat Mass in Interleukin-1 Receptor Antagonist–Deficient Mice
Open accessAbstract
Interleukin (IL)-1 is a regulator of inflammation but is also implicated in the control of energy homeostasis. Because the soluble IL-1 receptor antagonist (IL-1Ra) is markedly increased in the serum of obese patients and is overexpressed in white adipose tissue in obesity, we studied the metabolic consequences of genetic IL-1Ra ablation in mice. We have shown that IL-1Ra−/− mice have a lean phenotype due to decreased fat mass, related to a defect in adipogenesis and increased energy expenditure. The adipocytes were smaller in these animals, and the expression of genes involved in adipogenesis was reduced. Energy expenditure as measured by indirect calorimetry was elevated, and weight loss in response to a 24-h fast was increased in IL-1Ra−/− animals compared with wild-type mice. Lipid oxidation of IL-1Ra−/− mice was higher during the light period, reflecting their reduction in diurnal food intake. Interestingly, IL-1Ra−/− and IL-1Ra+/− mice presented an attenuation in high-fat diet–induced caloric hyperphagia, indicating a better adaptation to hypercaloric alimentation, which is in line with the role of IL-1Ra as a mediator of leptin resistance. Taken together, we show that IL-1Ra is an important regulator of adipogenesis, food intake, and energy expenditure.
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Increased abdominal fat mass is associated with chronic elevation of circulating inflammatory mediators including CRP, cytokines, adhesion molecules and pro-thrombotic molecules.
“The increase in abdominal fat mass is associated with a chronic elevation of the circulating concentrations of inflammatory mediators including several acute-phase inflammatory proteins such as CRP (46,47) , proand anti-inflammatory cytokines, adhesion molecules and pro-thrombotic molecules (22,47 -49) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [46]
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- Authors
- Somm, E., Henrichot, E., Pernin, A., Juge-Aubry, C. E., Muzzin, P., Dayer, J.-M., Nicklin, M. J. H., & Meier, C. A.
- Affiliations
- University Hospital of Geneva (CH)
- Endocrine Unit, Department of Internal Medicine, University Hospital, and Department of Cellular Physiology and Metabolism, University Medical Center, Geneva, Switzerland
- University of Geneva (CH)
- Royal Hallamshire Hospital (GB)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-12-01
- Volume
- 54
- Issue
- 12
- Pages
- 3503-3509
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2144150240
- Cited by
- 114
- References
- 42
- Citations by year
- 2026: 1 · 2025: 3 · 2023: 2 · 2022: 7 · 2021: 4 · 2020: 5 · 2019: 2 · 2018: 3 · 2017: 5 · 2016: 1 · 2015: 6 · 2014: 5 · 2013: 9 · 2012: 9
- FWCI
- 6.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- interleukin-1 receptor antagonist, fat mass, adipogenesis, energy expenditure, obesity, leptin resistance, dietary intake, high-fat diet, lipid oxidation, diurnal feeding, adipocyte size, energy homeostasis
- MeSH terms
- Adipose Tissue, Animals, Body Composition, Energy Intake, Energy Metabolism, Gene Amplification, Interleukin-1, Introns, Male, Obesity, Sialoglycoproteins, Weight Gain, Weight Loss, Interleukin-6, Mice, Knockout, Mice, Interleukin 1 Receptor Antagonist Protein
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