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Decreased Fat Mass in Interleukin-1 Receptor Antagonist–Deficient Mice

Impact on Adipogenesis, Food Intake, and Energy Expenditure

¹ Endocrine Unit, Department of Internal Medicine, University Hospital, and Department of Cellular Physiology and Metabolism, University Medical Center, Geneva, Switzerland
² Department of Cellular Physiology and Metabolism, University Medical Center, Geneva, Switzerland
³ Division of Immunology and Allergology, Department of Internal Medicine, University Hospital, Geneva, Switzerland
⁴ Division of Genomic Medicine, University of Sheffield, Royal Hallamshire Hospital, Sheffield, U.K

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.

Key Words: C/EBP, CAAT enhancer–binding protein • eWAT, epididymal white adipose tissue • IL, interleukin • IL-1Ra, IL-1 receptor antagonist • LPL, lipoprotein lipase • PPAR, peroxisome proliferator–activated receptor • RER, respiratory exchange ratio • TNF, tumor necrosis factor • UCP, uncoupling protein • WAT, white adipose tissue

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