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Mature-Onset Obesity in Interleukin-1 Receptor I Knockout Mice

¹ Department of Physiology and Wallenberg Laboratory, Göteborg University, Göteborg, Sweden
² Medical Genetics Department of Medical Biochemistry, Göteborg University, Göteborg, Sweden
³ Department of Clinical Immunology, Göteborg University, Göteborg, Sweden
⁴ Department of Radiation Physics, Institute of Selected Sciences, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden
⁵ Department of Medicine, Lund University, Malmö, Sweden
⁶ Research Centre for Endocrinology, Sahlgrenska University Hospital, Göteborg, Sweden

Address correspondence and reprint requests to John-Olov Jansson, Department of Physiology, Medicinargatan 9A, SE-405 30 Gothenburg, Sweden. E-mail: john-olov.jansson{at}medic.gu.se

Abbreviations: DEXA, dual-energy X-ray absorptiometry; IL-1, interleukin-1; IL-1Ra, IL-1 receptor antagonist; IL-1RI, IL-1 type I receptor; LBM, lean body mass; MC4-R, melanocortin-4 receptor; MRI, magnetic resonance imaging; RER, respiratory exchange ratio; WAT, white adipose tissue

Interleukin-1 (IL-1) is a major mediator of inflammation that exerts its biological activities through the IL-1 type I receptor (IL-1RI). The body weights of IL-1RI^–/– mice of both sexes started to deviate from those of wild-type mice at 5–6 months of age and were 20% higher at 9 months of age. Visceral and subcutaneous fat mass, measured by dual-energy X-ray absorptiometry and magnetic resonance imaging, was markedly (1.5- to 2.5-fold) increased. Lean body mass and crown-rump length were also slightly (11 and 5%, respectively) increased, as was serum IGF-I. Obese IL-1RI^–/– mice were insulin resistant, as evidenced by hyperinsulinemia, decreased glucose tolerance, and insulin sensitivity. To elucidate the mechanisms for the development of obesity, young preobese IL-1RI^–/– mice were investigated. They showed decreased suppression of body weight and food intake in response to systemic leptin treatment. The decreased leptin responsiveness was even more pronounced in older obese animals. Moreover, spontaneous locomotor activity and fat utilization, as measured by respiratory quotient, were decreased in preobese IL-1RI^–/– mice. In conclusion, lack of IL-1RI–mediated biological activity causes mature-onset obesity. This obese phenotype is preceded by decreased leptin sensitivity, fat utilization, and locomotor activity.

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