The activity of brown adipose tissue (BAT), a site of non-shivering metabolic thermogenesis, has been reported to increase after interleukin (IL)-1 / lipopolysaccharide injection. To clarify the possible contribution of BAT thermogenesis to whole body febrile response, we investigated febrile and thermogenic response to IL-1 using mice deficient in uncoupling protein (UCP) 1, a key molecule for BAT thermogenesis. In wild-type (WT) mice, IL-1 injection (5µg/kg, i.p.) increased plasma corticosterone level (+1220 % at 1 hr) and body temperature (+1.82 °C at 20 min), and decreased physical activity (-37 % at 1 hr), and produced a slight and insignificant rise (+15 % at 1 hr) in oxygen consumption (VO₂). VO₂ dependent on metabolic thermogenesis (VO_{2-thermogenesis}) calculated by correcting the effect of physical activity was increased after IL-1 injection (726 ± 200 ml/h/kg at 1 hr). Almost the same responses were observed in UCP1-deficient mice, showing 638 ± 87 ml/h/kg of VO_{2-thermogenesis} at 1 hr. In contrast, CL316,243, a selective activator of BAT thermogenesis, increased body temperature, decreased physical activity, and produced a significant rise in VO₂ in WT mice, showing 1229 ± 35 ml/h/kg of VO_{2-thermogenesis} at 1 hr. These changes were not observed in UCP1-deficient mice. These results, conflicting with a previously proposed idea of a role of BAT in fever, suggest a minor contribution of BAT thermogenesis to IL-1-induced fever. In support of this, we found no effect of IL-1 on triglyceride content and UCP1 mRNA level in BAT, in contrast with apparent effects of CL316,243.