Fever has been shown to increase metabolic rate and there is evidence that there is an induction of heat production in brown adipose tissue (BAT). This thesis examines heat production in BAT during fever by measuring GDP-binding to BAT mitochondria and the gene expression of UCP and lipoprotein lipase (LPL). Rats were injected iv. with lipopolysaccharide (LPS; 10 μg/kg body weight) and developed a triphasic fever characterized by an initial decrease in core temperature. Ketoprofen (3 mg/kg body weight), an inhibitor of prostaglandin synthesis, attenuated the increases in core temperature throughout the response but had no effect on the initial hypothermia. Animals made febrile with LPS showed no increase in GDP-binding to BAT mitochondria when compared to saline controls. UCP mRNA and LPL mRNA levels in BAT were also unaffected by the fever. Acute cold exposure induced increases in all of the above parameters. Measurements of the quantity of <I>ob</I> mRNA and LPL mRNA in the WAT of febrile rats revealed no changes in the expression of either gene. Acute cold exposure decreased the levels of <I>ob</I> mRNA, with smaller, but statistically insignificant decreases in LPL mRNA. Genetically obese (<I>fa/fa</I>) Zucker rats and lean controls responded to iv. LPS (10 μg/kg body weight) with a fever characterized by an initial hypothermia. The obese rats had lower levels of UCP mRNA in BAT, but not LPL mRNA, than lean controls. In addition, levels of <I>ob</I> mRNA were considerably elevated in the obese variant but, surprisingly, these differences were not statistically significant. It is concluded that fever does not necessarily involve thermogenesis in BAT and, that changes in energy balance during fever are not manifested as changes in the expression of the <I>ob</I> gene in WAT.