Daily body temperature (DBT) rhythm of mice lacking one of the transient receptor potential (TRP) family of proteins, the capsaicin receptor or TRPV1, was recorded by biotelemetry and found to have significantly higher amplitude than that of wild-type mice. Capsaicin-desensitized wild-mice exhibited an even higher DBT amplitude than did TRPV1 deficient mice. A standard heat load (radiant temperature of 36-37 degrees C) resulted in similar rises in body core temperature in wild-type mice and in TRPV1 deficient mice, while capsaicin-desensitized wild-type mice exhibited a robust heat-intolerance. The lack of TRPV1 slightly modifies amplitude of daily body temperature rhythm but does not seem to influence physiological heat defence in mice. In vivo evidence for a TRP protein functioning in the physiological heat-defence range is still lacking.

The purpose of this study was to determine, using push-pull perfusion, the levels of interleukin (IL)-1-like, IL-6-like, and tumor necrosis factor-alpha (TNF)-like activity in the anterior hypothalamus during lipopolysaccharide (LPS)-induced fever in rats. Additionally, slow anterior hypothalamic infusions of human recombinant IL-6 (hrIL-6) or TNF (hrTNF) for several hours were performed to determine possible febrile effects of these two cytokines. Artificial cerebrospinal fluid (aCSF) was infused as a control. Samples of cerebrospinal fluid were collected 60 min before and 60, 180, 300, and 420 min after the intraperitoneal injection of LPS. A control group was injected intraperitoneally with saline. The core temperature (measured by biotelemetry) of LPS-injected rats was significantly higher (P < 0.05) than the temperature of the rats injected with saline at 180, 300, and 420 min after the injection. The average postinjection IL-6 levels were significantly higher (P < 0.05) in the LPS-injected group. TNF was significantly higher (P < 0.05) than the baseline only at 180 min. There were no changes in levels of IL-1-like activity. Infusion of hrIL-6 at a level similar to the peak IL-6 level measured during LPS-induced fever resulted in a slowly developing and long-lasting increase in core temperature. Infusion of hrTNF at a level corresponding to the peak TNF level measured during LPS-induced fever did not induce a significant increase in core temperature. These results support the hypothesis that elevated hypothalamic concentrations of IL-6 are involved in the induction of fever elicited by peripheral (intraperitoneal) injection of LPS.

The purpose of this study was to test the hypothesis that tumor necrosis factor-alpha (TNF) limits fever induced by lipopolysaccharide (LPS) in rats and to determine whether such antipyretic action of this cytokine is outside or inside the central nervous system (CNS). The CNS effects on LPS-induced fever were tested by injecting a subpyrogenic amount (0.20 microgram) of human recombinant TNF (hrTNF) intracerebroventricularly or by slowly infusing into the anterior hypothalamus an amount previously measured in this brain region during LPS fever (0.24 U in 0.13 microliter of artificial cerebrospinal fluid/min). The peripheral effects of this cytokine on LPS fever were tested by injecting 1 micrograms/kg of hrTNF intraperitoneally or by intraperitoneal administration of 300 micrograms/kg of the hrTNF soluble receptor p80 (hrTNFsr). The core temperature (measured by biotelemetry) during LPS fever was not significantly affected by administration of hrTNF intracerebroventricularly or intrahypothalamically. An intraperitoneal injection of hrTNF (1 microgram/kg) had a significant antipyretic effect on febrile response to LPS (mean temperature 2-8 h after injections was 37.28 +/- 0.12 degrees C in rats injected with hrTNF and LPS vs. 38.73 +/- 0.04 degrees C in rats injected with saline and LPS; analysis of variance among groups, P = 0.0001; Fisher's protected least significant difference, P < 0.05). When rats were injected intraperitoneally with hrTNFsr, the febrile response to LPS was enhanced (analysis of variance among groups, P = 0.0001; Fisher's protected least significant difference, P < 0.05). These results support the hypothesis that TNF acts to limit the magnitude of LPS-induced fever and that this action occurs outside the CNS.

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OBJECTIVE:To assess cardiorespiratory exercise function in obese children with and without metabolic syndrome (MS). DESIGN: Comparing three groups of subjects with different cardiovascular risk pro®les. SUBJECTS: Twenty-two MS (body weight (mean AE s.d.) 97.3 AE 15.3 kg; age (mean AE s.d.) 14.2 AE 1.9 y), 17 obese (82.6 AE 15.7 kg; 14.2 AE 2.6 y) and 29 normal weight control (64.3 AE 8.5 kg; 15.3 AE 1.0 y) boys. MEASUREMENTS: Exercise duration (ED), resting heart rate (HR 0 ), peak heart rate (HR peak ), physical working capacity at 170 beatamin (PWC-170), peak oxygen consumption (VO 2peak ) and the lactic acidosis threshold (LAT) were determined on treadmill, using a continuous ramp protocol. RESULTS: ED (MS (mean AE s.d.); 655 AE 86 s; obese 703 AE 64 s; control 750 AE 0 s) in absolute value and PWC-170 normalised for body weight (139 AE 40 w; 177 AE 40 w; 211 AE 40 w) were signi®cantly shorter and lower in the MS group, as compared to obese and control groups (P`0.05). VO 2peak (2.2 AE 0.4 lamin; 2.4 AE 0.5 lamin; 2.9 AE 0.4 lamin) and LAT (1.3 AE 0.4 lamin; 1.5 AE 0.4 la min; 1.8 AE 0.4 lamin) normalised for body weight, were signi®cantly shorter and lower in the MS group, as compared to control group (P`0.05). HR 0 was signi®cantly higher (P`0.05) in MS group than in obese and control groups (88 AE 12 bpm; obese 78 AE 10 bpm; 73 AE 10 bpm). CONCLUSION: Cardiorespiratory exercise performance capacity in MS boys are reduced. It still remains to be elucidated whether the metabolic alterations or the decreased physical activity is responsible for the observed reduction in cardiorespiratory performance. International Journal of Obesity (2001) 25, 966 ± 970

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