Abstract
BACKGROUND AND OBJECTIVE: A decreased resistance to infection and impairments of immunity are common in obese humans and in rodents with hereditary obesity. Since brown fat thermogenesis is also suppressed in obese rodents, we hypothesized that obesity leads to a decreased febrile responsiveness.
METHODS: We compared the fever responses to intravenous E. coli lipopolysaccharide (10 µg/kg) between Zucker fa/fa (obese due to a defective leptin receptor) and Fa/? (lean) rats and between Otsuka Long–Evans Tokushima Fatty (OLETF; obese due to the lacking cholecystokinin-A receptor) and Long-Evans Tokushima Otsuka (lean) rats. Obesity of Zucker fa/fa and OLETF rats was verified by increased body mass and fat content, hypertriglyceridemia and hypercholesterolemia.
RESULTS: Neither fa/fa nor OLETF animals exhibited a decreased febrile responsiveness; if anything, their fevers tended to be higher than those in their lean counterparts.
CONCLUSION: Obesity per se does not lead to antipyresis.
International Journal of Obesity (2001) 25, 586–589
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Acknowledgements
This study was supported in part by the National Institutes of Health (NS 41233), Collins Medical Trust, Good Samaritan Foundation, Oregon Health Sciences Foundation (Medical Research Foundation of Oregon), and Dr Temple Fay Memorial Account (AAR). VAK was on leave from the Institute of Physiology, Minsk Belarus. The authors acknowledge the gift of the OLETF and LETO rats by the Tokushima Research Institute, Otsuka Pharmaceutical, and thank JA Foley, JF Herman, PR Hills, MK Schulmerich, KB Ulrich, and RK Velander for performing the biochemical assays.
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Ivanov, A., Kulchitsky, V. & Romanovsky, A. Does obesity affect febrile responsiveness?. Int J Obes 25, 586–589 (2001). https://doi.org/10.1038/sj.ijo.0801523
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DOI: https://doi.org/10.1038/sj.ijo.0801523