BACKGROUND AND OBJECTIVE: A decreased resistance to infection and impairmen
ts of immunity are common in obese humans and in rodents with hereditary ob
esity. Since brown fat thermogenesis is also suppressed in obese rodents, w
e hypothesized that obesity leads to a decreased febrile responsiveness.
METHODS: We compared the fever responses to intravenous E. coil lipopolysac
charide (10 mug/kg) between Zucker fa/fa (obese due to a defective leptin r
eceptor) and Fa/? (lean) rats and between Otsuka Long - Evans Tokushima Fat
ty (OLETF; obese due to the lacking cholecystokinin-A receptor) and Long-Ev
ans Tokushima Otsuka (lean) rats. Obesity of Zucker fa/fa and OLETF rats wa
s verified by increased body mass and fat content, hypertriglyceridemia and
hypercholesterolemia.
RESULTS: Neither fa/fa nor OLETF animals exhibited a decreased febrile resp
onsiveness; if anything, their fevers tended to be higher than those in the
ir lean counterparts.
CONCLUSION: Obesity per se does not lead to antipyresis.