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 microg/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.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1038/sj.ijo.0801523 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!