Visfatin Induces Sickness Responses in the Brain
- Authors
- Park, Byong Seo; Jin, Sung Ho; Park, Joong Jean; Park, Jeong Woo; Namgoong, Il Seong; Kim, Young Il; Lee, Byung Ju; Kim, Jae Geun
- Issue Date
- 20-1월-2011
- Publisher
- PUBLIC LIBRARY SCIENCE
- Citation
- PLOS ONE, v.6, no.1
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLOS ONE
- Volume
- 6
- Number
- 1
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/113258
- DOI
- 10.1371/journal.pone.0015981
- ISSN
- 1932-6203
- Abstract
- Background/Objective: Visfatin, also known as nicotiamide phosphoribosyltransferase or pre-B cell colony enhancing factor, is a pro-inflammatory cytokine whose serum level is increased in sepsis and cancer as well as in obesity. Here we report a pro-inflammatory role of visfatin in the brain, to mediate sickness responses including anorexia, hyperthermia and hypoactivity. Methodology: Rats were intracerebroventricularly (ICV) injected with visfatin, and changes in food intake, body weight, body temperature and locomotor activity were monitored. Real-time PCR was applied to determine the expressions of proinflammatory cytokines, proopiomelanocortin (POMC) and prostaglandin-synthesizing enzymes in their brain. To determine the roles of cyclooxygenase (COX) and melanocortin in the visfatin action, rats were ICV-injected with visfatin with or without SHU9119, a melanocortin receptor antagonist, or indomethacin, a COX inhibitor, and their sickness behaviors were evaluated. Principal Findings: Administration of visfatin decreased food intake, body weight and locomotor activity and increased body temperature. Visfatin evoked significant increases in the levels of pro-inflammatory cytokines, prostaglandin-synthesizing enzymes and POMC, an anorexigenic neuropeptide. Indomethacin attenuated the effects of visfatin on hyperthermia and hypoactivity, but not anorexia. Further, SHU9119 blocked visfatin-induced anorexia but did not affect hyperthermia or hypoactivity. Conclusions: Visfatin induced sickness responses via regulation of COX and the melanocortin pathway in the brain.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
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