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, prostaglandinsynthesizing 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.
| Original language | English |
|---|---|
| Article number | e15981 |
| Journal | PLoS One |
| Volume | 6 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2011 Feb 3 |
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ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Agricultural and Biological Sciences(all)
Cite this
Visfatin induces sickness responses in the brain. / Park, Byong Seo; Jin, Sung Ho; Park, Joong Jean; Park, Jeong Woo; Seong Namgoong, I. L.; Kim, Young I.L.; Lee, Byung Ju; Kim, Jae Geun.
In: PLoS One, Vol. 6, No. 1, e15981, 03.02.2011.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Visfatin induces sickness responses in the brain
AU - Park, Byong Seo
AU - Jin, Sung Ho
AU - Park, Joong Jean
AU - Park, Jeong Woo
AU - Seong Namgoong, I. L.
AU - Kim, Young I.L.
AU - Lee, Byung Ju
AU - Kim, Jae Geun
PY - 2011/2/3
Y1 - 2011/2/3
N2 - 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, prostaglandinsynthesizing 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.
AB - 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, prostaglandinsynthesizing 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.
UR - http://www.scopus.com/inward/record.url?scp=79251645369&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79251645369&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0015981
DO - 10.1371/journal.pone.0015981
M3 - Article
C2 - 21283791
AN - SCOPUS:79251645369
VL - 6
JO - PLoS One
JF - PLoS One
SN - 1932-6203
IS - 1
M1 - e15981
ER -