Visfatin induces sickness responses in the brain

Byong Seo Park, Sung Ho Jin, Joong Jean Park, Jeong Woo Park, I. L. Seong Namgoong, Young I.L. Kim, Byung Ju Lee, Jae Geun Kim

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30 Citations (Scopus)


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 languageEnglish
Article numbere15981
JournalPloS one
Issue number1
Publication statusPublished - 2011
Externally publishedYes

ASJC Scopus subject areas

  • General


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