Visfatin induces sickness responses in the brain

Area of Science:

• Neuroimmunology
• Cytokine Signaling

Background:

• Visfatin (nicotinamide phosphoribosyltransferase) is a pro-inflammatory cytokine with elevated serum levels in conditions like sepsis, cancer, and obesity.
• This study investigates the pro-inflammatory role of visfatin within the central nervous system.

Purpose of the Study:

• To elucidate the role of visfatin in mediating sickness responses in the brain.
• To identify the molecular pathways, specifically cyclooxygenase (COX) and melanocortin signaling, involved in visfatin-induced sickness behaviors.

Main Methods:

• Rats received intracerebroventricular (ICV) injections of visfatin.
• Measurements included food intake, body weight, body temperature, and locomotor activity.
• Gene expression analysis (Real-time PCR) for inflammatory cytokines, POMC, and prostaglandin-synthesizing enzymes was performed.
• The involvement of COX and melanocortin pathways was assessed using indomethacin (COX inhibitor) and SHU9119 (melanocortin receptor antagonist).

Main Results:

• ICV visfatin administration led to decreased food intake, body weight, and locomotor activity, alongside increased body temperature.
• Visfatin significantly upregulated pro-inflammatory cytokines, prostaglandin-synthesizing enzymes, and proopiomelanocortin (POMC).
• Indomethacin partially blocked visfatin's effects on hyperthermia and hypoactivity, while SHU9119 specifically inhibited visfatin-induced anorexia.

Conclusions:

• Visfatin induces central sickness responses, including anorexia, hyperthermia, and hypoactivity.
• These effects are mediated through the regulation of the cyclooxygenase (COX) pathway and the melanocortin signaling pathway in the brain.