Anorexia induced by chronic central administration of cytokines at estimated pathophysiological concentrations.

Interleukin-1 beta (IL-1 beta), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) induce acute anorexia by direct action in the central nervous system (CNS) at estimated pathophysiological concentrations reported in the cerebrospinal fluid (CSF). Cytokine-induced anorexia may also participate in the long-term anorexia observed during disease. Here, we studied the effects of chronic intracerebroventricular (ICV) microinfusion (through osmotic minipumps) of various cytokines on feeding and drinking in rats.

Antisense oligodeoxynucleotides to G-protein alpha-subunit subclasses identify a transductional requirement for the modulation of normal feeding dependent on G alpha OA subunit.

A variety of G-protein-coupled receptors are proposed to participate in the modulation of ingestive behavior and in the mode of action of antiobesity drugs. In the present study, we investigated the involvement of G-protein alpha-subunit subclasses (molecular transducers of multiple chemical signals) in the control of ingestive behavior. We report here that the chronic intracerebroventricular (i.

Modulation of feeding by beta 2-microglobulin, a marker of immune activation.

Increased levels of beta 2-microglobulin (part of the class I major histocompatibility complex molecules) in body fluids are associated with activation of the immune system and pathophysiological processes. Various anorexigenic cytokines, including interferon-gamma and tumor necrosis factor-alpha, induce the expression of class I molecules. Therefore, it is possible that beta 2-microglobulin may participate in the feeding suppression induced by cytokines or may have direct effects on feeding.

Chemokines/intercrines and central regulation of feeding.

Chemokines/intercrines are structurally and functionally related cytokines that induce specific actions on the immune system and are released in response to infection, inflammation, and trauma. These pathological processes are frequently accompanied with food intake suppression. In the present study, the action of chemokines/intercrines on the regulation of feeding was investigated using the intracerebroventricular microinfusion of chemokine/intercrine-alpha subfamily members [interleukin-8 (IL-8); growth-related cytokine/melanoma growth-stimulating activity (GRO-alpha/MGSA); platelet factor-4 (PF-4); beta-thromboglobulin (beta-TG); and interferon-inducible protein-10 (IP-10)] and beta-subfamily members [monocyte chemotactic protein-1/monocyte chemotactic and activating factor (MCP-1/MCAF); regulated upon activation normal T-cell expressed and presumably secreted (RANTES); macrophage inflammatory protein-1 alpha (MIP-1 alpha); and macrophage inflammatory protein-1 beta (MIP-1 beta)].

Centrally administered bacterial lipopolysaccharide depresses feeding in rats.

Bacterial lipopolysaccharide (LPS) suppresses feeding in rats when administered peripherally in the microgram range. In the present study, the effects of LPS (Escherichia coli serotype 0111:B4) on the central regulation of feeding in rats maintained ad lib was investigated. Intracerebroventricular (ICV) microinfusion of LPS (0.