Interleukin 1b triggers catabolism via a central nervous system-mediated pathway in mice and rat

Hypothalamic interleukin-1 beta (IL-1β) production is induced in multiple inflammatory diseases associated with muscle catabolism. To determine whether IL-1β signaling in the CNS plays a role in the muscle wasting of inflammatory disease, we examined the ability of intracerebroventricular (ICV) IL-1β injection at pathophysiologically relevant concentrations, to generate catabolic changes in skeletal muscle. Changes in gene expression associated with these catabolic changes were monitored using gene expression exon arrays. 28 samples were analyzed. The following comparisons were made: 6 groups were defined on the basis of treatment and time. Differences between groups were assesed by one way-ANOVA. P values were corrected for multiple comparisons using the Benjamini Hochberg correction at a false discovery rate of 1%. Probes were considered that showed a 1.75 fold or greater up or down regulation at any of the three timepoints.