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

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. Overall design: 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.