Regardless of the influence of PPARβ/δ on other metabolic changes accompanying muscle wasting, the present results provide strong evidence that activation of PPARβ/δ results in upregulation of genes in the ubiquitin-proteasome pathway, stimulation of protein degradation, and atrophy of muscle cells and, importantly, that inhibition of PPARβ/δ improves glucocorticoid- and sepsis-induced muscle wasting. This evidence concerns the gene PPARD and Sepsis.