Peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily. PPARgamma regulates several metabolic pathways by binding to sequence-specific PPAR response elements in the promoter region of target genes, including lipid biosynthesis and glucose metabolism. It has also been reported that has an anti-inflammatory effect. Sepsis is an acute inflammation process associated with an hypercatabolic state that include a decrease in serum concentrations of insulin-like growth factor I (IGF-I), liver IGF-I gene expression, and alterations in adipose tissue metabolism. The aim of this study was to analyse the effect of the PPARgamma agonist rosiglitazone in the hypercatabolic state in sepsis induced by lipopolysaccharide (LPS). Adult male Wistar rats were simultaneously intraperitoneally injected with LPS (1mg/kg) and/or rosiglitazone (3mg/kg) 19 and 4 hours before decapitation. Food was removed to avoid possible effects of food intake. Serum IGF-I was measured using radioimmunoassay (RIA). Gene expression of leptin and hormone-sensitive lipase (HSL) in white adipose tissue, TNF-alpha, IGF-I and PPARgamma in liver and white adipose tissue were quantified using RT-PCR. In LPS-injected animals, hepatic expression of PPARgamma decreased (P<0.01), as well as circulating IGF-I and its hepatic gene expression (P<0.05). In white adipose tissue leptin and HSL were increased (P<0.05) after LPS injections. Rosiglitazone administration decreased white adipose tissue leptin and TNF-alpha mRNA in vehicle rats (P<0.05), but it did not modify any of the parameters studied in LPS-injected rats either in the liver or white adipose tissue. These data suggest that the administration of the PPAR gamma agonist rosiglitazone don’t seem to modify the catabolic response studied in sepsis.