Aim: Recently, it has been proposed that inflammation triggered by macrophages as the pathogenic mechanism linked to the development of obesity-related insulin resistance. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists which increase the insulin receptor sensitivity. might improve glycemic control by enhancing insulin sensitivity and ameliorate the impaired lipid profile. In this study, we assessed the effect of rosiglitazone (PPAR-gamma agonist) on the insulin resistance and inflammatory markers. Material and Method: Thirty patients (11 men. 19 women) with type II diabetes mellitus (DM) were taken into the study. They were treated by rosiglitazone in a dose of 4mg/day as well as a diet for 12 weeks. Results: Rosiglitazone treatment significantly decreased HbA1c (p<0,01), IR-HOMA, hsCRP (p<0,01), triglyceride levels (p<0,05), CETP activity (p<0,01) and basal serum oxidation (TBARS levels, p<0,05). However, Chitotriosidase activity significantly increased after Rosiglitazone treatment (p<0,01). TNF, IL-6, sTNFR1, and sTNFR2 levels showed no statistically significant difference compared to their basal levels. Discussion: Rosiglitazone might treat diabetes by mediating glucose/lipid metabolism and preventing lipid oxidation in patients with DM. On the other hand, it has a dual role on inflammation; while it might induce macrophage activation suggesting its pro-inflammatory effect, It might also reduce the CRP levels by lowering gene expression suggesting its anti-inflammatory effect.