Objective:To observe the expression of CD36 in peripheral monocytes in patients with Type 2 diabetes, and to study the influence of rosiglitazone on CD36 expression and the related the mechanism. Methods: The expression of CD36 in the peripheral monocytes of patients with Type 2 diabetes was measured by flow cytometry before and after rosiglitazone treatment; the correlation between monocytes CD36 expression and metabolic index was analyzed. Results: Flow cytometry showed that the mean fluorescence intensity (MFI ) of monocyte CD36 in Type 2 diabetes was significantly higher than that in the healthy controls(745.9±281.3 vs 406.3±80.2,P<0.01). CD36 MFI in patients with Type 2 diabetes atherosclerosis was significantly higher than that in patients with Type 2 diabetes non-atherosclerosis(878.2±296.1 vs 584.2±148.3,P<0.01). Besides, we also found that CD36 expression, fasting blood glucose(FBG), post-prandial blood glucose(PBG), hemoglobin A1c(HbA1c), FIN, PIN, and HOMA-IR were all significantly decreased after rosiglitazone intervention compared with those before rosiglitazone intervetion and placebo group(P<0.05 or P<0.01). There was a positive correlation between monocyte CD36 expression with FBG(r=0.55,P<0.05), HbA1c(r=0.62,P<0.01), and HOMA-IR(r=0.64,P<0.01); but the expression was not correlated with PBG, FIN, or PIN. Conclusion: The increased expression of CD36 in monocytes of patients with Type 2 diabetes may be one of the mechanisms for accelerated atherosclerosis in diabetic patients. Rosiglitazone can decrease CD36 expression in monocytes through effectively controlling the blood glucose and decreasing insulin resistance.