Aim To investigate the changes of platelet activation and vascular endothelial function in patients with impaired glucose tolerance (IGT). Methods 40 patients with IGT were chosen and the level of platelet alpha granule membrane protein (GMP-140) was measured in these patients. Meanwhile, flow-mediated endothelium dependent dilation of branchial arteries was observed with high resolution ultrasound by celermajer's method. The diameter of branchial arteries were respectively measured at rest (basal diameter, BD), during reactive hyperemia (increased flow causing endothelium-dependent dilation, FMD) and after sublingual nitroglycerine (nitroglycerine causing endothelium-independent dilation, NCD). Data of 30 healthy persons were taken as the control group. Results There was no significant difference in the level of fasting blood glucose (FBG) between the control group and the IGT group. However, after 75 g oral glucose loading for 2 h, the level of blood glucose (2hBG) in the IGT group was higher than that in the control group. In the fasting state, the level of FMD was significantly reduced and the level of platelet GMP-140 was significantly increased in the IGT group as compared with those in the control group. After 75 g oral glucose loading, the level of FMD (2hFMD) was lower than that in the fasting state and the level of platelet GMP-140 (2hGMP-140) was higher than those in the fasting state. Linear correlation analysis showed that there was no significant relation between FBG and the levels of GMP-140 and FMD. However, before and after oral glucose loading, the changes of blood glucose [△(2hBG-FBG)] were positively correlated with the changes of platelet GMP-140 [△(2hGMP-140-GMP-140)], and the changes of blood glucose [△(2hBG-FBG)] were negatively correlated with the changes of FMD [△(2hFMD-FDM)]. The level of platelet GMP-140 was negatively correlated with the level of FMD. Conclusion Platelet activation was increased and vascular endothelial function was impaired in the patients with IGT, and oral glucose loading aggravate the increasing platelet activation and the endothelial dysfunction.