Type 2 diabetes (DT2) is a major risk factor of atherosclerosis. As Hypertension or dyslipidemia, DT2 can occur in patients with metabolic syndrome and may result in endothelial dysfunction. Physical activity is a part of the preventive treatment of endothelial dysfunction. The aims of this study were to develop a new animal model of induced DT2 and to investigate the impact of exercise on the DT2 development. Male Wistar rats were supplemented with a fructose enriched drink (20% w/v) for 12 weeks. Randomly selected rats were either trained on a treadmill at moderate intensity (60-70% maximal aerobic speed) for 6 weeks (0° incline, 1h/day, 5 days/week) or kept sedentary. Rats were weighed and their drink and food consumption were measured weekly. Fasting glycaemia and systolic pressure were monitored. Glucose tolerance was evaluated using an oral glucose tolerance test; insulinemia was measured concomitantly. Endothelial function was studied on isolated aorta rings. After only 6 weeks of fructose supplementation rats had a higher energy intake (p<0.001) but were not overweight. These rats also presented an elevated glycaemia (+14.3%, p<0.001) and a reduced glucose tolerance (p<0.01). Systolic blood pressure (+23.4%, p<0.001) and heart volume (p<0.05) were increased. After 12 weeks of fructose supplementation, sedentary rats were overweighed and presented an insulin resistance. In fructose supplemented rats, exercise helped to reduce overweight, fasting glycaemia (p<0.01), heart volume (–13.1%, p<0.01) and insulin resistance (p<0.001). Surprisingly, exercise enhanced endothelial dysfunction in both diabetic and control rats (p<0.01) but no effect of the fructose supplementation was observed. Thus, indicating that exercise reduced only age related endothelial dysfunction. In this new model of Wistar rats with induced DT2, moderate exercise improved some DT2 markers like fasting glycaemia and insulin resistance.