Genetic rodent models of type 2 diabetes are routinely utilized in studies of diabetes-related cardiovascular disease; however, these models frequently exhibit abnormalities that are not consistent with diabetic complications. The aim of this study was to develop a model of diabetes that leads to cardiovascular dysfunction commonly seen in diabetic patients with minimal non-diabetes related pathologies. Young male rats received either control (CON), high fat (HF; 60%) or western (WES; 40% fat, 45% carbohydrate) diets for two weeks after which streptozotocin (STZ) was administered to induce diabetes (DIA). Blood glucose levels were higher in CON+DIA and WES+DIA compared to HF+DIA (25 ± 1, 25 ± 2 and 15 ± 1mmol/l respectively; P<0.05). Plasma levels of alanine aminotransferase, bilirubin and blood urea nitrogen were higher in all diabetic groups indicating liver and kidney dysfunction. Despite lower heart rates in CON+DIA and HF+DIA, mean arterial, pulse, end-systolic and end-diastolic pressures were not different between any of the groups. All diabetic groups had diastolic dysfunction but only HF+DIA and WES+DIA exhibited elevated diastolic wall stress, arterial stiffness (augmentation index) and systolic dysfunction (velocity of circumferential shortening, systolic wall stress, end-systolic volume elastance). These findings suggest that the combination of a high fat (60%) diet and a moderate dose of STZ results in a model of type 2 diabetes with moderate hyperglycemia that mimics the cardiovascular dysfunction seen in patients. Also, the combination of hyperglycemia and dietary fat appears to be more detrimental to endothelial and cardiovascular function than either intervention alone.