Objective To establish and evaluate a mouse model of diabetic hindlimb ulcers, study the changes in blood flow and pathophysiology in mice with diabetic hindlimb ulcers, and explore the pathogenesis of the ulcers to provide a basis and reference for studying peripheral vascular diseases in diabetes. Methods ICR mice were divided into the diabetic hindlimb ulcer, hindlimb ischemia, and diabetic groups. Mice in the diabetic hindlimb ulcer and diabetes groups were intraperitoneally injected with streptozotocin to establish a model of type 1 diabetes. Mice in the diabetic hindlimb ulcer and hindlimb ischemia groups had their femoral arteries and veins ligated and their femoral artery severed. Sham surgery was performed in the diabetic group. Blood flow changes postoperation were detected via laser Doppler, and ischemic necrosis of the limbs was observed. Twenty-one days postoperation, hematoxylin and eosin staining was used to observe morphological changes in the ischemic tissue. Changes in CD31 and SMA expressions were analyzed. Results After the operation, the weight of the diabetic hindlimb ulcer group decreased significantly compared with that of the hindlimb ischemia group, and the hindlimb necrosis was more severe. Additionally, the diabetic hindlimb ulcer and hindlimb ischemia groups showed significantly decreased blood perfusion, which recovered gradually on days 3, 7, and 14 postoperation. Blood perfusion in the hindlimb ischemia group was near normal 21 days postoperation, but that of the diabetic hindlimb ulcer group decreased slightly. No significant change occurred in the diabetes group. In the diabetic hindlimb ulcer and hindlimb ischemia groups, muscle structure destruction and inflammatory infiltration occurred in the gastrocnemius tissues, and CD31 expression was increased. SMA expression was increased in the diabetic hindlimb ulcer and diabetes groups but not in the hindlimb ischemia group. Conclusions The diabetic hindlimb ulcer mouse model is successfully established. Limb necrosis and impaired recovery of blood perfusion are obvious in the diabetic hindlimb ulcer model compared with those of the hindlimb ischemia model. This model can be used to study the pathogenesis of diabetic vascular diseases and to screen therapeutic drugs.