Objective To establish a rat model of hyperuricemia, and explore the possible secondary cardiovascular disease that could be induced by hyperuricemia in the model rats. Methods 32 male SD rats were randomly divided into control group (Group C), potassium oxonate model group (Group M1), potassium oxonate combined with high-sugar model group (Group M2), potassium oxonate combined with yeast extract feed model group (Group M3), 8 rats were treated in each group for 3 weeks. At the end of the experiment, the serum levels of uric acid (UA), blood urea nitrogen, creatinine, insulin (INS), blood glucose (GLU) and triglyceride (TG) were measured, and histopathological examination of liver, renal, and heart tissue was performed. Results Compared with the control group, a significant increase in serum levels of UA ( P <0. 01) and the number of rats showing renal lesions was found in the experimental group (3/8, 37. 5%) after oral administration of potassium oxonate at a dose of 750 mg/ kg, combined with yeast extract feed (Group M3). Also, the changes in GLU, INS, TG and the histopathology of heart tissue (3/8, 37. 5%) suggesting that rats in this group had secondary cardiovascular alterations. Conclusions Compared with the basic potassium oxonate model, the model of potassium oxonate combined with yeast extract feed is more suitable for the study of rat chronic hyperuricemia, accompanied by glucose metabolic impairment. It can also be used in rat models to establish mutual intervention mechanisms between hyperuricemia and cardiovascular disorders, and be applied in comprehensive preclinical pharmacodynamic evaluation of therapeutic drugs for hyperuricemia.