Objective To study effects of captopril on cardiac function and structure in the experimental type 2 diabetic cardiomyopathy (T2DC) rat model. Methods The experimental type 2 DC model rats were induced by feeding with high sucrose-fat diet and intraperitoneal (i.p.) injection with 30 mg/kg of streptozotocin. The model rats were intragastric given with captopril at the dose of 45 mg/kg for six months totally. At the thirteenth week, the parameters of cardiac output (CO), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), the maximum rate of myocardial contraction (+dp/dtmax) and the maximum rate of myocardial diastole (-dp/dtmax) were detected using MP150 polygraph physiological signal recorder to evaluate cardiac function. The thickness of interventricular septal (IST) and left ventricular wall (LVWT) was measured to assess cardiac structure. Levels of fasting blood sugar (i.e., fasting plasma glucose (FPG) and glycated hemoglobin A1c (HbA1c)), blood lipid (i.e., total cholesterol (TC) and triglyceride (TG)) and myocardial non-esterified fatty acids (NEFA) and creatine kinase (CK) were determined by ultraviolet spectrophtometric method. The genes expression of cardiac peroxisome proliferator activated receptor-α (PPAR α) and glucose transporter-4 (GLUT4) mRNA were detected by real-time PCR method. Results When compared with the drug-untreated T2DC rat model, the parameters of LVSP, +dp/dtmax, absolute value of -dp/dtmax and CO were significantly increased by 15%, 77%, 52% and 54%, respectively, after treated with 45 mg/kg of captopril. Meanwhile, the value of IST was decreased by 40% after treatment of captopril in T2DC rats. Levels of plasma HbA1c and myocardial NEFA were remarkably decreased by 31% and 24%, when compared with T2DC group. Furthermore, expression of PPAR α was significantly decreased while GLUT4 mRNA increased, when compared with drug-untreated model rats. Conclusion Captopril treatment could effectively attenuate the diastolic and systolic dysfunction and inhibit the cardiac hypertrophy in experimental type 2 diabetic cardiomyopathy rats, and the therapeutic mechanism might be relate to mediating energy metabolism and lowering lipid accumulation in the heart.