Introduction and Objective: Diabetic nephropathy (DN) is a common complication of type 2 diabetes, and physical activity along with proper nutrition may help control its associated inflammation. The present study aimed to investigate the effects of eight weeks of combined training and taurine supplementation on the gene expression of CCL2 and HIF1α in the kidney tissue of diabetic male rats. Materials and Methods: In this experimental study,50 eight-week-old male Wistar rats were randomly assigned into five equal groups: healthy control, diabetic control, diabetic supplement, diabetic training, and diabetic training+supplement. Diabetes was induced by intraperitoneal injection of streptozotocin. The combined training program (resistance and endurance) was performed for eight weeks, five sessions per week. Resistance training started with three sets of four repetitions and progressed to three sets of five repetitions using weights equivalent to 3% of body weight. Endurance training began at 15 m/min for 15 minutes and increased to 20m/min for 40minutes. Taurine supplementation was administered intraperitoneally at a dose of 20 mg/kg after exercise sessions. 48hours after the final session, kidney tissues were collected and gene expression was analyzed using Real-Time PCR. Data were analyzed using ANOVA at a significance level of p≤0.05. Results:CCL2 gene expression was significantly reduced in the diabetic training+supplement group (p=0.001) and the diabetic training group (p=0.03) compared with the diabetic control group. However, no significant difference was observed between the diabetic training and diabetic training+supplement groups (p=0.19). In addition, HIF1α gene expression showed no significant changes in the diabetic training+supplement group (p=0.99) or the diabetic training group (p=0.78) compared with the diabetic control group. Conclusion: Combined training and taurine supplementation may reduce diabetes-related renal inflammation through decreasing CCL2 expression; however, adding taurine to exercise did not produce additional effects on CCL2 expression. Moreover, these interventions did not show significant effects on hypoxia-related pathways.