Objective To investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy(LVH) in type 2 diabetic rats. Methods Type 2 diabetic mellitus(DM) model rats were established by intraperitoneally injecting with 30 mg/kg streptozotocin. After 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy(LVH) by ultrasound examination, and randomly assigned into three groups: untreated(DM-LVH, n=7), treated with insulin(DM-LVH+INS, n=6), and treated with 1, 25-(OH)2D3(DM-LVH+VD, n=6). Healthy male rats were used as the controls group(n=6). The fasting blood glucose and the insulin level were determined weekly. The left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor level were determined by 4 weeks later. Results In the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group(P<0.05), whereas the blood glucose, left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor expression were significantly increased(all P<0.05). In the DM-LVH+INS and DM-LVH+VD groups, the insulin levels were significantly increased compared with the DM-LVH model group(P<0.05), whereas the other parameters were significantly decreased(all P<0.05). Conclusion 1, 25-(OH)2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating insulin secretion and reducing blood glucose via direct up-regulation of 1, 25-(OH)2D3-receptor expression. Objective To investigate the impact of 1, 25- (OH) 2D3 on left ventricular hypertrophy (LVH) in type 2 diabetic rats. Methods Type 2 diabetic mellitus (DM) model rats were established by intraperitoneally injecting with 30 mg / kg streptozotocin. 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy (LVH) by ultrasound examination, and randomly assigned into three groups: untreated (DM-LVH, n = 7) = 6), and treated with 1, 25- (OH) 2D3 (DM-LVH + VD, n = 6). The Healthy male rats were used as the controls group were determined weekly. The left ventricular mass index, collagen content, and 1, 25- (OH) 2D3-receptor level were determined by 4 weeks later. Results In the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group (P <0.05), while the blood glucose, left ventricular mass index, myocardial In the DM-LVH + INS and DM-LVH + VD groups, the insulin levels were, and 1, 25- (OH) 2D3-receptor expression were significantly increased (all P <0.05) Conclusion 1, 25- (OH) 2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating (all P <0.05) compared with the DM-LVH model group insulin secretion and reducing blood glucose via direct up-regulation of 1, 25- (OH) 2D3-receptor expression.