Impact of 1, 25-(OH)2D3 on Left Ventricular Hypertrophy in Type 2 Diabetic Rats.
- Author:
Ying FAN
;
Shan-xiao ZHANG
;
Meng REN
;
Li-feng HONG
;
Xiao-ni YAN
- Publication Type:Journal Article
- MeSH: Animals; Blood Glucose; analysis; Calcitriol; therapeutic use; Diabetes Mellitus, Experimental; blood; complications; Diabetes Mellitus, Type 2; blood; complications; Hypertrophy, Left Ventricular; prevention & control; Insulin; blood; Male; Rats; Rats, Wistar; Receptors, Calcitriol; analysis; Streptozocin
- From: Chinese Medical Sciences Journal 2015;30(2):114-120
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy (LVH) in type 2 diabetic rats.
METHODSType 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.
RESULTSIn 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).
CONCLUSION1, 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.