论文部分内容阅读
目的利用大鼠糖尿病模型探讨不同血糖水平对心肌GLUT1和GLUT4 mRNA表达的影响。方法 SD大鼠50只,随机选取10只为正常对照组(NC组),另外40只建立糖尿病模型。取建模成功糖尿病大鼠36只(DM组),随机分为糖尿病血糖未控制组(A组,血糖>16.7 mmol/L)、糖尿病血糖控制较差组(B组,血糖14~16.7 mmol/L)、糖尿病血糖控制一般组(C组,血糖10~13.9 mmol/L)和糖尿病血糖控制良好组(D组,血糖<10 mmol/L),每组9只。腹腔注射甘精胰岛素,12周后称体质量,取血测空腹血糖(FBG)、糖化血红蛋白(Hb A1c),并将大鼠处死取心肌组织,采用RT-PCR法检测GLUT1和GLUT4 mRNA。结果与NC组相比,DM组心肌组织GLUT1和GLUT4mRNA表达水平显著降低(P<0.05)。经胰岛素控制血糖后,DM组心肌组织GLUT1和GLUT4mRNA表达水平有所升高,A组、B组、C组和D组表达量依次升高,各组间差异有统计学意义(P<0.05)。DM组心肌组织GLUT1和GLUT4mRNA表达水平与血糖及Hb A1c水平呈显著负相关(P<0.05)。结论血糖长期慢性升高可使DM大鼠心肌组织GLUT1和GLUT4mRNA的表达降低,是机体对长期高血糖的一种代偿性保护。
Objective To investigate the effect of different blood glucose levels on the expression of GLUT1 and GLUT4 mRNA in the rat model of diabetes. Methods Fifty SD rats were randomly divided into normal control group (NC group) and control group (NC group). Another 40 diabetic rats were established. Thirty-six diabetic rats were randomly divided into diabetic uncontrolled group (group A, blood glucose> 16.7 mmol / L), poor glucose control group (group B, blood glucose 14-16.7 mmol / (Group C, blood glucose 10 ~ 13.9 mmol / L) and diabetic patients with good glycemic control (group D, blood glucose <10 mmol / L), with 9 rats in each group. The glargine was injected intraperitoneally. After 12 weeks, the body weight was measured. Fasting blood glucose (FBG) and Hb A1c were measured. The myocardium was sacrificed and the GLUT1 and GLUT4 mRNA were detected by RT-PCR. Results Compared with NC group, the expression of GLUT1 and GLUT4 mRNA in DM group was significantly decreased (P <0.05). The level of GLUT1 and GLUT4 mRNA in myocardium of diabetic rats increased after insulin was controlled by blood glucose. The expression of GLUT1 and GLUT4 mRNA in DM group was increased, and the expression of GLUT1 and GLUT4 in DM group was higher than that of DM group (P <0.05) . The levels of GLUT1 and GLUT4mRNA in myocardium of DM group were significantly negatively correlated with the level of Hb A1c (P <0.05). Conclusion The long-term chronic increase of blood glucose can decrease the expression of GLUT1 and GLUT4mRNA in the myocardium of diabetic rats, which is a compensatory protection of long-term hyperglycemia.