The Effect Of Hyperglycemia On The Expression Of Glucose Transporter 1 MRNA In Renal Cortex Of Rats

ObjectiveWith the increase of the living standards of people and aging of population,the incidence of diabetes mellitus is going up year by year,followed with rising of number of the patients with diabetic nephropathy(DN).DN, as a serious chronic implication of diabetes, has become one of the mainetiological factors resulting in renal failure.It is very important to clarify thepathogenesis for seeking the methods to prevent and treat DN. Recent reports have indicated that many factors, including metabolic abnormality induced by hyperglycemia, changes of glomerular hemodynamics, cytokines, growth factors and genetic factors,are involved in the pathogenesis of DN.Hyperglycemia is the basic biochemical feature of diabetes and has been believed to play major role in the development of diabetes and diabetic complications.Glucose transporter located in cytoplasm is the main carrier mediating glucose intake, and expression and activity of it are important forglucose intake of cells. Isoforms of glucose transporter have sevenkinds,which are distributed in different tissues. GLUT1 is the main isoform of glucose transporter located in mesangial cells of kidneys,which has a close affinity to glucose and is not regulated by insulin. In the present study, to study the effect of hyperglycemia on the expression of glucose transporter 1 mRNA in renal cortex of rats, and to investigate the relationship between glucose transporter 1 mRNA and diabetic nephropathy.Methods1. The groups of expremental animal: a total of 46 healthy male wistar rats weighing 180-220g were randomly divided into four groups: (1)Normal control group: 10(2)Type 2 diabetic rat model: 13(3) High-fat diet model of insulin resistance: 10(4) High-glucose rat model: 132. Methods(1) Type 2 diabetic rat model were induced by intraperitoneally administered low dose of streptozocin(STZ) in rats and fed with food of high fat, High-fat diet model of insulin resistancewere induced by fedding with food of high fat, High-glucose rat model were induced by intraperitoneally administered high dos of streptozocin (STZ) in rats and fed with normal food.(2) After ten weeks, haemospasia form heart, sacrificed all the rats,extracted the renal cortex of rats,detected the clinical and biochemical index: body weitht,the kidney weight,the kidney weight×100/the body weight,Bun,FBG , FINS, ISI, TG , TC, LDL, HDL.(3) Semiquantitative analysis on the expression of GLUT1mRNA in renal cortex were investigated by reverse transcriptase polymerase chain reaction.3. Statistics anylysisDatas were analyzed by the Statistical Package of the SPSS 11.5. Descriptive data were given as means±SD.Datas with non-mormal distribution were changed by logarithm,the comparison between different groups were analyzed by analysis of variance.The p-values are two-tailed and a p-value of less than 0.05 being considered to be significant.ResultsGLUT1 expressed in renal cortex in all groups in this study. The GLUT1mRNA expressions were significantly higher in the renal cortex of type 2 diabetic rats and high-glucose model rats than the control and high-fat diet groups (P<0.01), The GLUT1mRNA expression in the renal cortex in High-glucose model rats were higher than that in type 2 diabetic rats (P<0.01).ConclusionGLUT1 expressed in renal cortex .Hyperglycemia can increase the expression of GLUT1 mRNA in renal cortex of rats, the increase of the expression of GLUT1mRNA maybe correlate with diabetic nephropathy.