| Objective: Dyslipidemia induce insulin resistance. Insulin resistance is the basic pathologic physiology phenomenon of type 2 diabetes mellitus and is the bases of the metabolic syndrom such as diabetes mellitus ,hypertension and hyperlipidemia. Dyslipidemia also play an important role in the development of diabetic microvascuiar and macrovascular complications. So it is important to investigate the mechanism of dyslipidemia in the insulin resistance,type 2 diabetes mellitus and diabetic chronic complication. To feed SD femal rat with a high-sucrose-high-fat diet induce insulin resistance. After 4 weeks streptozotion (STZ,25mg/kg) was injected intrapenitoneally to induce hyperglycemia. So a rat model with the characteristics of hyperglycemia hyperlipidemia insulin resistance was set up , which stimulates the metabolic abnormalites of human type 2 diabetes mellitus. It may provide a particular advantage for investigating the relationship between dyslipidemia and insulin resistance,type 2 diabetes mellitus and diabetic nephropathy.Method: The rats were randomly assigened into twogroups :normal control rats(group A) and diabetic rats(group B). Group A was fed with normal diet .Group B was fed with a high-sucrose-high-faf diet and a low dose of STZ was injected to induce hyperglycemia after 4 weeks. Body weight, fasting blood glucose, fasting serum insulin, serum triglyceride, cholestrol were observed after 4 8 26 weeks After 26 weeks, kidney weight, serum creatinine, urinary albumin, urinary creatinine were observed?The expressions of protein of TGF- P was examined utilizing immunohistochemistyoThe renal tissue were observed by light microscopy and electronic microscope Morever , the correlation between insulin sensitivity index (ISI) and serum lipid level , the average positive expressing rate of TGF-P and urinary alumin were respectively analyzed To calculate kidney weight/body weight, creatinine clearance ratio (Ccr) and insulin sensitivity index, mean glomerular area (MGA), mean glomerular volume (MGV)Result: In the group B, fed with high-sucrose-high-fat diet for 4 weeks, body weight, fasting insulin, serum triglyceride, cholestrol were markedly increase as compared with those of group A ISI was reduced as compared with group A Fasting blood glucose had no difference with group A (p>0.05) . So insulin resistance was induced in group B. After 8 weeks, in group B, serum triglyceride, cholestrol, fasting blood glucose significantly increased. The fasting plasma inshlin, body weight were the same level comparedwith group A(p>0.05). ISI was markedly reduced as compared with group B(p<0.01). Insulin resistance also exist in group B o The rat model of type 2 diabetes mellitus has the characteristics of high blood glucose, hyperlipidemia, insulin resistance. After 26 weeks, compared with group A, there was a significantly increase in fasting blood glucose, urinary albumin, Ccr in group B. The body weight,fasting blood insulin in both groups had significance. The insulin sensitivity index in group B, kidney weight/body weight, GMA, GMV were significantly increase. Electronic microscopic finds showed expanded mesangial matrix, glomerular basement membrane thickening in group B. The PAS positive substance in glomeruli of group B was highly expressed than group A There was a significant positive correlation between the positive expressing ratio of TGF- 3 and urinary albumin in group B(r=0.7150, p<0.01). While there was a significant correlation between ISI and serum triglyceride, cholestrol(r=-0.7319, p<0.01;r=-0.6814, p<0.01). Conclusion:1 Insulin resistance was induced in femal SD rats fed with a high-sucrose-high-fat diet for 4 weeks.2 After streptozotion injected intraperitoneally hyperglycemia was induced. The rat model has hyperglycemia, hyperlidemia, insulin resistance, which stimulates the metabolic abnormalites of human type 2 diabetes mellitus.3 Compared the insulin sensitivity after injecting STZwith before injecting STZ , insulin resistance... |
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