Expression Of CD36 In High-Fat-Diet Induced Diabetic Rats And Type 2 Diabetes

Objective:To investigate the expression of scavenger receptor CD36 in High-Fat-Diet induced diabetic rats and Type 2 diabetes and the possible mechanism, and to observe the effects of thiazolidinediones—rosiglitazone intervention.Method:Type 2 diabetic rat models were induced by High-Fat-Diet SD rats combined with intraperitoneal injection streptozotocin(STZ) 35mg/kg once.The expression of CD36 in monocytes from High-Fat-Diet induced diabetic rats and Type 2 diabetes were measured before and after rosiglitazone intervention by laser flow cytometry.Expressions of CD36 mRNA,Peroxisome proliferator-activated receptorγ(PPARγ) mRNA,Glucose transporter 4(GLUT4) mRNA and their protein in skeletal muscle,subcutaneous adipose tissue and epididymal adipose tissue from High-Fat-Diet induced diabetic rats were investigated before and after rosiglitazone intervention by real time RT-PCR and Western blot analysis respectively.Assay the correlation between monocytes CD36 expression and PPARγ,GLUT4 and other cytokines,metabolic parameters.Results:(1) Similar to Type 2 diabetes metabolic disorder,High-Fat-Diet combined intraperitoneal injection STZ once SD rats appeared evident hyperglycemia,hyperinsulinemia,lipid metabolic disorder and body weight gain.(2) Flow cytometry showed that the MFI of monocytes CD36 expressions in diabetic rats were significantly higher in comparison with controls(P＜0.01).After rosiglitazone intervention the MFI of monocytes CD36 expressions were significantly decreased(P＜0.01).There was a positive correlation between monocytes CD36 MFI and FBG,HOMA-IR.(3) Expressions of CD36 mRNA,PPARγmRNA and their protein in skeletal muscle, subcutaneous adipose tissue and epididymal adipose tissue from diabetic rats were significantly increased and expressions of GLUT4 mRNA and protein in above-mentioned tissues were significantly decreased(P＜0.01).There was a coincidence change between expressions of CD36 and PPARγmRNA or protein. After rosiglitazone intervention,expressions of CD36mRNA,PPARγmRNA and their protein in skeletal muscle were significantly decreased(P＜0.05),expressions of GLUT4 mRNA and protein in skeletal muscle were significantly increased (P＜0.01).Expressions of CD36mRNA,PPARγmRNA,GLUT4 mRNA and their protein in subcutaneous adipose tissue and epididymal adipose tissue were all increased but only in epididymal adipose tissue there was a statistics significance (P＜0.05).(4) The MFI of monocytes CD36 expressions were significantly higher in Type 2 diabetes in comparison with healthy controls(P＜0.01).The MFI of monocytes CD36 expressions in atherosclerosis diabetes were significantly higher in comparison with nonatherosclerosis diabetes(P＜0.01).There was a positive correlation between monocytes CD36 MFI and diabetes duration,FBG,HbA1_C,HOMA-IR.(5) After rosiglitazone intervention,the MFI of monocytes CD36 expressions were significantly decreased in comparison with controls and before rosiglitazone intervention(P＜0.01).The serum levels of sVCAM-1 and TNFαwere significantly decreased(P＜0.01) and the serum levels of adiponectin were significantly increased (P＜0.01).There was a positive correlation between monocytes CD36 MFI and serum levels of sVCAM-1 and TNFα,a inverse correlation between monocytes CD36 MFI and serum levels of adiponectin.Conclusion:High-Fat-Diet combined intraperitoneal injection STZ once SD rats were good Type 2 diabetic rat models.The increased expression of scavenger receptor CD36 in monocytes in the condition of Type 2 diabetes may be one of the mechanism of accelerated atherosclerosis in diabetic,hyperglycemia and insulin resistance were the main up-regulation factors.Rosiglitazone could reduce CD36 expression in monocytes,the mechanism might lie in the good glycaemic control,relief of oxidative stress,improvement of insulin resistance and relief of inflammatory reaction.The expression of CD36 in rat skeletal muscle and adipose tissue was regulated by PPARγand exist tissue specificity.There may be exist different mechanism between subcutaneous adipose tissue and epididymal visceral adipose tissue in insulin resistance,metabolism of lipid and atherosclerosis.