Na+-K+-ATPase activity of the erythrocyte plasma membrane in noninsulin-de- pendent diabetes mellitus (NIDDM) was studied together with the red cell deform-ability (RCD) and other influencing factors. Comparing with the normal controls, Na+-K+-ATPase activity, Mg++-ATPase activity, and RCD in diabetics were significantly decreased, and the erythrocyte membrane cholesterol and lipid peroxide, fasting blood glucose, and glycosylated hemoglobin were significantly increased. The change of Na+-K+-ATPase activity was positively correlated with RCD, and inversely correlated with fasting blood glucose, erythrocyte membrane cholesterol, and lipid peroxide. The results suggested that the change of Na+-K+-ATPase activity in erythrocyte may contribute to the alterations of RCD in diabetics

Pioglitazone treatment significantly improved the euglycemic clamp-determined insulin sensitivity (IS), raised adiponectin level, decreased TNF-α and FFA levels in rats with obese and hyperglycemia.

Objective To investigate the relationship among p38 mitogen-activated protein kinase (p38MAPK), NF-KB and monocyte chemoattractant protein-1 (MCP-1), and to study the role of p38MAPK, NF-κB and MCP-1 in diabetic nephropathy. Methods Protein expressions of p38MAPK and NF-κB, and mRNA expression of MCP-1 were initially investigated in rat mesangial cell line HBZY-1, which were incubated separately with 25mmol/L glucose, 100nmol/L insulin, 100 μmol/L H2 O2 and 100mg/L advanced glycosylation end products (AGEs). The relationship among p38MAPK, NF-κB and MCP-1 expression Was observed by usingSB203580, a specific inhibitor of p38MAPK. Results The expressions of p38MAPK, NF-κB and MCP-1 were increased in HBZY-1 cells incubated separately with 25mmol/L glucose, 100nmol/L insulin, 100μmol/L H2 O2and 100 mg/L AGEs. Expressions of NF-κB and MCP-1 were significantly reduced when p38MAPK was inhibited by SB203580. Conclusion p38MAPK, NF-κB and MCP-1 are involved in development of diabetic nephropathy, and p38MAPK stimulation is essential for the expressions of NF-κB and MCP-1.

The association of serum adiponectin concentration with coronary heart disease (CHD) in Chinese Han population was evaluated. Present evidence demonstrated that the lowered serum adiponectin concentration was a susceptibility risk factor for CHD, while the precise relationship between serum adiponectin concentration and CHD in Chinese population requires further study.

0.9 mm(n = 26).Twenty-five healthy individuals served as a control group.Clinical data including age,sex,BMI,ABI,HbA1c,fasting glucose and insulin were collected.Insulin resistance index in Homa model was calculated following the equation:Homa IR = FINS ? FPG) /22.5.Serum adiponectin level was measured by ELISA.Results The serum adiponectin level was significantly lower in atherosclerosis group than in non-atherosclerosis and control groups(P

Objective To investigate the relationship between p38MAPK and PPAR-?,and to study the role of p38MAPK and PPAR-? for diabetic nephropathy. Methods The expression of p38MAPK protein and PPAR-? mRNA was investigated in rat mesangial cells line HBZY-1 that was incubated respectively with 25 mmol/L glucose,100 nmol/L insulin,100 ?mol/L H_2O_2 and 100 mg/L AGEs. The relationship between p38MAPK and PPAR-? expression was studied by using SB203580,a specific inhibitor of p38MAPK. Results p38MAPK had significantly higher expression,while the expression of PPAR-? was significantly decreased in rat mesangial cells line HBZY-1 incubated with 25 mmol/L glucose,100 nmol/L insulin,100 ?mol/L H_ 2 O_ 2 and 100 mg/L AGEs respectively. PPAR-? activity was significantly reduced when p38MAPK was inhibited by SB203580. Conclusion p38MAPK is involved in development of diabetic nephropathy and may antagonize the expression of PPAR-?. PPAR-? activity might protect the function of kidney.

AIM: To investigate the blocking effects of sodium ferulate (SF) on the nonenzymatic glycation and oxidation in kidneys of diabetic rats. METHODS: The diabetic rats induced by streptozotocin (STZ) were treated with SF (110 mg/kg) per day for 8 weeks. The renal weight/body weight, clearance rate of creatinine (Ccr), proteinuria, advanced glycation end products (AGEs) in renal cortex, and the malonyldialdehyde (MDA), fructosamine (FMN), antioxidant enzymes in serum and renal cortex were measured. The pathologic changes of kidneys were also observed. RESULTS: The levels of Ccr, proteinuria, FMN and AGEs in renal cortex, FMN in serum, and renal weight/body weight in diabetic group were significantly higher than those in normal control group. In the diabetic group, there was a highter level of MDA and a lower activity of superoxide dismutase (SOD) and catalase (CAT) in serum and renal cortex than those in normal control group. Except for FMN in renal cortex, the abnormalities were significantly ameliorated in the treatment group. The pathologic changes was significant in the diabetic group, which was significantly ameliorated with the treatment of SF. CONCLUSIONS: SF protects the activity of antioxidant enzymes, clears away oxygen radicals and inhibits the deposit of AGEs in kindey, which may be the mechanisms of protecting effects of SF on kindey in diabetic rats. [

0.05), but did inhibit activity of iNOS (P

The expression of cyclooxygenase-2 (COX-2) mRNA and protein was significantly increased in rat glomerular mesangial cells (RCMC) treated separately with high glucose, high insulin, H2 O2 and advanced glycosylation end products. The expressions of COX-2 mRNA and protein in RCMC induced by above 4 factors were distinctly inhibited by sodium selenite, suggesting that sodium selenite might play a significant role in the prevention of diabetic nephropathy via this mechanism.

0.05), but insulin sensitivity was actually improved (P