| 中文摘要 |
期刊連結：http://www.gouthyperuricemia.com Objective: The association between hyperuricemia and hyperglycemia may be causal or an epiphenomenon, which was investigated. Methods: Seventy Wistar rats were divided into two groups. Thirty rats were fed a normal diet (control group, group A,), whereas 40 rats were administered a high purine diet (model group, group B,). Oral glucose tolerance test (OGTT) was performed by oral administration of 30% glucose solution, to 2g/kg every week. After fasting for 12 hours, fasting serum glucose was monitored using glucose Kit. Then two hours later, 5-10 μl blood was obtained from the tail vein and glucose concentration was measured. Pancreatic morphology at 10th week after induction of hyperuricemia was observed with HE and immunohistochemical staining. Experimental data were reported as mean ± standard error of the mean (SEM) and compared using t-tests. All analyses were performed using SPSS 13.0 software, with P <0.05 considered statistically significant. Results: Beginning at 8 weeks, fasting blood glucose concentrations were significantly higher in the hyperuricemic than in the control group (p=0.008). Two hour oral glucose tolerance tests also showed that blood glucose concentrations were significantly higher (p=0.017) and serum insulin concentrations significantly lower in model rats than controls (p=0.007), beginning at week 7. Then immunohistochemical staining was done, which showed that, in hyperuricemic rats, islet shapes became more irregular, and the number and area of islets were decreased, compared with control rats. Conclusion: These findings support that sustained hyperuricemia in these rats induced hyperglycemia, diabetes and pancreatic islet damaged. |
