Study Of Glucose Metabolism In Spontaneously Hyperuricemia Model

Objective:To observe spontaneous hyperuricemia induce glucose metabolic disorders mice pancreas islet beta cell effect,in order to discuss the pathogenesis of hyperuricemia induce and enhance the glucose metabolic disorders.Methods: Choose six weeks old male urate oxidase gene knockout homozygote mice 8 were spontaneous hyperuricemia group and male urate oxidase gene knockout wild-type mice 12 were control group.At the same time,two groups of mice were given streptozotocin by intraperitoneal injection,according to 40 mg per kilogram,for five consecutive days to construct spontaneous hyperuricemia induce glucose metabolic disorders mice.After given streptozotocin 5 days,observe the general status of two groups of mice and monitor the body weight changes in the two groups of mice every day.Before injection streptozotocin,after injection streptozotocin fasting blood glucose(FBG)and serum uric acid(UA)levels of two groups mice were determined by regularly.After injection streptozotocin seven days,real time blood glucose(RBG)were determined by regularly.Fasting serum insulin levels were measured by enzyme linked immunosorbent assay(ELISA).According to the fasting blood glucose and fasting serum insulin levels to calculate the insulin resistance index(HOMA-IR).The pathological sections and immunohistochemical of mouse pancreas were also performed,in order to observe the anatomic structure of the pancreas and the quantity of the islets in mice.Results: 1.Before the intraperitonneal injection of streptozotocin,the body weight of urate oxidase gene knockout homozygote mice were(20.6±1.9)g were lower than urate oxidase gene knockout wild-type mice(23.3±2.0)g,(P ﹤ 0.05),until the end of the experiment.2.Before the intraperitonneal injection of streptozotocin,the fasting blood glucose of homozygote mice were(7.85±0.69)mmol/L,wild-type mice were(7.11±0.66)mmol/L,were no significant difference(P>0.05).At 7th and10 th of injection of streptozotocin,the fasting blood glucose of homozygote mice were((6.36±0.73)mmol//L,(8.11±1.71)mmol//L)higher than wild-type mice((5.52±0.73)mmol//L,(5.45±0.47)mmol//L)(P ﹤ 0.05).3.Before the intraperitonneal injection of streptozotocin,the serum insulin levels of homozygote mice were(82.99±15.52)m U//L higher than wild-type mice(50.22±12.67)m U//L(P﹤0.05).4.From the 7th of injection of streptozotocin,real time blood glucose of homozygote mice were(12.0±2.2)mmol/L higher than wild-type mice(9.3±1.0)mmol/L(P﹤0.05).until the end of the experiment.5.Before the intraperitonneal injection of streptozotocin,the serum uric acid of homozygote mice were(524.17±72.75)umol/L higher than wild-type mice(189.33±30.19)umol/L(P﹤0.05).At 10 th days of injection of streptozotocin,the serum uric acid of homozygote mice higher amplitude is greater than wild-type mice.6.Before the intraperitonneal injection of streptozotocin,the insulin resistance index of homozygote mice were(1.49±0.07)higher than wild-type mice(1.20±0.15)(P﹤0.05).7.The pathological sections and immunohistochemical of mouse pancreas,the number of islet cells in homozygous mice was less than in the wild-type mice,the difference was statistically significant(P﹤0.05).Conclusions: Continuous hyperuricemia can increase blood glucose,induce or aggravate islet beta cell injury.