Changes in blood glucose and metabolism in hyperuricemia mice

The aim of this study is to explore the changes in blood uric acid level, blood glucose, and metabolism in hyperuricemia (HUA) mice. The urate oxidase gene of C57BL/6J mouse is knocked out by targeted gene modification technology, and a spontaneous HUA mouse model is established. In the experiment, 20 urate oxidase gene knockout homozygous and wild type C57BL/6J mice are selected to construct the experimental group (EG) and the control group (CG), and the mice in both groups receive multiple intraperitoneal injections of low dose streptozotocin (STZ) solution. The changes in metabolic related indicators such as blood glucose, pancreatic β cell function, water intake, urination, food intake, and body weight are observed and compared between the EG and CG mice. Baseline indicators other than body weight between the two groups of mice before the experiment have no significant difference, P > 0.05. After the injection of STZ solution, body weight between the two groups has significant difference, P < 0.05. Before the experiment and less than 19 days after the start of the experiment, daily water intake and urine output between the two groups of mice have no significant difference, P > 0.05. After the experiment reaches 19 days, two groups' water intake and urine output have significant difference, P < 0.05. Daily food intake between the two groups of mice has no significant difference, P > 0.05. Before the injection of STZ solution, fasting blood glucose levels between the two groups of mice has no significant difference, P > 0.05. The plasma insulin level of the EG mice was higher than that of the CG mice, with significant difference (P < 0.05). At the same time, the Homeostasis Model Assessment of Insulin Resistance index and fasting blood uric acid level of the EG mice were overall higher than those of the CG mice, with significant difference (P < 0.05). From the seventh day after the injection of STZ solution, the random blood glucose level, fasting blood glucose level, fasting insulin level, and blood uric acid level of the EG mice were higher than those of the CG mice, with significant difference (P < 0.05). For spontaneous HUA mice, the continuous increase in blood uric acid level caused by the disease may cause the increase in blood sugar content, thus promoting the occurrence of diabetes. Second, the content of uric acid in spontaneous HUA mice is maintained at a high level, which will bring or aggravate the damage of pancreatic islet β cells.