Abstract：
Hyperuricemia is a state in which the serum levels of uric acid (UA) are elevated. This study was to determine the roles of rosuvastatin in fasting blood glucose (FGB) and insulin levels in hyperuricemic rats.
Thirty-six Sprague-Dawley (SD) rats were randomized divided into the control, model and rosuvastatin groups: the control was given no intervention, the model group was established by administrating yeast extract powder and oxonic acid potassium salt, and the rosuvastatin group was given intravenous administration of rosuvastatin for 28 days in hyperuricemic rats. Serum uric acid (SUA), fasting blood glucose (FBG), fasting blood insulin (FBI), glutamic acid decarboxylase antibody (GADA), oral glucose tolerance test (OGTT) levels, and the ultrastructure of pancreatic β-cells were measured. Also, homeostasis model assessment of insulin resistance (HOMA-IR) scores was computed in three groups.
Compared to the model group, SUA were decreased, while the FBG, GADA, OGTT and HOMA-IR at week 4 were significantly increased in rosuvastatin group. However, FBI was not significantly changed between three groups. It was also showed that the structure of pancreatic β-cells was damaged and the number of β-cells was changed in hyperuricemic rats while they were aggravated in rosuvastatin group.
Rosuvastatin has roles in inducing FGB, GADA, OGTT and pancreatic β-cells damage in hyperuricemic rats.
Thirty-six Sprague-Dawley (SD) rats were randomized divided into the control, model and rosuvastatin groups: the control was given no intervention, the model group was established by administrating yeast extract powder and oxonic acid potassium salt, and the rosuvastatin group was given intravenous administration of rosuvastatin for 28 days in hyperuricemic rats. Serum uric acid (SUA), fasting blood glucose (FBG), fasting blood insulin (FBI), glutamic acid decarboxylase antibody (GADA), oral glucose tolerance test (OGTT) levels, and the ultrastructure of pancreatic β-cells were measured. Also, homeostasis model assessment of insulin resistance (HOMA-IR) scores was computed in three groups.
Compared to the model group, SUA were decreased, while the FBG, GADA, OGTT and HOMA-IR at week 4 were significantly increased in rosuvastatin group. However, FBI was not significantly changed between three groups. It was also showed that the structure of pancreatic β-cells was damaged and the number of β-cells was changed in hyperuricemic rats while they were aggravated in rosuvastatin group.
Rosuvastatin has roles in inducing FGB, GADA, OGTT and pancreatic β-cells damage in hyperuricemic rats.
摘要：
高尿酸血症是血清尿酸（UA）水平升高的状态。本研究旨在确定瑞舒伐他汀对高尿酸血症大鼠空腹血糖（FGB）和胰岛素水平的影响。
36只SD大鼠随机分为对照组，模型组和瑞舒伐他汀组:对照组不给予干预,采用酵母浸膏粉和含氧酸钾盐建立模型组，瑞舒伐他汀组给予高尿酸血症大鼠瑞舒伐他汀静脉给药28天。血清尿酸（SUA），空腹血糖（FBG），空腹血胰岛素（FBI），谷氨酸脱羧酶抗体（GADA），口服葡萄糖耐量试验（OGTT）水平，并测定胰腺β细胞的超微结构。此外，在三组中计算胰岛素抵抗的稳态模型评估(HOMA-IR)评分.
与模型组相比，SUA减少，而FBG,GADA,瑞舒伐他汀组第4周时OGTT和HOMA-IR显著升高。然而,FBI在三组之间没有显着变化。瑞舒伐他汀组高尿酸血症大鼠胰岛β细胞结构受损,胰岛β细胞数量改变,但加重。
瑞舒伐他汀在诱导FGB，GADA,OGTT与高尿酸血症大鼠胰腺β细胞损伤.
36只SD大鼠随机分为对照组，模型组和瑞舒伐他汀组:对照组不给予干预,采用酵母浸膏粉和含氧酸钾盐建立模型组，瑞舒伐他汀组给予高尿酸血症大鼠瑞舒伐他汀静脉给药28天。血清尿酸（SUA），空腹血糖（FBG），空腹血胰岛素（FBI），谷氨酸脱羧酶抗体（GADA），口服葡萄糖耐量试验（OGTT）水平，并测定胰腺β细胞的超微结构。此外，在三组中计算胰岛素抵抗的稳态模型评估(HOMA-IR)评分.
与模型组相比，SUA减少，而FBG,GADA,瑞舒伐他汀组第4周时OGTT和HOMA-IR显著升高。然而,FBI在三组之间没有显着变化。瑞舒伐他汀组高尿酸血症大鼠胰岛β细胞结构受损,胰岛β细胞数量改变,但加重。
瑞舒伐他汀在诱导FGB，GADA,OGTT与高尿酸血症大鼠胰腺β细胞损伤.
