摘要
目的探讨丙酮酸激酶(PK)水平变化与高甘油三酯(TG)并尿酸(UA)、血糖(GLU)代谢紊乱的病理联系。方法高果糖食饵复制高TG血症动物模型基础上,并拓展塑造高TG并高UA、高GLU血症动物模型,动态检测模型大鼠血清TG、UA、GLU水平变化,并根据模型动物血清TG水平单纯明显升高(21 d)和血清TG、UA、GLU三者同时明显升高(57 d)先后分2批结束实验。动物处死后用比色法测定血清、肝脏中PK活性,用免疫组化法显示肝脏PK的蛋白表达。结果造模21d,高果糖模型大鼠血清TG较正常对照组明显升高,UA、GLU水平无明显变化;造模29 d,模型大鼠血清TG、UA、GLU水平均较正常对照组明显升高并持续至造模57 d仍维持较高水平,大鼠血清、肝脏中PK活性均明显降低,肝脏中PK蛋白表达均明显减弱。结论PK活性降低可能是模型大鼠出现高TG及其并发症的原因之一。
Objective To investigate the pathological relationship between pyruvate kinase (PK) level and hypertriglyceridemia complicated by the metabolism disorder of uric acid (UA) and glucose (GLU). Methods On the base of copied hypertriglyceridemia model by high fructose diet, the model of hypertriglyceridemia complicated by hyperuricemia and hyperglycemia was established. The changes of serum levels of triglyceride (TG), UA and GLU in model rats were detected dynamically. The experiments were stopped respectively when only TG level markedly increased (on 21st day) and TG, UA and GLU levels increased synchronously (on 57th day). The activity of PK in the serum and liver were detected by spectrophotometry and PK protein expression in the liver was detected by immunohistochemistry assay after killing rats. Results The serum TG level was increased obviously in the model group than that in the normal control group, and UA and GLU levels were not changed 21 days after model establishment. The levels of TG, UA and GLU were obviously increased in the model group than those in the normal control group 29 days after model establishment, and kept higher levels till to 57th day. The PK activity and protein expression in the serum or liver in the model group were obviously decreased. Conclusion The decrease of PK activity may be one of the causes of hypertriglyceridemia and its complications in rats.
出处
《北京中医药大学学报》
CAS
CSCD
北大核心
2008年第2期98-101,共4页
Journal of Beijing University of Traditional Chinese Medicine
基金
国家自然科学基金资助项目(No.30472282)
北京市自然科学基金资助项目(No.7052036)
博士点基金资助项目(No.20040026005)
关键词
丙酮酸激酶
高甘油三酯并高尿酸高血糖血症
蛋白表达
大鼠
pyruvate kinase
hypertriglyceridemia complicated by hyperuricemia and hyperglycemia
protein expression
rats