目的:模拟临床人类饮食结构改变,观察高嘌呤食饵对鹌鹑尿酸及糖脂代谢的影响,探讨高尿酸血症并糖脂代谢紊乱的发病规律与病理机制。方法:采用高嘌呤食饵诱导法塑造鹌鹑尿酸及糖脂代谢紊乱模型,动态观察各组鹌鹑血清尿酸(UA)、甘油三酯(TG)、血糖(GLU)及相关代谢酶黄嘌呤氧化酶(XOD)、鸟嘌呤脱氨酶(GuDa)、腺苷脱氨酶(ADA)、三磷酸甘油醛脱氢酶(GAPDH)酶活性、胰岛素(Ins)水平变化。结果:高嘌呤食饵诱导鹌鹑造模10-140 d血清UA水平显著升高;60-140 d伴发血清TG水平显著升高;90-140 d同时伴发血清GLU水平显著升高;造模第10、60、140 d血清XOD活性显著升高;造模第60-140 d模型组鹌鹑全血GAPDH活性显著降低;造模第60-140 d模型组鹌鹑Ins水平显著升高。结论:(1)高嘌呤饮食可诱发鹌鹑UA、TG、GLU多代谢紊乱,模拟临床尿酸及糖脂多代谢紊乱的疾病表现。(2)其发病特点表现为单纯高尿酸血症,而后伴发高甘油三酯血症,最终发展成为高尿酸并高甘油三酯/高血糖血症。(3)该病理机制可能与血清XOD活性、Ins水平升高及全血GAPDH活性降低有关。
AIM:To investigate the pathomechanisms in a coturnix model of high-purine diet and the metabolic characteristics of glucose and lipids.METHODS: Twenty-four French male quails were randomly divided into 2 groups: control group and model group.The animals in control group were fed with normal diet and the quails in model group were fed with high-purine diet.The body weight,serum uric acid(UA),triglyceride(TG),glucose(GLU),the activity of xanthine oxidase(XOD),guanine deaminase(GuDa) and glyceraldehyde phosphate dehydrogenase(GAPDH),and the level of insulin(Ins) were determined.RESULTS: No change of body weight in model group was observed.In model group,the serum levels of UA,TG and GLU were significantly increased from 10 d to 140 d,60 d to 140 d and 90 d to 140 d,respectively.At 10 d,60 d and 140 d,the activity of XOD in model group was significantly higher than that in control group.From 30 d to 140 d,the activity of GAPDH was significantly decreased.From 60 d to 140 d,the level of Ins was significantly increased.CONCLUSION: (1) High-purine diet induces multiple metabolic disorders of UA,TG and GLU.(2) The pathologic processes can be divided into three stages: simple hyperuricemia in the first stage,hyperuricemia combined with hypertriglyceridemia in the second stage and hyperuricemia combined with hypertriglyceridemia and hyperglycemia in the third stage.(3) The pathomechanisms may relate to the increased activity of XOD,decreased activity of GAPDH and increased level of Ins.