腹型肥胖、血脂谱异常与高尿酸血症并存鹌鹑模型的病理机制

目的 观察高脂饮食诱导的腹型肥胖鹌鹑的血清尿酸含量、脂质谱、脂代谢及尿酸代谢相关酶活性，探讨腹型肥胖伴脂质谱异常、高尿酸血症的可能机制。方法 采用高脂饲料诱导腹型肥胖鹌鹑模型，分别于高脂饮食的第7和14天检测正常(n=12)和腹型肥胖鹌鹑模型(n=12)的血清尿酸及血糖水平、脂质谱、脂代谢及尿酸代谢相关酶活性以及体重、腹部脂肪重量、腹脂率。结果 研究第7天模型组鹌鹑的体重、腹部脂肪重量及腹脂率与正常组的差异无统计学意义（P均＞0.05）。第14天两组鹌鹑体重的差异无统计学意义(P＞0.05)，模型组的腹部脂肪重量(3.91±2.13)比(2.40±0.96)g，P=0.0468]及腹脂率（1.92％±0.97％比1.22％±0.45％，P=0.0447）均显著高于正常组。研究第7及14天模型组鹌鹑血清总胆固醇（P值分别为0.0042和0.0006）和低密度脂蛋白胆固醇（P值分别为0.0045和0.0010）水平均显著高于正常组；甘油三酯水平显著低于正常组（P值分别为0.0006和0.0024）；尿酸代谢相关酶腺苷脱氨酶（P值分别为0.0237和0.0060）及黄嘌呤氧化酶活性（P值分别为0.0142和0.0071）均显著高于正常组。第14天模型组的尿酸水平显著高于正常组(P=0.0320)；高密度脂蛋白胆固醇水平显著低于正常组(P=0.0197)；模型组脂代谢相关酶脂蛋白脂酶活性显著高于正常组（P=0.0419）。结论 高脂饮食不但可诱发鹌鹑血脂谱异常，并随造模时间的延长而伴发腹型肥胖与高尿酸血症。脂代谢及尿酸代谢相关酶活性改变可能是腹型肥胖伴发血脂谱异常、高尿酸血症的病理机制。

Mechanisms of abdominal obesity combined with blood lipid spectrum disorder and hyperuricemia on quail model

Objective To observe the changes of uric acid level and lipid spectrum, and activities lipid metabolism related enzyme as well as uric acid metabolism-related enzymes on quail abdominal obesity model and then investigate the underlying mechanism of abdominal obesity combined with blood lipid spectrum disorder and hyperuricemia model. Methods The quail model of abdominal obesity was induced by feeding with high-fat diet.The body weight and abdominal fat content were measured and the abdominal fat index was calculated. The levels of total cholesterol (TC), high density lipoprotein cholesterol, low density lipoprotein cholesterol (LDL-C), triglyceride (TG), glucose, and uric acid in serum were determined. The changes of adenosine deaminase (ADA),xanthine oxidase (XOD), lipoprotein lipase (LPL), hepatic lipase (HL), and total esterase (TE) activities were also determined. Results On the 7th day, the body weight, abdominal fat content, and abdominal fat index were not significantly different between the model group and control group ( all P ＞0.05 ). On the 14th day, the body weight was not significantly different between these two groups ( P ＞ 0.05 ), while the abdominal fat content (3.91 ±2. 13) vs. (2.40±0.96) g, P=0.0468] and abdominal fat index (1.92％ ±0.97％ vs. 1.22％ ±0.45％, P =0.0447) were significantly higher in the model group. On the 7th and 14th day, the levels ofTC (P =0.0042 and P =0.0006, respectively), LDL-C ( P =0.0045 and P =0.0010, respectively) in the model group were significantly higher than those in control group, while the level of TG significantly decreased ( P =0.0006 and P =0.0024, respectively ). On the 7th day, compare with the control group, the activities of ADA ( P =0.0237 )and XOD (P =0.0142) in the model group significantly increased, while the activities of LPL, HL, and TE had no significant changes. On the 14th day, compared with the control group, the activities of ADA ( P =0.0060),XOD ( P =0.0071 ), and LPL ( P =0.0419) in the model group significantly increased, while the activities of HL and TE had no significant changes. Conclusions High-fat diet can induce disorders in blood lipid profiles in quail model, but also may incur abdominal obesity and multiple metabolic disorders. Changes in the activities of uric acid and lipid metabolism related enzymes may be the underlying mechanism of disorders in blood lipid profile and its associated hyperuricemia and abdominal accumulation.