低蛋白饮食可抑制链脲佐菌素诱导的糖尿病大鼠的尿酸合成并减轻肾脏损伤。
Low protein diet inhibits uric acid synthesis and attenuates renal damage in streptozotocin-induced diabetic rats.
作者信息
Ran Jianmin, Ma Jing, Liu Yan, Tan Rongshao, Liu Houqiang, Lao Gancheng
机构信息
Department of Endocrinology, Guangzhou Red Cross Hospital, Medical College of Jinan University, No. 396 Tong Fu Zhong Road, Guangzhou 510220, China.
Department of Nephrology, Guangzhou Red Cross Hospital, Medical College of Jinan University, No. 396 Tong Fu Zhong Road, Guangzhou 510220, China.
出版信息
J Diabetes Res. 2014;2014:287536. doi: 10.1155/2014/287536. Epub 2014 Mar 13.
AIM
Several studies indicated that hyperuricemia may link to the worsening of diabetic nephropathy (DN). Meanwhile, low protein diet (LPD) retards exacerbation of renal damage in chronic kidney disease. We then assessed whether LPD influences uric acid metabolism and benefits the progression of DN in streptozotocin- (STZ-) induced diabetic rats.
METHODS
STZ-induced and control rats were both fed with LPD (5%) and normal protein diet (18%), respectively, for 12 weeks. Vital signs, blood and urinary samples for UA metabolism were taken and analyzed every 3 weeks. Kidneys were removed at the end of the experiment.
RESULTS
Diabetic rats developed into constantly high levels of serum UA (SUA), creatinine (SCr) and 24 h amounts of urinary albumin excretion (UAE), creatinine (UCr), urea nitrogen (UUN), and uric acid (UUA). LPD significantly decreased SUA, UAE, and blood glucose, yet left SCr, UCr, and UUN unchanged. A stepwise regression showed that high UUA is an independent risk factor for DN. LPD remarkably ameliorated degrees of enlarged glomeruli, proliferated mesangial cells, and hyaline-degenerated tubular epithelial cells in diabetic rats. Expression of TNF-α in tubulointerstitium significantly decreased in LPD-fed diabetic rats.
CONCLUSION
LPD inhibits endogenous uric acid synthesis and might accordingly attenuate renal damage in STZ-induced diabetic rats.
目的
多项研究表明，高尿酸血症可能与糖尿病肾病（DN）的恶化有关。同时，低蛋白饮食（LPD）可延缓慢性肾脏病肾损伤的加重。因此，我们评估了LPD是否会影响尿酸代谢以及对链脲佐菌素（STZ）诱导的糖尿病大鼠DN的进展是否有益。
方法
将STZ诱导的糖尿病大鼠和对照大鼠分别给予LPD（5%）和正常蛋白饮食（18%），持续12周。每3周采集并分析生命体征、用于尿酸代谢的血液和尿液样本。实验结束时取出肾脏。
结果
糖尿病大鼠血清尿酸（SUA）、肌酐（SCr）以及24小时尿白蛋白排泄量（UAE）、肌酐（UCr）、尿素氮（UUN）和尿酸（UUA）持续处于高水平。LPD显著降低了SUA、UAE和血糖，但SCr、UCr和UUN未变。逐步回归分析显示，高UUA是DN的独立危险因素。LPD显著改善了糖尿病大鼠肾小球增大、系膜细胞增殖和肾小管上皮细胞玻璃样变性的程度。LPD喂养的糖尿病大鼠肾小管间质中TNF-α的表达显著降低。
结论
LPD抑制内源性尿酸合成，因此可能减轻STZ诱导的糖尿病大鼠的肾损伤。
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