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Journal of Diabetes Research
Volume 2014, Article ID 287536, 10 pages
http://dx.doi.org/10.1155/2014/287536
Research Article

Low Protein Diet Inhibits Uric Acid Synthesis and Attenuates Renal Damage in Streptozotocin-Induced Diabetic Rats

1Department of Endocrinology, Guangzhou Red Cross Hospital, Medical College of Jinan University, No. 396 Tong Fu Zhong Road, Guangzhou 510220, China
2Department of Nephrology, Guangzhou Red Cross Hospital, Medical College of Jinan University, No. 396 Tong Fu Zhong Road, Guangzhou 510220, China
3Clinical Institute of Nutrition, Guangzhou Red Cross Hospital, Medical College of Jinan University, No. 396 Tong Fu Zhong Road, Guangzhou 510220, China

Received 27 December 2013; Revised 9 February 2014; Accepted 10 February 2014; Published 13 March 2014

Academic Editor: Francesco Chiarelli

Copyright © 2014 Jianmin Ran et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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), creatintine (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.