Low Protein Diet Inhibits Uric Acid Synthesis and Attenuates Renal Damage in Streptozotocin-Induced Diabetic Rats
| Autor: | Gancheng Lao, Houqiang Liu, Jing Ma, Yan Liu, Jianmin Ran, Rongshao Tan |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Male
medicine.medical_specialty Article Subject Endocrinology Diabetes and Metabolism Hyperuricemia Kidney lcsh:Diseases of the endocrine glands. Clinical endocrinology Streptozocin Diabetes Mellitus Experimental Rats Sprague-Dawley Diabetic nephropathy Excretion Random Allocation chemistry.chemical_compound Endocrinology hemic and lymphatic diseases Internal medicine Diabetes mellitus Diet Protein-Restricted medicine Albuminuria Animals Diabetic Nephropathies Cell Proliferation Cell Size Creatinine lcsh:RC648-665 Tumor Necrosis Factor-alpha business.industry Extracellular Fluid medicine.disease Streptozotocin Rats Uric Acid Kidney Tubules medicine.anatomical_structure chemistry Hyperglycemia Mesangial Cells Uric acid business Research Article medicine.drug |
| Zdroj: | Journal of Diabetes Research Journal of Diabetes Research, Vol 2014 (2014) |
| ISSN: | 2314-6753 2314-6745 |
| DOI: | 10.1155/2014/287536 |
| Popis: | 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-αin 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. |
| Databáze: | OpenAIRE |
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