西亞試劑：Restricted intake of dietary advanced glycation end product

Restricted intake of dietary advanced glycation end products retards renal progression in the remnant kidney model

J X Feng1, F F Hou1, M Liang1, G B Wang1, X Zhang1, H Y Li1, D Xie1, J W Tian1 and Z Q Liu1

1Department of Medicine, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, PR China

Correspondence: FF Hou, Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China. E-mail: ffhou@public.guangzhou.gd.cn

Received 27 October 2006; Revised 12 December 2006; Accepted 9 January 2007; Published online 7 March 2007.

Diet-derived advanced glycation end products (AGEs) contribute significantly to accumulation of AGEs in renal insufficiency. To test whether modulation of dietary AGEs would impact on progression of chronic renal disease, 5/6 nephrectomy rats were randomly placed on three diets that differed only in AGEs content (low AGEs diet (LAD), high AGEs diet (HAD), and standard rodent diet (SRD)) for 5–13 weeks. Compared with SRD- or HAD-fed rats, LAD-treated animals showed decreased proteinuria and retarded decline of creatinine clearance without alteration of blood pressure. Glomerular volume was reduced by 23% compared with HAD-fed rats at week 13 (P<0.001). Renal fibrosis progressed with time in the remnant kidneys from HAD-fed rats. However, LAD-fed animals presented a better-preserved structure of the kidneys. LAD-fed rats demonstrated significantly decreased serum and renal AGEs concentration (P<0.01 and P<0.01). This was associated with marked decrease of intrarenal advanced oxidation protein products and thiobarbituric acid reactive substances, as well as increase of glutathione peroxidase activity. LAD treatment also downregulated expression of monocyte chemoattractant protein-1 and transforming growth factor-1 and ameliorated macrophage infiltration in the remnant kidney. These results demonstrated that restriction of dietary AGEs intake retards progression of renal fibrosis and dysfunction in the remnant kidney model.