Issue 3, 2016

Ellagic acid inhibits non-enzymatic glycation and prevents proteinuria in diabetic rats

Abstract

The formation of advanced glycation end products (AGEs) is a characteristic feature of diabetic tissues and accumulation of these products has been implicated in the pathogenesis of micro- and macrovascular complications of diabetes including diabetic nephropathy (DN). Compelling evidence suggests that AGEs mediate progressive alteration in the renal architecture and loss of renal function whereas inhibitors of AGEs prevent the progression of experimental DN. We have investigated the potential of ellagic acid (EA), a polyphenol present abundantly in fruits and vegetables, to prevent in vivo accumulation of AGE and to ameliorate renal changes in diabetic rats. Streptozotocin-induced diabetic rats were fed with either 0.2% or 2% of EA in the diet for 12 weeks. Dietary supplementation of EA to diabetic rats prevented the glycation mediated RBC-IgG-cross-links and HbA1c accumulation. EA inhibited the accumulation of N-carboxymethyl lysine (CML), a predominant AGE in the diabetic kidney. Further, EA also prevented the AGE-mediated loss of expression of podocyte slit diaphragm proteins: nephrin and podocin. By inhibiting CML formation, EA improved renal function in rats as evidenced by urinary albumin and creatinine levels. In conclusion, EA inhibited AGE accumulation in the diabetic rat kidney and ameliorated AGE-mediated pathogenesis of DN.

Graphical abstract: Ellagic acid inhibits non-enzymatic glycation and prevents proteinuria in diabetic rats

Article information

Article type
Paper
Submitted
12 Nov 2015
Accepted
07 Feb 2016
First published
12 Feb 2016

Food Funct., 2016,7, 1574-1583

Author version available

Ellagic acid inhibits non-enzymatic glycation and prevents proteinuria in diabetic rats

G. Raghu, S. Jakhotia, P. Yadagiri Reddy, P. Anil Kumar and G. Bhanuprakash Reddy, Food Funct., 2016, 7, 1574 DOI: 10.1039/C5FO01372K

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