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BioMed Research International
Volume 2014 (2014), Article ID 823879, 10 pages
http://dx.doi.org/10.1155/2014/823879
Research Article

Impact of Gentamicin Coadministration along with High Fructose Feeding on Progression of Renal Failure and Metabolic Syndrome in Sprague-Dawley Rats

1Department of Pharmacology and Toxicology, School of Medicine and Health Science, Universiti Putra Malaysia, 47300 Serdang, Selangor, Malaysia
2Department of Clinical Laboratory Science, Faculty of Pharmacy, Baghdad University, Baghdad, Iraq
3Department of Anatomy, School of Medicine and Health Science, Universiti Putra Malaysia, 47300 Serdang, Selangor, Malaysia
4Department of Veterinary Surgery, School of Veterinary Medicine, Universiti Putra Malaysia, 47300 Serdang, Selangor, Malaysia
5Department of Pathology, School of Medicine and Health Science, Universiti Putra Malaysia, 47300 Serdang, Selangor, Malaysia
6Department of Pathology, School of Dentistry, Universiti Technology MARA, 48600 Shah Alam, Selangor, Malaysia

Received 13 February 2014; Revised 24 April 2014; Accepted 3 May 2014; Published 23 June 2014

Academic Editor: Emmanuel A. Burdmann

Copyright © 2014 Zaid O. Ibraheem 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

The current study evaluates the impact of high fructose feeding in rat model of gentamicin induced nephrotoxicity. Sprague-Dawley rats weighing 180–200 g were randomized into four groups; (C) received standard rodents chow with free access to ad libitum drinking water for 8 weeks and was considered as control, (F) received standard rodents chow with free access to drinking water supplemented with 20% (W/V) fructose for the same abovementioned period, (FG) was fed as group F and was given 80 mg/kg (body weight)/day gentamicin sulphate intraperitoneally during the last 20 days of the feeding period, and (G) was given gentamicin as above and fed as group C. Renal function was assessed at the end of the treatment period through measuring serum creatinine, uric acid and albumin, creatinine clearance, absolute and fractional excretion of both sodium and potassium, twenty-four-hour urinary excretion of albumin, and renal histology. For metabolic syndrome assessment, fasting plasma glucose and insulin were measured and oral glucose tolerance test was performed throughout the treatment period. Results showed that gentamicin enhances progression of fructose induced metabolic syndrome. On the other hand, fructose pretreatment before gentamicin injection produced a comparable degree of renal dysfunction to those which were given fructose-free water but the picture of nephrotoxicity was somewhat altered as it was characterized by higher extent of glomerular congestion and protein urea. Overall, more vigilance is required when nephrotoxic drugs are prescribed for patients with fructose induced metabolic syndrome.