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1 Medicine, University of Florida, Gainesville, Florida, United States; Medicine, North Florida South Georgia VA Medical Center, 1601 Archer Road, Gainesville, 32610, United States
2 Medicine, University of Florida, Gainesville, Florida, United States
3 Medicine, University of Florida, Gainesville, Florida, United States; Medicine, KhonKaen University, 123 Mittraparp Road, KhonKaen, 40002, Thailand
* To whom correspondence should be addressed. E-mail: gerscms{at}medicine.ufl.edu.
The metabolic syndrome has recently been recognized as a risk factor for kidney disease but the mechanisms mediating this risk remain unclear. High fructose consumption by animals produces a model of the metabolic syndrome with hypertension, hyperlipidemia, and insulin resistance. The present study was conducted to test the hypothesis that consumption of a high fructose diet could accelerate the progression of chronic kidney disease. Three groups of fourteen male Sprague-Dawley rats were pair-fed a specialized diet containing 60% fructose (FRU), 60% dextrose (DEX), or standard rat chow (CON). After six weeks of the diet, 5/6 nephrectomy was performed and the animals were continued on their diets for more 11 weeks. Compared to the control or dextrose fed animals, the fructose treated animals had significantly increased proteinuria, decreased creatinine clearance, and higher blood urea nitrogen. The kidneys from the fructose-fed animals were markedly larger than the kidneys from control or dextrose diet treated rats. The kidneys from the fructose treated animals showed markedly worse glomerular sclerosis, tubular atrophy, tubular dilatation, and cellular infiltration compared to the dextrose or control treated animals. Monocyte chemoattractant protein-1 (MCP-1) was measured in renal tissue homogenate and found to be increased in the fructose treated animals. In order to determine the mechanism for increased renal MCP-1, in vitro studies were conducted; and fructose stimulation of proximal tubular cells resulted in the production of MCP-1. In conclusion, consumption of a high fructose diet greatly accelerates progression of CKD in the rat remnant kidney model.
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