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Dietary Fructose Inhibits Intestinal Calcium Absorption and Induces Vitamin D Insufficiency in CKD

Veronique Douard^*, Abbas Asgerally^*, Yves Sabbagh, Shozo Sugiura, Sue A. Shapses, Donatella Casirola^* and Ronaldo P. Ferraris^*

*Department of Pharmacology and Physiology, New Jersey Medical School, Newark, New Jersey;
Endocrine and Renal Sciences, Genzyme Corporation, Framingham, Massachusetts;
Department of Biological Resource Management, School of Environmental Sciences, University of Shiga Prefecture, Shiga-ken, Japan; and
New Jersey Obesity Group, Department of Nutritional Science, Rutgers University, New Brunswick, New Jersey

Correspondence: Dr. Ronaldo P. Ferraris, Department of Pharmacology and Physiology, UMDNJ-New Jersey Medical School, Newark, NJ 07101-1709. Phone: 973-972-4519; Fax: 973-972-7950; E-mail: ferraris{at}umdnj.edu

Received for publication August 3, 2009. Accepted for publication September 23, 2009.

Renal disease leads to perturbations in calcium and phosphate homeostasis and vitamin D metabolism. Dietary fructose aggravates chronic kidney disease (CKD), but whether it also worsens CKD-induced derangements in calcium and phosphate homeostasis is unknown. Here, we fed rats diets containing 60% glucose or fructose for 1 mo beginning 6 wk after 5/6 nephrectomy or sham operation. Nephrectomized rats had markedly greater kidney weight, blood urea nitrogen, and serum levels of creatinine, phosphate, and calcium-phosphate product; dietary fructose significantly exacerbated all of these outcomes. Expression and activity of intestinal phosphate transporter, which did not change after nephrectomy or dietary fructose, did not correlate with hyperphosphatemia in 5/6-nephrectomized rats. Intestinal transport of calcium, however, decreased with dietary fructose, probably because of fructose-mediated downregulation of calbindin 9k. Serum calcium levels, however, were unaffected by nephrectomy and diet. Finally, only 5/6-nephrectomized rats that received dietary fructose demonstrated marked reductions in 25-hydroxyvitamin D₃ and 1,25-dihydroxyvitamin D₃ levels, despite upregulation of 1-hydroxylase. In summary, excess dietary fructose inhibits intestinal calcium absorption, induces marked vitamin D insufficiency in CKD, and exacerbates other classical symptoms of the disease. Future studies should evaluate the relevance of monitoring fructose consumption in patients with CKD.

Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673