J Am Soc Nephrol. 2010 Feb;21(2):261-71. Epub 2009 Dec 3.
Douard V, Asgerally A, Sabbagh Y, Sugiura S, Shapses SA, Casirola D, Ferraris RP.
Department of Pharmacology and Physiology, UMDNJ-New Jersey Medical School, Newark, NJ 07101-1709, USA.
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 D(3) and 1,25-dihydroxyvitamin D(3) levels, despite upregulation of 1alpha-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.
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