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Impaired vitamin D synthesis and intestinal Ca transport compromise growth in fructose‐fed young rats
Author(s) -
Douard Veronique,
Lee Jackie,
Sabbagh Yves,
Shapses Sue A,
Lin Sheldon S,
Ferraris Ronaldo P
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.603.16
Subject(s) - fructose , endocrinology , medicine , calcitriol , chemistry , vitamin d and neurology , biology , biochemistry
Sufficient Ca intake is essential in supporting rapid growth of young mammals. We recently discovered in adult rat models of kidney disease that dietary fructose reduces rates of intestinal Ca transport and levels of calcitriol regulating Ca homeostasis. However, the effects of fructose on growth rate are not known. Three groups of young male rats were fed a 63% fructose, glucose or starch diet from 21 to 50 d of age. Feeding rate was similar but fructose significantly impaired the growth rate after 15 d of feeding. Rats fed fructose weighed 10% less than those fed glucose or starch at 50 d old, and had lower bone mineral content in the carcass. The femur of fructose‐fed rats demonstrated lower torsional rigidity and lower shear modulus. Duodenal transport of Ca and CaBP9k expression were reduced in fructose‐fed rats by ~50%. This effect is specific since total intestinal Pi and glucose transporter activity and expression were each independent of diet. Calcitriol levels were 2‐fold lower in fructose‐fed rats. Since calcidiol levels did not change, fructose feeding may impair the renal synthesis or enhance the breakdown of calcitriol in the kidney. These results may explain the deleterious impact of fructose on growth rate since reduced absorption of calcium arising from calcitriol deficiency may limit statural growth (NSF IBN722365, NIH RDK075617).