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High renal calcium (Ca) excretion does not reduce femur bone density in mice fed adequate or low dietary Ca
Author(s) -
Fernandez Perla Citlali Reyes,
Fleet James C
Publication year - 2013
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.27.1_supplement.867.5
Subject(s) - medicine , endocrinology , calcitriol receptor , weanling , ileum , vitamin d and neurology , calcium metabolism , bone remodeling , excretion , chemistry , cancellous bone , small intestine , calcium , jejunum , biology , anatomy
Active vitamin D, 1,25(OH) 2 D 3 (1,25D) regulates intestinal Ca absorption (Ca Abs) under low dietary Ca intake by inducing gene expression through the vitamin D receptor (VDR). Vitamin D‐regulated Ca Abs is greatest in the proximal small intestine but VDR is highest in the large intestine. We generated transgenic (TG) mice using a CDX2P9.5 promoter‐Cre transgene to drive deletion of floxed VDR alleles from the lower bowel to test whether this disrupts whole body Ca metabolism. Weanling, male TG and control mice were fed diets with low (0.25%) or normal (0.5%) Ca levels until 10 wks of age. Transgene expression was seen in the distal ileum, cecum, and colon as well as the kidney, a 1,25D target tissue. Serum 1,25D was not different between genotypes and serum Ca was normal in all groups. TG mice had low serum PTH (p<0.001) which explains the 10‐fold higher urinary Ca/creatinine ratio (p<0.001) we observed. However, no genotype effects were found in femur cancellous or cortical bone density. These data show that while Ca metabolism is disturbed in TG mice, high renal Ca excretion does not negatively affect bone density or adaption to restricted Ca intake. Grant Funding Source : NIH award DK54111 (JCF)