25-Hydroxyvitamin D requirement for maintaining skeletal health utilising a Sprague-Dawley rat model

被引:29
作者
Anderson, P. H.
Sawyer, R. K.
May, B. K.
O'Loughlin, P. D.
Morris, H. A.
机构
[1] Inst Med & Vet Sci, Endocrine Bone Res Lab, Hanson Inst, Adelaide, SA 5000, Australia
[2] Inst Med & Vet Sci, Div Clin Biochem, Adelaide, SA 5000, Australia
[3] Univ Adelaide, Sch Mol & Biomed Sci, Adelaide, SA 5005, Australia
关键词
vitamin D-deficiency; kidney; osteomalacia; osteoporosis; 25-hydroxyvitamin D-l alpha-hydroxylase; 25-hydroxyvitamin D-24 hydroxylase;
D O I
10.1016/j.jsbmb.2006.12.086
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To study the role of vitamin D to optimise bone architecture, we have developed an animal model to investigate the effects of frank vitamin D-deficiency as well as graded depletion of circulating 25-hydroxyvitamin D-3 (25D) levels on the skeleton. Rats fed on dietary vitamin D levels from 0 to 500ng/day achieved diet-dependent circulating levels of 25D ranging from 11 to 115 nmol/L. Levels of serum 1,25-dihydroxyvitamin D-3 (1,25D) increased as dietary vitamin D increased between 0 and 200 ng/day at which point a maximum level was achieved and retained with higher vitamin D intakes. The renal levels of 25-hydroxyvitamin D-la-hydroxylase (CYP27B1) mRNA were highest in animal groups fed on vitamin D between 0 and 300 ng/day. In contrast, renal 25-hydroxyvitamin D 24-hydroxylase (CYP24) mRNA levels increased as dietary vitamin D increased achieving maximum levels in animals receiving 500 ng vitamin D/day. This animal model of vitamin D depletion is suitable to provide invaluable information on the serum levels of 25D and dietary calcium intake necessary for optimal bone structure. Such information is essential for developing nutritional recommendations to reduce the incidence of osteoporotic hip fractures. (c) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:592 / 595
页数:4
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