Experimental Evidence for the Effects of Calcium and Vitamin D on Bone: A Review

Nutrients

Howard A. Morris¹  Peter D. O’Loughlin² 

[1] School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia 5001, AustraliaEndocrine Bone Research Laboratory, Hanson Institute, SA Pathology, Adelaide, South Australia 5000, Australia;

关键词: osteomalacia;    osteoporosis;    dietary calcium;    vitamin D;    oophorectomy;    bone architecture;    bone strength;    calcium balance;   

DOI  :  10.3390/nu2091026

来源: mdpi

【 摘 要 】

Animal models fed low calcium diets demonstrate a negative calcium balance and gross bone loss while the combination of calcium deficiency and oophorectomy enhances overall bone loss. Following oophorectomy the dietary calcium intake required to remain in balance increases some 5 fold, estimated to be approximately 1.3% dietary calcium. In the context of vitamin D and dietary calcium depletion, osteomalacia occurs only when low dietary calcium levels are combined with low vitamin D levels and osteoporosis occurs with either a low level of dietary calcium with adequate vitamin D status or when vitamin D status is low in the presence of adequate dietary calcium intake. Maximum bone architecture and strength is only achieved when an adequate vitamin D status is combined with sufficient dietary calcium to achieve a positive calcium balance. This anabolic effect occurs without a change to intestinal calcium absorption, suggesting dietary calcium and vitamin D have activities in addition to promoting a positive calcium balance. Each of the major bone cell types, osteoblasts, osteoclasts and osteocytes are capable of metabolizing 25 hydroxyvitamin D (25D) to 1,25 dihydroxyvitamin D (1,25D) to elicit biological activities including reduction of bone resorption by osteoclasts and to enhance maturation and mineralization by osteoblasts and osteocytes. Each of these activities is consistent with the actions of adequate circulating levels of 25D observed in vivo.

【 授权许可】

CC BY   
© 2010 by the authors; licensee MDPI, Basel, Switzerland