Abstract
Vitamin A plays a prominent role for maintaining optimal bone status, but its impact upon the bone in response to vitamin A deficiency is not well defined. The purpose of this study was to evaluate how replenishing vitamin A by either whole food cod liver oil (COD) or the active metabolite of vitamin A, retinoic acid (RA), altered bone thickness of vitamin A-deficient (VAD) rats. Weanling rats were administered a control diet (CTRL) or VAD diet for 9 weeks. This was followed by four weeks of treatment in which the VAD group was divided into the following 4 subgroups: (1) VAD (9 weeks)-VAD (4 weeks); (2) VAD-CTRL; (3) VAD-COD; and (4) VAD-RA. Compared to controls, VAD rats had thicker bones which showed marked dysplasia. VAD-rats treated with COD produced a thinner bone that was not significantly different from that of untreated rats. In contrast, RA did not significantly change the thicker bone, and also had significantly greater periosteal and endosteal osteoblast numbers compared to VAD-COD. Active osteoclasts were not detected in VAD rats, nor during the treatment period. These findings suggest that the abnormal bone thickness in VAD rats appears to be more effectively restored to bone thickness of untreated control rats when treated with COD.
Highlights
After we evaluated the impact of vitamin A-deficient (VAD) on bone status, we replenished vitamin A in the form of the whole food cod liver oil or its active metabolite retinoic acid, to determine which form was most effective in restoring the bone
Twelve rats were euthanized at week 9 to examine the impact of VAD rats on bone status in the VAD group (n = 6) and the control diet (CTRL) group (n = 6)
We showed that 9 weeks of VAD caused thickening of the cortical bone in rats
Summary
Active osteoclasts were not detected in VAD rats, nor during the treatment period These findings suggest that the abnormal bone thickness in VAD rats appears to be more effectively restored to bone thickness of untreated control rats when treated with COD. Important roles in maintaining proper bone structure through activating osteoclasts and osteoblasts, respectively, in the continual bone degradation and formation process. This continual renewal of bone structure allows for bone to adapt to stressors that are placed upon it and for bone growth. Vitamin A, in the form of all-trans-retinoic acid, has been found to directly promote bone resorption, which leads to decreased bone mineral density (BMD) in rats independent of cholecalciferol (vitamin D3 ), calcium or phosphorus levels [6]. All-trans-retinoic acid has been found to stimulate mature isolated osteoclasts through increased gene expression of cathepsin K/osteoclast-2 (OC-2) and increased expression of retinoic acid receptor α mRNA and retinoid X-receptor β mRNA [7]
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