1/1/2018 · A bolus administration of vitamin D compounds into mice induced hypercalcemia with enhanced bone resorption. This proresorptive activity of vitamin D compounds was not observed in Ob-VDR-cKO mice, suggesting that VDR in osteoblastic cells played a role in induction of osteoclastogenesis in vivo. On the other hand, long-term treatment of mice with a pharmacological dose of vitamin D.
Vitamin D, when administered for severe vitamin D deficiency or in large doses, stimulates osteoclastic bone resorption, presumably through a molecular interaction between recently identified receptor activator of NF-?B ligand/osteoprotegerin ligand on marrow stromal cells and receptor activator of NF-?B on osteoclast precursors.
Mature osteoclasts express the vitamin D receptor (VDR) and are able to synthesise and respond to 1,25 (OH) 2 D 3 via CYP27B1 enzyme activity. Whether vitamin D signalling within osteoclasts is necessary for the regulation of osteoclastic bone resorption in an in vivo setting is unclear.
10/1/2010 · In summary, we provide evidence that vitamin D metabolizes in osteoclasts in an autocrine manner, and the circulating level of 25D appears to be a determinant of osteoclast differentiation and function. As reported previously , as circulating 25D levels fall, the initial response is for an increase in circulating PTH and 1,25D levels. High 1,25D levels are believed to stimulate RANKL expression on.
The active form of vitamin D, 1,25-dihydroxyvitamin D3, carries out its diverse range of biological activities by binding to the nuclear vitamin D receptor, present in almost every cell of the body. It is well established that adequate serum 25-hydroxyvitamin D levels correlate with a reduction in the incidence of osteoporosis; however, the physiological basis for this relationship remains elusive.
The direct action of active vitamin D compounds on osteoclast precursors has also been proposed to explain its suppressive effect on osteoclastogenesis. 1?,25(OH) 2 D 3 inhibits RANKL-induced osteoclastic differentiation in cultures of osteoclast precursors in the absence of osteoblastic cells. 1?,25(OH) 2 D 3 suppressed the expression of c-Fos, a transcription factor essential for …
