Plasma vitamin D metabolite levels in phosphorus deficient rats during the development of vitamin D deficient rickets

Harrison, Joan E.; Hitchman, A. J. W.; Jones, Glenville; Tam, Carolyn; Heersche, J. N. M.

doi:10.1016/0026-0495(82)90162-7

Cited by 21 publications

(3 citation statements)

References 27 publications

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“…The serum 25(OH)D values observed in normal rats in this study are lower than those previously described by ourselves (36) and by other workers (37)(38)(39). Whereas the animals were not dosed individually there was sufficient vitamin D in the diet (125 IU/100 g diet) to protect against vitamin D deficiency.…”

Section: Discussioncontrasting

confidence: 80%

Bioactive Parathyroid Hormone in the Rat: Effects of Calcium and Calcitriol*

Seshadri¹,

Frankel²,

Lissner³

et al. 1985

Endocrinology

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Bioactive PTH was measured in Wistar rats under a variety of experimental conditions. The mean activity in normal rat sera was 0.17 +/- 0.12 ng/ml (expressed in terms of bovine PTH 1-34). Sera from animals reared on a vitamin D deficient diet showed a mean value of 0.46 +/- 0.24 ng/ml (P less than 0.01), whereas sera from animals with 1,25-dihydroxyvitamin D (1,25(OH)2D) deficiency had a mean activity of 0.62 +/- 0.23 ng/ml (P less than 0.01). Dietary calcium deficiency also resulted in high serum PTH levels (0.71 +/- 0.34 ng/ml, P less than 0.01) in spite of marked elevations of serum 1,25(OH)2D concentrations in these animals. A significant negative correlation was noted between serum calcium and bioactive PTH. Calcium infusions into hypocalcemic, vitamin D-deficient rats caused a fall in serum bioactive PTH concentrations to a mean of 13% of control values within 10 min. Intraperitoneal administration of 1,25(OH)2D3 to hypocalcemic, 1,25(OH)2D-deficient rats did not suppress serum bioactive PTH concentrations after 30 or 60 min even though serum 1,25(OH)2D concentrations were greater than 900 pmol/liter in each animal at these time points. To our knowledge, this is the first study using PTH bioassays for physiological experiments in rats.

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Section: Discussioncontrasting

confidence: 80%

Bioactive Parathyroid Hormone in the Rat: Effects of Calcium and Calcitriol*

Seshadri¹,

Frankel²,

Lissner³

et al. 1985

Endocrinology

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“…Inability ofcalcitriol to carry out all the functions of vitamin D has also been inferred from discrepancies between the plasma concentrations of various metabolites and the histologic changes in bone in patients (6,12,(35)(36)(37)(38)(39) or in experimental animals (11,40) receiving only vitamin D. In this circumstance any calcitriol present is of endogenous origin from the kidney, so that its short half life would not impair its biologic effectiveness. There have been several reports of patients with adequate histologic documentation of osteomalacia due to vitamin D deficiency in whom plasma calcitriol levels have fallen within the range found in healthy subjects (35)(36)(37)41), and in patients with intestinal malabsorption of vitamin D, even above that range (6).…”

Section: Discussionmentioning

confidence: 99%

Calcitriol but no other metabolite of vitamin D is essential for normal bone growth and development in the rat.

Parfitt¹,

Mathews²,

Brommage³

et al. 1984

J. Clin. Invest.

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As bstract. To determine the relative importance of different metabolites of vitamin D in bone growth and development, weanling male rat pups suckled by vitamin D-deficient mothers were given either calcitriol (1,25-dihydroxycholecalciferol) by continuous subcutaneous infusion, oral calcidiol (25-hydroxycholecalciferol), or oral 24,24-difluoro-25-hydroxycholecalciferol, a synthetic compound that can undergo 1-hydroxylation but not 24-hydroxylation, as their sole source of vitamin D for 40 d. Pups raised in the same manner, but given no vitamin D, served as controls. The three metabolites compared were given in doses that restored normal plasma calcium levels and normal increments in body weight. After in vivo double tetracycline labeling, bone histomorphometry by standard methods was performed on one femur and one tail vertebra. There were no significant differences between the three metabolite-treated groups in length, periosteal or endosteal diameter, cortical cross-sectional area, cortical porosity, osteoid thickness and volume, appositional rate and bone formation rate in the femur, or in qualitative and quantitative indices of endochondral ossification in the tail vertebra. All three groups differed markedly from the untreated controls with respect to all measurements. Collectively, the data indicate that neither calcidiol nor any 24-hydroxylated metabolite of calcidiol is needed in the rat (other than as a precursor) for longitudinal or transverse bone growth, for normal endochondral ossification, or for normal periosteal and endosteal formation, mineralization, and resorption ofbone. Calcitriol was fully active with respect to each of the indices listed when given in a manner resembling its continuous endogenous production by the kidney, suggesting that previous reports of incomplete skeletal response to calcitriol result from its rapid clearance and infrequent oral administration. We demonstrated that calcitriol is the only metabolite that is both necessary and sufficient for normal bone growth and development in the rat, but our data do not indicate the extent to which its beneficial skeletal effects were mediated by direct action on bone, either of calcitriol itself or of some metabolite thereof, or by restoration of normal plasma levels of calcium and phosphate.

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“…For histology, the coccyx at experimental day 30 was prepared, undecalcified, sectioned, and stained with hematoxylin and eosin as reported previously [24]. Then the apparently trabecular bone volume was estimated as a percentage of the sum of trabeculae and marrow volume.…”

Section: Bone Morphologymentioning

confidence: 99%

Altered bone turnover in chlorpromazine-challenged rats and its effect on 1α-hydroxyvitamin D 3 administration in vivo

Oh-ie

Miyazaki

Koyama

et al. 2002

Journal of Bone and Mineral Metabolism

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We reported previously that Ca and Pi levels are elevated and alkaline phosphatase (ALP) activity and 1alpha,25(OH)2D3 levels are reduced in chlorpromazine (CPZ)-challenged rats. In the present study, we determined the serum levels of interleukin (IL)-6 and acid phosphatase (ACP) in CPZ-challenged rats, in addition to levels of ALP protein. ALP mRNA and coccyx morphology were examined in CPZ-challenged rats as well as the effect of CPZ on 1alpha(OH)D3 production in vivo. Although Ca, Pi, IL-6, and ACP activity levels in CPZ-challenged rats were markedly increased on day 30, the elevated serum levels were restored to within normal ranges by the in vivo addition of 1alpha(OH)D3 to CPZ administration. The gain in body weight in CPZ-treated rats was significantly improved by the addition of 1alpha(OH)D3. Reduced levels of 1alpha,25(OH)2D3 in CPZ-treated rats were restored to normal levels by the administration of 1alpha(OH)D3. Moreover, the decreased ALP activity and ALP mRNA levels in the rat coccyx marrow in CPZ-treated rats were also restored by the administration of 1alpha(OH)D3 with CPZ. However, the molecular sizes of rat ALP molecules and ALP mRNA were the same for each group. Furthermore, bone morphometry showed that trabecular bone in the rat coccyx was decreased in CPZ-treated rats. However, the reduced volume of trabecular bone in CPZ-treated rats was restored by the addition of 1alpha(OH)D3 to CPZ administration. Taken together, altered bone metabolism in CPZ-treated rats can be improved by the addition of 1alpha(OH)D3.

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Plasma vitamin D metabolite levels in phosphorus deficient rats during the development of vitamin D deficient rickets

Cited by 21 publications

References 27 publications

Bioactive Parathyroid Hormone in the Rat: Effects of Calcium and Calcitriol*

Bioactive Parathyroid Hormone in the Rat: Effects of Calcium and Calcitriol*

Calcitriol but no other metabolite of vitamin D is essential for normal bone growth and development in the rat.

Altered bone turnover in chlorpromazine-challenged rats and its effect on 1α-hydroxyvitamin D 3 administration in vivo

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