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  • Articles  (7)
  • 1,25(OH)2D3  (7)
  • Springer  (7)
  • American Chemical Society (ACS)
  • American Geophysical Union
  • National Academy of Sciences
  • 2015-2019
  • 2005-2009
  • 1990-1994
  • 1980-1984  (7)
  • 2017
  • 1984  (7)
  • Physics  (7)
  • Nature of Science, Research, Systems of Higher Education, Museum Science
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  • Articles  (7)
Publisher
  • Springer  (7)
  • American Chemical Society (ACS)
  • American Geophysical Union
  • National Academy of Sciences
Years
  • 2015-2019
  • 2005-2009
  • 1990-1994
  • 1980-1984  (7)
Year
Topic
  • Physics  (7)
  • Nature of Science, Research, Systems of Higher Education, Museum Science
  • Biology  (7)
  • Medicine  (7)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. 114-122 
    ISSN: 1432-0827
    Keywords: 1,25(OH)2D3 ; 24,25(OH)2D3 ; Vitamin D3 ; Vitamin D-deficiency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The ability of 1,25(OH)2D3 and of 24,25(OH)2D3 to prevent or to heal rickets in chicks was evaluated by studies of plasma biochemistry, growth plate histology, bone morphometry and microradiography, and bone mineralization. 1,25(OH)2D3 at a dose of 100 ng/day produced fewest abnormalities compared with vitamin D3-treated control chicks. Bone growth was slightly greater than vitamin D3-treated controls in chicks given a lower dose of this metabolite; the reverse was observed in chicks given a higher dose. 24,25(OH)2D3 was less effective than 1,25(OH)2D3 in preventing rickets even at doses as high as 400 ng/day. Treatment of rachitic chicks with doses of 24,25(OH)2D3 up to 300 ng/day produced no healing effect on the bone lesions, in marked contrast to the beneficial effects observed with 1,25(OH)2D3.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. 384-391 
    ISSN: 1432-0827
    Keywords: 1,25(OH)2D3 ; Vitamin D metabolities ; Parathyroid hormone ; PTH secretion regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of vitamin D metabolites on parathyroid hormone secretion was studied using rat parathyroid gland cultured in basal medium Eagle containing 5% serum obtained from thyroparathyroidectomized rat, 1 mM magnesium, and calcium concentration varying from 0.75–2.25 mM, and radioimmunoassay for rat parathyroid hormone (rPTH). 1,25 dihydroxycholecalciferol (1,25(OH)2D3), 5×10−10−2.5×10−8M, consistently decreased rPTH secretion in dose-related manner; the effect reached steady state after 24 hin vitro addition of 1,25(OH)2D3 and was also observed at different medium calcium concentrations (0.75, 1.25, 1.75 mM). Comparison of dose-responses for inhibitory activity of some vitamin D metabolites on rPTH secretion showed: 1,25(OH)2D3=1,24,25(OH)3D3〉1α OHD3〉25 OHD3. Cholecalciferol (10−5M), 24,25-dihydroxycholecalciferol (10−8−10−6M) and 25,26-dihydroxycholecalciferol (5×10−9−5×10−7M) did not inhibit rPTH secretion. Analysis of structural activity relation of vitamin D metabolites studied indicated that 1α or pseudo-1α hydroxylated metabolites or analogs were active in inhibiting rPTH secretion, while, non-1α hydroxylated metabolites were without or were weakly inhibitory only at very high concentrations. This study provides further evidence for a direct role of 1,25(OH)2D3 on a negative feedback loop for regulation of parathyroid gland function.
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  • 3
    ISSN: 1432-0827
    Keywords: Osteoblastlike cells ; Cyclic AMP ; Dexamethasone ; 1,25(OH)2D3 ; Hormone interactions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Parathyroid hormone (PTH)-stimulated cyclic adenosine monophosphate (cAMP) in rat osteoblastlike (OB) cells has been shown to be modulated by steroid hormones; glucocorticoids are known to increase the level, while the effects of 1,25(OH)2D3 are inhibitory. In the present study, we found that the PTH-stimulated cAMP responses are similar in neonatal mouse and fetal rat OB cells. Dexamethasone (0.13–13nM) augmented PTH-stimulated cAMP in both species. Mouse cells showed a higher maximal response to dexamethasone (100% increment) than rat cells (60–70% increment) with similar sensitivity to dexamethasone (ED50 ∼ 1.0 nm). On the other hand, 1,25(OH)2D3 decreased PTH-stimulated cAMP, but the effect required pharmacological levels of hormone; mouse cells responded at a lower dose (1.3 nM) and were more sensitive than rat cells (responded at 13 nM) to 1,25(OH)2D3 treatment. Introduction of physiological concentrations of 1,25(OH)2D3 (0.013–1.3 nm) in addition to dexamethasone (13 nM) resulted in a synergistic enhancement of PTH-stimulated cAMP in rat cells. In contrast, a dose-dependent antagonistic effect was observed in mouse cells. In summary, our findings demonstrate species and concentration-dependent differences in hormonal responses to 1,25(OH)2D3 and a complex interplay among PTH, dexamethasone, and 1,25(OH)2D3.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. 153-157 
    ISSN: 1432-0827
    Keywords: 1,25(OH)2D3 ; Glucocorticoids ; Triamcinolone acetonide ; Receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We have used cultured osteoblastlike rat osteogenic sarcoma cells (ROS 17/2) which have receptors for 1,25(OH)2D3 and for glucocorticoids, and have examined the modulation of the 1,25(OH)2D3 receptor by the potent glucocorticoid triamcinolone acetonide. We report that triamcinolone acetonide caused an increase of the 1,25(OH)2D3 receptor concentration in these cells but it did not affect the affinity of the receptor to 1,25(OH)2D3; this phenomenon occurred in a dosedependent fashion for triamcinolone (10−9 to 10−7 M) with a maximum increase of 1,25(OH)2D3 receptor concentration of ⋍twofold. During the culture period, the 1,25(OH)2D3 receptor concentration was altered both in untreated as well as in triamcinolone-treated cells, being highest at the early logarithmic phase and diminished progressively as cells approached confluence. However, throughout the culture period, the 1,25(OH)2D3 receptor concentration was higher in the triamcinolone-treated cells.
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  • 5
    ISSN: 1432-0827
    Keywords: Calcium ; Vitamin D deficiency ; 1,25(OH)2D3 ; Parathyroidectomy ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Studies presented here were designed to investigate further the basis for an impaired cAMP response to parathyroid hormone (PTH) in osteoblastlike calvarial bone cells isolated from vitamin D-deficient rat pups. The goal was to perturb Ca, PTH, and vitamin Din vivo in order to see which factors might be responsible for the impairedin vitro bone cell cAMP response. Pups either were parathyroidectomized (PTX) 3–5 days, implanted with osmotic minipumps delivering high doses of PTH, given repeated, high doses of 1,25(OH)2D3, or were D-deficient (-D, i.e., born and suckled by D-deficient mothers). Osteoblastlike bone cells, isolated by sequential enzyme digestion and centrifugation, were exposed to PTH for 5 min in the presence of a phosphodiesterase inhibitor. In bone cells isolated from -D rat pups, both basal and PTH-induced cAMP accumulation were significantly lower than in +D bone cells. Earlier, we had shown that two daily injections of -D pups with 50 ng 1,25(OH)2D3 restores this reduced bone cAMP response of -D pups toward normal. In the present study, neither basal nor PTH-induced bone cell cAMP accumulation was affected by subjecting D-replete pups to PTX, PTH infusion, or repeated high doses of 1,25(OH)2D3 despite the fact that each treatment markedly changed serum Ca or serum immunoreactive PTH. The results indicate that the impaired bone cell cAMP response seen in -D pups is not a direct result of chronic hypocalcemia and that the “heterologous desensitization” seenin vitro with added 1,25(OH)2D3 could not be duplicated byin vivo treatment of +D pups with supraphysiologic doses of 1,25(OH)2D3. Finally the lack of alteration in the bone cell cAMP response to PTHin vitro after chronic PTH infusionin vivo fails to support the notion that the impaired response in -D bone cells can be explained entirely by “homologous desensitization” induced by high circulating levels of PTH in the hypocalcemic, -D rat pup.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. 608-614 
    ISSN: 1432-0827
    Keywords: 1,25(OH)2D3 ; Glucocorticoids ; Calcium and phosphate absorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The interrelation of glucocorticoids and 1,25 dihydroxycholecalciferol (1,25(OH)2D3) on intestinal calcium and phosphate absorption was investigated. The active and passive transport of calcium and phosphate was evaluated by thein situ intestinal loop technique. Administration of cortisone resulted in a decrease of the luminal fluid and an increase of the luminal calcium and phosphate concentration. Under active transport conditions, administration of cortisone resulted in a decrease of net calcium absorption through two mechanisms: (1) depressed vitamin D-dependent calcium absorption, (2) increased vitamin D-independent calcium backflux. The enhancement of bidirectional phosphate flux by cortisone was independent of 1,25(OH)2D3. An enhancement of water movement by cortisone resulted in an increase of luminal calcium and phosphate concentration which favors the passive diffusion of these ions. Enhanced calcium diffusion by cortisone compensates for the inhibitory effect of cortisone on vitamin D-dependent calcium transport. However, enhanced phosphate diffusion by cortisone is additive to the effect of 1,25(OH)2D3.
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  • 7
    ISSN: 1432-0827
    Keywords: Fracture ; (Glucocorticoid ; 1,25(OH)2D3 ; Osteoporosis ; Rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary A closed tibial fracture, which was controlled by an intramedullary stainless steel pin, was created in 16 rabbits. Eight rabbits were treated with 75 ng of 1,25(OH)2D3 daily as subcutaneous (s.c.) injections. After three weeks, the fractured tibia resisted a force of 101,7±21.0 Newtons in the control group and 57.3±8.0 Newtons in animals given 1,25(OH)2D3 (m±SE,P〈0.05). In another group of eight rabbits, the left hindleg was immobilized in a plastic splint. Four rabbits were given 75 ng of 1,25(OH)2D3/day s.c. and the effect of immobilization was studied on the calcaneus. Bone ash/cm3 of the calcaneus on the immobilized side was decreased by 11±2% in control rabbits and by 20±2% in the group treated with 1,25(OH)2D3 indicating a more advanced immobilization osteoporosis (m±SE,P〈0.05), which was also demonstrated by studies of bone density. Eighteen rabbits were used in a study of the effects of 1,25(OH)2D3 on the development of prednisolone osteoporosis. The dose of prednisolone was 2.5 mg per day, given by the oral route. After four months, the density of the femur was 1.53±0.02 g/cm2 in control rabbits and 1.42±0.01 in prednisolonetreated animals (P〈0.01). In rabbits additionally given 1,25(OH)2D3, the mean value for bone density was further lowered (n.s.). It appears that 1,25(OH)2D3 exaggerates disuse osteoporosis and prednisolone osteoporosis and impairs fracture healing in rabbits. These results differ from what has been shown earlier with 1,25(OH)2D3 treatment in the rat.
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