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  • 1
    Electronic Resource
    Electronic Resource
    Calvarial cells synthesize 1.alpha.,25-dihydroxyvitamin D3 from 25-hydroxyvitamin D3 (1983)
    s.l. : American Chemical Society
    Biochemistry 22 (1983), S. 1073-1076 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00274a012
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  • 2
    Electronic Resource
    Electronic Resource
    Evidence for abnormal regulation of circulating 1α,25-dihydroxyvitamin D in patients with pulmonary tuberculosis and normal calcium metabolism (1984)
    Springer
    Calcified tissue international 36 (1984), S. 541-544 
    Details
    ISSN: 1432-0827
    Keywords: 1α25(OH)2D ; Hypercalcemia ; Normocalcemia ; Pulmonary tuberculosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Available evidence indicates that hypercalcemia in pulmonary tuberculosis results from increases in circulating 1α,25-dihydroxyvitamin D [1α,25(OH)2D]. To further characterize vitamin D metabolism in this disorder, the effects of vitamin D, 100,000 units a day for 4 days, were compared in 25 normal subjects and 11 patients with active pulmonary tuberculosis who were normocalcemic and had not had hypercalcemia. Serum calcium, phosphorus, 25-hydroxyvitamin D (25-OHD) and 1α,25(OH)2D were measured. Whereas vitamin D increased mean serum 25-OHD from 20±2 (±SE) to 40±5 ng/ml (P〈0.001) and did not change mean serum 1α,25(OH)2D in the normals (33±2 vs. 31±2 pg/ml), it increased mean serum 25-OHD from 21±4 to 55±13 ng/ml (P〈0.05) and mean serum 1α,25(OH)2D from 28±2 to 35±3 pg/ml (P〈0.05) in the patients. Serum calcium was normal and remained within the normal range in all subjects and patients. The findings indicate that there is a modest but significant abnormality in the regulation of circulating 1α,25(OH)2D in normocalcemic patients with pulmonary tuberculosis. The results are similar to those previously reported by us in normocalcemic patients with sarcoidosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405362
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  • 3
    Electronic Resource
    Electronic Resource
    The renal metabolism of 25-hydroxyvitamin D3 in the rat: Regulation by 1,25-dihydroxyvitamin D3 (1983)
    Springer
    Calcified tissue international 35 (1983), S. 438-442 
    Details
    ISSN: 1432-0827
    Keywords: Vitamin D-deficiency ; Immunoreactive parathyroid hormone ; Serum calcium ; Renal 1-hydroxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary To determine the effects of 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] on the renal metabolism of 25-hydroxyvitamin D3 [25(OH)D3], the influence of 1,25(OH)2D3 and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] was compared in vitamin D-deficient rats. Serum calcium (Ca), serum immunoreactive parathyroid hormone (iPTH) and the specific activities (SA) of renal 25(OH)D3: 24-hydroxylase (24-hydroxylase) and 25(OH)D3: 1α-hydroxylase (1-hydroxylase) were measured. In vitamin D-deficient rats, mean serum Ca was low, serum iPTH was increased, renal 1-hydroxylase was increased, and renal 24-hydroxylase was below the limit of detection. Treatment with either 1,25(OH)2D3 or 24,25(OH)2D3, 50 ng/d for 2 days, significantly increased mean serum Ca but did not change serum iPTH, renal 1-hydroxylase SA, or renal 24-hydroxylase SA. 1,25(OH)2D3, 50 ng/d for 7 days, returned serum Ca and iPTH to normal, lowered renal 1-hydroxylase SA, and induced renal 24-hydroxylase activity. In contrast, 24,25(OH)2D3, 50 ng/d for 7 days, similarly lowered renal 1-hydroxylase SA but did not induce renal 24-hydroxylase activity. Thyroparathyroidectomy of vitamin D-deficient rats resulted in a rapid decline in 1-hydroxylase SA. The results indicate that in vitamin D-deficient rats a) 1,25(OH)2D3 reduces renal 1-hydroxylase SA and increases renal 24-hydroxylase SA and b) 24,25(OH)2D3 reduces renal 1-hydroxylase SA and does not alter renal 24-hydroxylase SA. Inhibition of renal 1-hydroxylase by the two metabolites is apparently mediated through changes in serum Ca and circulating iPTH, whereas stimulation by 1,25(OH)2D3 of renal 24-hydroxylase activity is direct.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405073
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  • 4
    Electronic Resource
    Electronic Resource
    Extrarenal metabolism of 25-hydroxycholecalciferol in the rat: Regulation by 1,25-dihydroxycholecalciferol (1984)
    Springer
    Calcified tissue international 36 (1984), S. 274-278 
    Details
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary To determine the role of the kidney in regulation of 25-hydroxycholecalciferol (25OHD3, metabolism, the effects of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] on3H-25OHD3 were compared in intact and nephrectomized vitamin D-deficient rats. Sixteen hours after the intravenous administration of3H-25OHD3, extracts of serum and pooled small intestinal mucosa were fractionated by Sephadex LH-20 column chromatography followed by high performance liquid chromatography. In intact rats, 1,25(OH)2D3 (50 ng/day i.p. for 7 days) increased mean serum3H-24,25-dihydroxycholecalciferol [3H-24,25(OH)2D3] from 2±2–210±80 fmol/ml (mean±1 SD), increased mean serum3H-25,26-dihydroxycholecalciferol [3H-25,26(OH)2D3] from 2±2–12±6 fmol/ml and lowered mean serum3H-1,25(OH)2D3 from 210±40–4±4 fmol/ml. Similarly, in nephrectomized animals, 1,25(OH)2D3 increased mean serum3H-24,25-(OH)2D3 from 6±11–115±30 fmol/ml and increased mean serum3H-25,26(OH)2D3 from 3±3–26 ± 10 fmol/ml. Nephrectomy increased serum3H-25(OH)D3 in untreated (from 1450±225–2675±225 fmol/ml serum) and 1,25(OH)2D3 treated rats (from 1600±175–3075±100 fmol/ml).3H-1,25(OH)2D3 averaged 74±16% of total radioactivity in intestinal mucosa of untreated intact rats and was not detected in either the serum or intestinal mucosa of nephrectomized animals. The results suggest that in intact animals, extrarenal synthesis can account for substantial 24,25(OH)2D3 production and for most 25,26(OH)2D3 production. Further, the observed stimulation of production of 24,25(OH)2D3 and 25,26(OH)2D3 by 1,25(OH)2D3 in anephric — D rats providesin vivo evidence for regulation of extrarenal 25OHD3: 24- and 26-hydroxylases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405330
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  • 5
    Electronic Resource
    Electronic Resource
    Ovarian status influences the skeletal effects of tamoxifen in adult rats (1996)
    Springer
    Breast cancer research and treatment 41 (1996), S. 71-79 
    Details
    ISSN: 1573-7217
    Keywords: antiestrogen ; Tamoxifen ; histomorphometry ; ovary-intact rat ; bone structure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tamoxifen (TAM), an antiestrogen used in adjuvant therapy for breast cancer, is currently being evaluated for prevention of breast cancer in premenopausal and postmenopausal disease-free women. In light of this clinical application in young women, the skeleton's potential predisposition for osteoporosis following long-term treatment with an antiestrogen is a concern. In postmenopausal women being treated for breast cancer TAM was shown to prevent bone loss. There is little information, however, about the skeletal effects of TAM in premenopausal women. Previous animal studies in ovariectomized (OVX'd) rats have consistently reported TAM to prevent cancellous and cortical bone loss. The effects of TAM on ovary-intact animals, however, are not well established. We have performed a histomorphometric analysis in order to evaluate the influence of ovarian function on the skeletal effects of long-term TAM treatment in the laboratory animal model. Sixmonth-old rats were implanted subcutaneously with pellets designed for the controlled release of TAM at a dose (5 mg/3 wks) previously shown to be effective at antagonizing short-term bone loss in OVX'd growing rats. TAM acted as an estrogen agonist on cortical bone measurements in tibia of ovary-intact as well as OVX'd rats. In cancellous bone of OVX'd rats, TAM reduced indices of bone formation and resorption and reduced the bone loss from over 90 percent to less than 50 percent. In ovary-intact rats, however, TAM produced a 31 percent loss of cancellous bone, a deficit associated with a 26 percent reduction in the trabecular number. These results clearly demonstrate an interaction between TAM and ovarian status whereby TAM partially prevents estrogen-deficient bone loss in OVX'd animals but antagonizes selective actions of estrogen on the skeleton of ovary-intact animals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01807038
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