Interaction of 24,25-Dihydroxyvitamin D3 and parathyroid hormone on bone enzymes in vitro

1979 ◽  
Vol 27 (1) ◽  
pp. 47-52 ◽  
Author(s):  
M. Lieberherr ◽  
M. Garabédian ◽  
H. Guillozo ◽  
M. Bailly du Bois ◽  
S. Balsan
Nature ◽  
1979 ◽  
Vol 281 (5729) ◽  
pp. 317-319 ◽  
Author(s):  
Y. Weisman ◽  
A. Harell ◽  
S. Edelstein ◽  
M. David ◽  
Z. Spirer ◽  
...  

1982 ◽  
Vol 242 (6) ◽  
pp. G575-G581 ◽  
Author(s):  
M. J. Favus ◽  
F. L. Coe ◽  
S. C. Kathpalia ◽  
A. Porat ◽  
P. K. Sen ◽  
...  

Previous studies have shown that thiazide diuretic agents reverse secondary hyperparathyroidism and reduce circulating 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and intestinal calcium absorption rates in patients with idiopathic hypercalciuria of the renal-leak variety. We have investigated whether thiazides can reverse the secondary increase in serum parathyroid hormone (PTH) and 1,25(OH)2D3 levels or intestinal calcium absorption induced by feeding rats a diet low in calcium (LCD, 0.02% calcium) but adequate in phosphorus and vitamin D. We found that LCD increased circulating immunoreactive PTH [chow vs. LCD, 0.52 +/- 0.06 vs. 1.06 +2- 0.1 (SE) ng/ml, P less than 0.001], 1,25(OH)2D3 (chow vs. LCD, 101 +/- 15 vs. 325 +/- 38 pg/ml, P less than 0.001), calcium uptake by everted gut sacs from duodenum, ileum, and descending colon, and net calcium absorption by descending colon studied in Ussing chambers in vitro. Chlorothiazide (CTZ) prevented the increase in PTH during LCD (chow + CTZ vs. LCD + CTZ, 0.69 +/- 0.07 vs. 0.73 +/- 0.06, NS) but not the increase in 1,25(OH)2D3 (chow + CTZ vs. LCD + CTZ, 88 +/- 10 vs. 277 +/- 31, P less than 0.002) or intestinal calcium transport. The drug caused no change in serum 1,25(OH)2D3 or intestinal calcium absorption in rats fed normal chow. In rats given exogenous 1,25(OH)2D3 to stimulate intestinal calcium absorption, CTZ reduced urine calcium excretion greatly but did not alter intestinal calcium absorption.


1983 ◽  
Vol 35 (1) ◽  
pp. 449-454 ◽  
Author(s):  
Marcos Rothstein ◽  
Klaus Olgaard ◽  
Mario Arbelaez ◽  
Delmar Finco ◽  
Saulo Klahr ◽  
...  

1987 ◽  
Vol 41 (1) ◽  
pp. 48-51 ◽  
Author(s):  
Larry K. Cantley ◽  
John B. Russell ◽  
Deborah S. Lettieri ◽  
Louis M. Sherwood

1978 ◽  
Vol 235 (3) ◽  
pp. E338 ◽  
Author(s):  
J W Pike ◽  
E Spanos ◽  
K W Colston ◽  
I MacIntyre ◽  
M R Haussler

The influence of estrogen on the metabolism of 25-hydroxyvitamin D3 was studied in 2- to 5-wk-old chicks. Single injections of at least 500 microgram diethylstibestrol (DES) increased the conversion of 25-hydroxyvitamin D3 to 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) and suppressed the production of 24,25-dihydroxyvitamin D3 in chick kidney homogenates. Acute (one 5-mg) injections of testosterone or progesterone did not enhance the 25-hydroxyvitamin D3-1alpha-hydroxylase, indicating specificity. However, chronic pretreatment with DES appeared to allow the potentiation of previously unstimulatory steroids such as progesterone and testosterone. In addition, the hormonal metabolite of vitamin D3, 1alpha,25-(OH)2D3, was measured in 4- to 6-wk chick plasma after steroid treatment. Greater than 1 mg DES per day for 5 days was necessary to enhance the circulating level of 1alpha,25-(OH)2D3; testosterone alone had no effect. This elevation was rapid, occurring within 12--24 h after injection. These data suggest that estrogen (as evidenced by DES treatment) is a modulator of vitamin D metabolism along with other known regulators such as parathyroid hormone, phosphate, and 1alpha,25-(OH)2D3. The mechanism of the regulation is as yet unknown.


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