Effect of vitamin D3, 25-hydroxyvitamin D3, and 24,25-dihydroxyvitamin D3 on parathyroid hormone secretion

1987 ◽  
Vol 41 (1) ◽  
pp. 48-51 ◽  
Author(s):  
Larry K. Cantley ◽  
John B. Russell ◽  
Deborah S. Lettieri ◽  
Louis M. Sherwood
1983 ◽  
Vol 35 (1) ◽  
pp. 449-454 ◽  
Author(s):  
Marcos Rothstein ◽  
Klaus Olgaard ◽  
Mario Arbelaez ◽  
Delmar Finco ◽  
Saulo Klahr ◽  
...  

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.


1985 ◽  
Vol 260 (25) ◽  
pp. 13625-13630
Author(s):  
K Jarnagin ◽  
S Y Zeng ◽  
M Phelps ◽  
H F DeLuca

1991 ◽  
Vol 260 (2) ◽  
pp. E220-E225 ◽  
Author(s):  
J. Fox

Plasma immunoreactive parathyroid hormone (irPTH) levels increase with aging. This study determined 1) whether NH2-terminal irPTH secretory responses to induced hypocalcemia differ between adult (6-mo-old) and aged (24- to 26-mo-old) male rats and 2) whether a higher set point for irPTH release by Ca is responsible for the elevated irPTH levels with aging. Basal irPTH levels were 68% higher and 1,25-dihydroxyvitamin D3 levels were 44% lower in aged rats. An acutely induced, constant hypocalcemic stimulus [0.32 mM decrement in ionized Ca (Ca2+) for 2 h] was developed in catheterized conscious adult and aged rats by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) infusion using the Ca clamp technique. The initial irPTH secretory response to acute hypocalcemia (5-10 min) was reduced in aged rats (1.9- vs. 3.1-fold increase), suggesting reduced hormone stores. However, higher sustained irPTH levels (30 min to 2 h) were maintained in aged rats, indicating increased irPTH synthesis and release. The EGTA infusion rate necessary to maintain constant hypocalcemia was less in aged rats, suggesting skeletal resistance to PTH. Slow EGTA and Ca infusions were used to determine irPTH secretion at plasma Ca2+ levels from 0.7 to 1.5 mM. In aged rats, irPTH levels were higher at all Ca2+ concentrations, but the set point for irPTH release by Ca2+ was the same as in adult rats. Thus the elevated irPTH secretion in aged rats is not caused by a change in the set point for irPTH release but does result in decreased irPTH stores.


1983 ◽  
Vol 65 (4) ◽  
pp. 429-436 ◽  
Author(s):  
S. Dekel ◽  
R. Salama ◽  
S. Edelstein

1. One-day-old chicks were depleted of vitamin D. At 3 weeks their right tibiae, and those of a control group given vitamin D3, were fractured and pinned. After fracture the controls were kept on vitamin D3. Another group was left vitamin D-deficient. The remaining depleted chicks, divided into four groups, were given vitamin D3, 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] or a combination of 24,25(OH)2D3 and 1,25(OH)2D3. 2. The callus obtained after 9 and 14 days was subjected to torsional stress. The callus of chicks given vitamin D continuously showed the greatest resistance, whereas that of vitamin D-deficient chicks showed the smallest resistance. Repletion with either vitamin D3 or its metabolites increased the strength of the callus. Repletion with the combination of 24,25(OH)2D3 and 1,25(OH)2D3 produced the most marked results, in that the callus was even stronger than that of chicks replete with vitamin D3. 3. It is concluded that 24,25(OH)2D3 is essential for bone formation in addition to the known active vitamin D metabolite 1,25(OH)2D3, and the possible clinical implications of these findings are discussed.


1980 ◽  
Vol 239 (6) ◽  
pp. E515-E523 ◽  
Author(s):  
B. S. Levine ◽  
N. Brautbar ◽  
M. W. Walling ◽  
D. B. Lee ◽  
J. W. Coburn

Effects of 6-9 days of vitamin D3 (D3), 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], or 1,24,25-trihydroxyvitamin D3 [1,24,25(OH)3D3] on Mg metabolism were studied in vitamin D-deficient (-D) rats. Mg absorption expressed as percent intake increased with 1,25(OH)2D3 and 1,24,25(OH)3D3. Urinary Mg (UMg) increased with no change in serum Mg (SMg) or Mg balance. 1,25(OH)2D3 was threefold more potent than 1,24,25(OH)3D3 in raising serum Ca and Mg absorption. In a separate experiment in pair-fed rats given D3, 1,25-(OH)2D3, or 1,24,25(OH)3D3, the diet contained either 0.03 or 0.2% Mg; 1,25(OH)2D3 and D3 lowered SMg after 3 days; UMg increased after 24 h to remain elevated. D3 and 1,25(OH)2D3 augmented Mg absorption; feeding 0.2% Mg lowered Mg absorption in -D animals. All sterols augmented Mg absorption in -D rats; both the earlier action of 1,25(OH)2D3 and 1,24,25(OH)3D3 suggests that 1-hydroxylation is necessary. Suppressed Mg absorption with 0.2% Mg in -D rats suggests two transport processes, with one vitamin D dependent. Higher UMg with decreased SMg with 1,25(OH)2D3 suggests reduced tubular reabsorption.


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