scholarly journals Evidence that 1,25-dihydroxyvitamin D3 inhibits the hepatic production of 25-hydroxyvitamin D in man.

1984 ◽  
Vol 74 (4) ◽  
pp. 1540-1544 ◽  
Author(s):  
N H Bell ◽  
S Shaw ◽  
R T Turner
Keyword(s):  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
25 Hydroxyvitamin D

Seasonal variations of serum 1,25-dihydroxyvitamin D3 and alkaline phosphatase in relation to the antler formation in the fallow deer (Dama dama L.)

1984 ◽  
Vol 107 (1) ◽  
pp. 141-144 ◽  
Author(s):  
B. Eiben ◽  
St. Scharla ◽  
K. Fischer ◽  
H. Schmidt-Gayk
Keyword(s):  
Alkaline Phosphatase ◽  
Seasonal Variation ◽  
Serum Alkaline Phosphatase ◽  
Serum Levels ◽  
Fallow Deer ◽  
Dama Dama ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
25 Hydroxyvitamin D

Abstract. Serum 1,25-dihydroxyvitamin D3 and serum alkaline phosphatase increased several fold during the antler formation period in July. Both maxima were observed in the second half of the antler formation period, where the mineralization of the antler takes place. In contrast serum levels of calcium and 25-hydroxyvitamin D3 showed no alternation or seasonal variation.

Regulation of serum 1,25-dihydroxyvitamin D3 in lactating rats

1990 ◽  
Vol 259 (5) ◽  
pp. E665-E671 ◽  
Author(s):  
B. Lobaugh ◽  
A. Boass ◽  
G. E. Lester ◽  
S. U. Toverud
Keyword(s):  
Bolus Injection ◽  
Basal Diet ◽  
Hydroxylase Activity ◽  
Lower Serum ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
Supplemental Calcium ◽  
25 Hydroxyvitamin D ◽  
Hormone Biosynthesis

To characterize further the mechanism(s) underlying the increased serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] concentration associated with lactation in the rat, we examined hormone biosynthesis [i.e., renal 25-hydroxyvitamin D-1 alpha-hydroxylase (1 alpha-hydroxylase) activity] and hormone disappearance in groups of lactating Holtzman rats and age- and sex-matched nonlactating controls. 1 alpha-Hydroxylase activity was significantly greater in kidneys from lactating rats (4.0 +/- 0.42 fmol.mg-1.min-1) on a basal diet than in those from nonmated females (1.4 +/- 0.08 fmol.mg-1.min-1), an increment sufficient to account for the observed fourfold elevation of 1,25(OH)2D3 in the dams. The increase occurs despite the lower serum 1,25(OH)2D3 levels in lactating than in nonlactating rats at 12 and 24 h after a bolus injection of 1,25(OH)2D3 (2 ng/g body wt). Elevation of serum 1,25(OH)2D3 is not a requisite consequence of lactation, however, because dams receiving supplemental calcium from food (1.6%) and water (0.3%) exhibited no increase of either serum 1,25(OH)2D3 or 1 alpha-hydroxylase activity compared with controls. In contrast, lactating rats that received a diet with only 0.1% calcium had 5-fold higher serum 1,25(OH)2D3 levels and 20-fold higher 1 alpha-hydroxylase activity than nonlactating rats on the same diet. We conclude that other factors in conjunction with lactation, but not the lactating state per se, promote the changes in 1,25(OH)2D3 metabolism observed.

scholarly journals Stimulation of 1,25-dihydroxyvitamin D3 production by 1,25-dihydroxyvitamin D3 in the hypocalcaemic rat

1983 ◽  
Vol 214 (3) ◽  
pp. 893-897 ◽  
Author(s):  
Y Tanaka ◽  
H F DeLuca
Keyword(s):  
Vitamin D3 ◽  
Hydroxylase Activity ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Low Phosphorus ◽  
25 Hydroxyvitamin D

Serum 1,25-dihydroxyvitamin D3 concentration and renal 25-hydroxyvitamin D 1 alpha-hydroxylase activity were measured in rats fed various levels of calcium, phosphorus and vitamin D3. Both calcium deprivation and phosphorus deprivation greatly increased circulating levels of 1,25-dihydroxyvitamin D3. The circulating level of 1,25-dihydroxyvitamin D3 in rats on a low-calcium diet increased with increasing doses of vitamin D3, whereas it did not change in rats on a low-phosphorus diet given increasing doses of vitamin D3. In concert with these results, the 25-hydroxyvitamin D 1 alpha-hydroxylase activity was markedly increased by vitamin D3 administration to rats on a low-calcium diet, whereas the same treatment of rats on a low-phosphorus diet had no effect and actually suppressed the 1 alpha-hydroxylase in rats fed an adequate-calcium/adequate-phosphorus diet. The administration of 1,25-dihydroxyvitamin D3 to vitamin D-deficient rats on a low-calcium diet also increased the renal 25-hydroxy-vitamin D 1 alpha-hydroxylase activity. These results demonstrate that the regulatory action of 1,25-dihydroxyvitamin D3 on the renal 25-hydroxyvitamin D3 1 alpha-hydroxylase is complex and not simply a suppressant of this system.

scholarly journals FGF23, αKLOTHO AND VITAMIN D MEDIATED CALCIUM-PHOSPHATE METABOLISM IN HEMODIALYSIS PATIENTS

2020 ◽  
Author(s):  
Ozge Tugce Pasaoglu ◽  
Ayse Senelmis ◽  
Ozant Helvaci ◽  
Ulver Derici ◽  
Hatice Pasaoglu
Keyword(s):  
Calcium Phosphate ◽  
Kidney Diseases ◽  
Mineral Metabolism ◽  
Hemodialysis Patients ◽  
Dihydroxyvitamin D3 ◽  
Chronic Kidney Diseases ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
Significant Difference ◽  
25 Hydroxyvitamin D

Background: Klotho is a protein that acts as a co-receptor for FGF23. FGF23-Klotho axis has great importance regarding to the regulation of mineral metabolism by kidneys. In this study, we analyzed FGF23, αKlotho, 1,25-dihydroxyvitamin D3, 25-hydroxyvitamin D, parathormone, calcium and phosphate levels of hemodialysis patients in order to investigate the nature of the mineral metabolism disruption in chronic kidney diseases. Methods: Sixty hemodialysis patients and 34 healthy controls were included in the study. Serum iFGF, cFGF, soluble αKlotho were analyzed using ELISA kits. 1,25-dihydroxyvitamin D3 was determined using LC-MS/MS. Calcium, phosphate, iPTH and 25-hydroxyvitamin D were measured using autoanalyzers. Results: In hemodialysis patients, iFGF23, cFGF23, iPTH and P levels were significantly higher and 1,25-dihydroxyvitamin D3, αKlotho and Ca levels were significantly lower compared with the control group. There was no significant difference in 25-hydroxyvitamin D levels. Conclusion: Our study showed that lack of sufficient amounts of αKlotho is crucial for mineral metabolism disruptions seen as a complication of chronic kidney diseases. Despite the high levels of the hormone, FGF23 is unable to accomplish its function properly, likely due to deteriorated kidney function in hemodialysis patients.

Expression of the renal 25-hydroxyvitamin D-24-hydroxylase gene: regulation by dietary phosphate

1996 ◽  
Vol 271 (1) ◽  
pp. F203-F208 ◽  
Author(s):  
S. Wu ◽  
J. Finch ◽  
M. Zhong ◽  
E. Slatopolsky ◽  
M. Grieff ◽  
...  
Keyword(s):  
Vitamin D ◽  
Gene Regulation ◽  
Mrna Level ◽  
Catabolic Pathway ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Pi Homeostasis ◽  
1,25 Dihydroxyvitamin D3 ◽  
Dietary Phosphate ◽  
25 Hydroxyvitamin D

1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] plays a key role in phosphate (Pi) homeostasis through its phosphatemic actions on intestine and bone. In turn, dietary Pi restriction increases serum 1,25(OH)2D3 by stimulating its production, but its effect on vitamin D catabolism is less clear. Here we have examined the effects of dietary Pi on the expression of the renal vitamin D-24-hydroxylase (24-OHase), the first enzyme in the catabolic pathway for vitamin D compounds. Rats fed a low Pi (0.02% P) diet showed a fivefold decrease in renal 24-OHase mRNA compared with rats fed a normal Pi (0.67% P) diet. 24-OHase mRNA and 24-OHase activity decreased within 24 h of Pi restriction, reached a minimum by 48 h, and remained low through 14 days. Decreased 24-OHase mRNA was observed with more moderate Pi restriction (0.2% P), but higher Pi (1.2% P) did not increase 24-OHase mRNA over the 0.8% P diet. 24-OHase mRNA correlated well with plasma Pi (r = 0.862, P < 0.001). In conclusion, renal 24-OHase expression is regulated by dietary phosphate at the mRNA level.

scholarly journals Chondrocyte-Specific Modulation of Cyp27b1 Expression Supports a Role for Local Synthesis of 1,25-Dihydroxyvitamin D3 in Growth Plate Development

Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4024-4032 ◽  
Author(s):  
Roy Pascal Naja ◽  
Olivier Dardenne ◽  
Alice Arabian ◽  
René St. Arnaud
Keyword(s):  
Growth Plate ◽  
Bone Volume ◽  
Long Bones ◽  
Differentiation Markers ◽  
Dihydroxyvitamin D3 ◽  
Hypertrophic Zone ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
25 Hydroxyvitamin D ◽  
Chondrocytic Differentiation

Abstract The Cyp27b1 enzyme (25-hydroxyvitamin D-1α-hydroxylase) that converts 25-hydroxyvitamin D into the active metabolite, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], is expressed in kidney but also in other cell types such as chondrocytes. This suggests that local production of 1,25(OH)2D3 could play an important role in the differentiation of these cells. To test this hypothesis, we engineered mutant mice that do not express the Cyp27b1 gene in chondrocytes. Inactivation of both alleles of the Cyp27b1 gene led to decreased RANKL expression and reduced osteoclastogenesis, increased width of the hypertrophic zone of the growth plate at embryonic d 15.5, increased bone volume in neonatal long bones, and increased expression of the chondrocytic differentiation markers Indian Hedgehog and PTH/PTHrP receptor. The expression of the angiogenic marker VEGF was decreased, accompanied by decreased platelet/endothelial cell adhesion molecule-1 staining in the neonatal growth plate, suggesting a delay in vascularization. In parallel, we engineered strains of mice overexpressing a Cyp27b1 transgene in chondrocytes by coupling the Cyp27b1 cDNA to the collagen α1(II) promoter. The transgenic mice showed a mirror image phenotype when compared with the tissue-specific inactivation, i.e. a reduction in the width of the hypertrophic zone of the embryonic growth plate, decreased bone volume in neonatal long bones, and inverse expression patterns of chondrocytic differentiation markers. These results support an intracrine role of 1,25(OH)2D3 in endochondral ossification and chondrocyte development in vivo.

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