Effect of the administration of 1,25-dihydroxyvitamin D3 on serum levels of 25-hydroxyvitamin D in postmenopausal osteoporosis

1982 ◽  
Vol 34 (1) ◽  
pp. 539-541 ◽  
Author(s):  
F. Loré ◽  
G. Di Cairano ◽  
P. Periti ◽  
A. Caniggia
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Serum Levels ◽  
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.

scholarly journals Severe Deficiency of 1,25-Dihydroxyvitamin D3 in Human Immunodeficiency Virus Infection: Association with Immunological Hyperactivity and Only Minor Changes in Calcium Homeostasis

1998 ◽  
Vol 83 (11) ◽  
pp. 3832-3838 ◽  
Author(s):  
Charlotte J. Haug ◽  
Pål Aukrust ◽  
Egil Haug ◽  
Lars Mørkrid ◽  
Fredrik Müller ◽  
...  
Keyword(s):  
Vitamin D ◽  
Human Immunodeficiency Virus ◽  
Nutritional Status ◽  
Serum Calcium ◽  
Serum Levels ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
Immunodeficiency Virus ◽  
25 Hydroxyvitamin D

The serum level of 1,25-dihydroxyvitamin D3[ 1,25-(OH)2D], the biologically most potent metabolite of vitamin D, is tightly regulated within narrow limits in human healthy adults. 1,25-(OH)2D deficiency is rare and is associated with disturbances in calcium and bone metabolism. We have previously reported a marked decrease in serum levels of 1,25-(OH)2D in human immunodeficiency virus (HIV)-infected patients. The present study was designed to further examine the causes and consequences of severe 1,25-(OH)2D deficiency in these patients. The design was a prospective cohort study. Fifty-four HIV-infected patients clinically classified according to the revised criteria from Centers for Disease Control and Prevention and healthy controls were studied. Parameters related to vitamin D and calcium metabolism as well as immunological and nutritional status were determined. Twenty-nine of the patients (54%) had serum levels of 1,25-(OH)2D below the lower reference limit, and 18 of these had undetectable levels. In contrast, HIV-infected patients had normal serum levels of 25-hydroxyvitamin D and vitamin D-binding protein. HIV-infected patients as a group had modestly depressed serum calcium and PTH levels. There were, however, no correlations between these parameters and serum levels of 1,25-(OH)2D. There were no differences in serum calcium or PTH levels or nutritional status when patients with severe 1,25-(OH)2D deficiency were compared to other patients, but patients with undetectable 1,25-(OH)2D had significantly elevated serum phosphate levels. Furthermore, patients with undetectable 1,25-(OH)2D levels were characterized by advanced clinical HIV infection, low CD4+ lymphocyte counts, and high serum levels of tumor necrosis factor-α (TNFα). We conclude that inadequate 1α-hydroxylation of 25-hydroxyvitamin D seems to be the most likely cause of 1,25-(OH)2D deficiency in HIV-infected patients, possibly induced by an inhibitory effect of TNFα. The low 1,25-(OH)2D and high TNFα levels observed may impair the immune response in HIV-infected patients both independently and in combination and may represent an important feature of the pathogenesis of HIV-related immunodeficiency. Markedly depressed 1,25-(OH)2D serum levels are also present in certain other disorders characterized by immunological hyperactivity. Thus, the findings in the present study may not only represent a previously unrecognized immune-mediated mechanism for induction of 1,25-(OH)2D deficiency in human disease, but may also reflect the importance of adequate serum levels of 1,25-(OH)2D for satisfactory performance of the immune system in man.

25 hydroxyvitamin D serum levels influence adequate response to bisphosphonate treatment in postmenopausal osteoporosis

Bone ◽  
2012 ◽  
Vol 51 (1) ◽  
pp. 54-58 ◽  
Author(s):  
Pilar Peris ◽  
Angeles Martínez-Ferrer ◽  
Ana Monegal ◽  
M. Jesús Martínez de Osaba ◽  
Africa Muxi ◽  
...  
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Serum Levels ◽  
Bisphosphonate Treatment ◽  
Hydroxyvitamin D ◽  
Adequate Response ◽  
25 Hydroxyvitamin D

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.

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