Age- and sex-dependent hormonal modulation of the expression of vitamin D receptor and 25-hydroxyvitamin D 1α hydroxylase in human bone cells

2014 ◽  
Vol 9 (3) ◽  
pp. 283-292
Author(s):  
Dalia Somjen ◽  
Sara Katzburg ◽  
David Hendel ◽  
Orli Sharon ◽  
Gary H Posner
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Bone Cells ◽  
Human Bone ◽  
Hydroxyvitamin D ◽  
Hormonal Modulation ◽  
25 Hydroxyvitamin D ◽  
Age And Sex

scholarly journals Prevalence of vitamin D level in the serum of patients living in Erbil city, Iraq, referred to private clinical laboratory and effect of age and sex on it

2018 ◽  
Vol 91 (1) ◽  
Author(s):  
Rabar M. Abdulrahman ◽  
Balen Muhsin Abdul Rahman
Keyword(s):  
Vitamin D ◽  
Clinical Laboratory ◽  
Mediterranean Country ◽  
Hydroxyvitamin D ◽  
Vitamin D Levels ◽  
Study Population ◽  
25 Hydroxyvitamin D ◽  
Country People ◽  
Effect Of Age ◽  
Age And Sex

This retrospective study aimed to determine the levels of 25- hydroxyvitamin D [25-(OH) D] in the individuals that have been referred to two laboratories (Bio Lab and King Lab) and to around 50 private side laboratories that use both Bio Lab and King Lab as a referral lab for their tests, in Erbil city, Iraq. Then show the range of deficiency and its relation with sunlight exposure, sex and age. Out of the total number of cases (N=10823), large percentage (nearly 78%) referred to both clinical laboratory based in Erbil city were found to have a deficiency in vitamin D levels, which means they had 25-(OH) D levels lower than 20 μg/L. This study found the percentage of vitamin D level in the serum of groups insufficient, deficient, adequate, optimal; intoxication were 52.8, 24.1, 11, 12 and 0.2% respectively. When the records have been compared according to gender, the results suggested that there was no difference between male and female within the study population (P>0.05), while there was difference in the grouped ages (P<0.05). Our results indicate that although Erbil is located in a Mediterranean country, people living there should periodically check their 25-(OH) D levels, in order to get appropriate supplements of vitamin D, which eventually prevents secondary chronic disease due to vitamin D deficiency.

scholarly journals Vitamin D-Mediated Hypercalcemia: Mechanisms, Diagnosis, and Treatment

2016 ◽  
Vol 37 (5) ◽  
pp. 521-547 ◽  
Author(s):  
Peter J. Tebben ◽  
Ravinder J. Singh ◽  
Rajiv Kumar
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Active Form ◽  
Elevated Serum ◽  
Diagnosis And Treatment ◽  
Vitamin D Metabolites ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Stone Formers ◽  
25 Hydroxyvitamin D

AbstractHypercalcemia occurs in up to 4% of the population in association with malignancy, primary hyperparathyroidism, ingestion of excessive calcium and/or vitamin D, ectopic production of 1,25-dihydroxyvitamin D [1,25(OH)2D], and impaired degradation of 1,25(OH)2D. The ingestion of excessive amounts of vitamin D3 (or vitamin D2) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH)2D, and the formation of 5,6-trans 25(OH)D, which binds to the vitamin D receptor more tightly than 25(OH)D. In patients with granulomatous disease such as sarcoidosis or tuberculosis and tumors such as lymphomas, hypercalcemia occurs as a result of the activity of ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages or tumor cells and the formation of excessive amounts of 1,25(OH)2D. Recent work has identified a novel cause of non-PTH-mediated hypercalcemia that occurs when the degradation of 1,25(OH)2D is impaired as a result of mutations of the 1,25(OH)2D-24-hydroxylase cytochrome P450 (CYP24A1). Patients with biallelic and, in some instances, monoallelic mutations of the CYP24A1 gene have elevated serum calcium concentrations associated with elevated serum 1,25(OH)2D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and on occasion, reduced bone density. Of interest, first-time calcium renal stone formers have elevated 1,25(OH)2D and evidence of impaired 24-hydroxylase-mediated 1,25(OH)2D degradation. We will describe the biochemical processes associated with the synthesis and degradation of various vitamin D metabolites, the clinical features of the vitamin D-mediated hypercalcemia, their biochemical diagnosis, and treatment.

Vitamin D metabolites regulate osteocalcin synthesis and proliferation of human bone cells in vitro

1985 ◽  
Vol 105 (3) ◽  
pp. 391-396 ◽  
Author(s):  
H. Skjødt ◽  
J. A. Gallagher ◽  
J. N. Beresford ◽  
M. Couch ◽  
J. W. Poser ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Bone Cells ◽  
Rank Order ◽  
Human Bone ◽  
Dependent Manner ◽  
Vitamin D Metabolites ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D

ABSTRACT The effects of six natural vitamin D metabolites of potential biological and therapeutic interest, 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), 25-hydroxyvitamin D3 (25-OH-D3), 24R,25-dihydroxyvitamin D3 (24R,25-(OH)2D3), 1,24R,25-trihydroxyvitamin D3 (1,24R,25-(OH)3D3), 25S,26-dihydroxyvitamin D3 (25S,26-(OH)2D3) and 1,25S,26-trihydroxyvitamin D3 (1,25S,26-(OH)3D3) on cell replication and expression of the osteoblastic phenotype in terms of osteocalcin production were examined in cultured human bone cells. At a dose of 5 × 10−12 mol/l, 1,25-(OH)2D3 stimulated cell proliferation, whereas at higher doses (5 × 10−9−5 × 10 −6 mol/l) cell growth was inhibited in a dose-dependent manner. The same pattern of effects was seen for the other metabolites in a rank order of potency: 1,25-(OH)2D3> 1,25S,26-(OH)3D3 = 1,24R,25-(OH)3D3>25S,26-(OH)2D3 = 24R,25-(OH)2D3 = 25-OH-D3. Synthesis of osteocalcin was induced by 1,25-(OH)2D3 in doses similar to those required to inhibit cell proliferation. Biphasic responses were observed for some of the metabolites in terms of osteocalcin synthesis, inhibitory effects becoming apparent at 5 × 10−6 mol/l. The cells did not secrete osteocalcin spontaneously. These results indicate that vitamin D metabolites may regulate growth and expression of differentiated functions of normal human osteoblasts. J. Endocr. (1985) 105, 391–396

scholarly journals Role of the vitamin D receptor in FGF23 action on phosphate metabolism

2005 ◽  
Vol 390 (1) ◽  
pp. 325-331 ◽  
Author(s):  
Yoshio Inoue ◽  
Hiroko Segawa ◽  
Ichiro Kaneko ◽  
Setsuko Yamanaka ◽  
Kenichiro Kusano ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Fibroblast Growth Factor 23 ◽  
Mrna Levels ◽  
Dna Encoding ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D ◽  
Naked Dna ◽  
25 Hydroxyvitamin D

FGF23 (fibroblast growth factor 23) is a novel phosphaturic factor that influences vitamin D metabolism and renal re-absorption of Pi. The goal of the present study was to characterize the role of the VDR (vitamin D receptor) in FGF23 action using VDR(−/−) (VDR null) mice. Injection of FGF23M (naked DNA encoding the R179Q mutant of human FGF23) into VDR(−/−) and wildtype VDR(+/+) mice resulted in an elevation in serum FGF23 levels, but had no effect on serum calcium or parathyroid hormone levels. In contrast, injection of FGF23M resulted in significant decreases in serum Pi levels, renal Na/Pi co-transport activity and type II transporter protein levels in both groups when compared with controls injected with mock vector or with FGFWT (naked DNA encoding wild-type human FGF23). Injection of FGF23M resulted in a decrease in 25-hydroxyvitamin D 1α-hydroxylase mRNA levels in VDR(−/−) and VDR(+/+) mice, while 25-hydroxyvitamin D 24-hydroxylase mRNA levels were significantly increased in FGF23M-treated animals compared with mock vector control- or FGF23WT-treated animals. The degree of 24-hydroxylase induction by FGF23M was dependent on the VDR, since FGF23M significantly reduced the levels of serum 1,25(OH)2D3 [1,25-hydroxyvitamin D3] in VDR(+/+) mice, but not in VDR(−/−) mice. We conclude that FGF23 reduces renal Pi transport and 25-hydroxyvitamin D 1α-hydroxylase levels by a mechanism that is independent of the VDR. In contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction of serum 1,25(OH)2D3 levels induced by FGF23 are dependent on the VDR.

scholarly journals Vitamin D receptor ChIP-seq in primary CD4+ cells: relationship to serum 25-hydroxyvitamin D levels and autoimmune disease

BMC Medicine ◽  
2013 ◽  
Vol 11 (1) ◽  
Author(s):  
Adam E Handel ◽  
Geir K Sandve ◽  
Giulio Disanto ◽  
Antonio J Berlanga-Taylor ◽  
Giuseppe Gallone ◽  
...  
Keyword(s):  
Vitamin D ◽  
Autoimmune Disease ◽  
Vitamin D Receptor ◽  
Cd4 Cells ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D
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