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PubMed1994

Release of endogenous ATP from the caudal artery in rats with arteriosclerosis.

Noradrenaline significantly increased (by a prazosin-sensitive mechanism) the overflow of ATP and its metabolites from the caudal arteries of rats treated with excess vitamin D2 and a high-cholesterol diet (arteriosclerotic rats), although the amount of the overflow was smaller than that in the normal rats. The arteries from the arteriosclerotic rats showed a marked increase in the calcium content and there was a significant negative correlation between the noradrenaline-induced overflow of ATP and the arterial calcium content. These findings indicate that ATP release from arteriosclerotic rat caudal arteries mediated by alpha 1-adrenoceptors is impaired in proportion to the extent of arterial calcification.

Adenosine Diphosphate↗
PubMed1994

Microsomal 25-hydroxylation of vitamin D2 and vitamin D3 in pig liver.

A microsomal cytochrome P-450 catalysing 25-hydroxylation of vitamin D2 was purified from both male and female pigs to apparent homogeneity and a specific cytochrome P-450 content of 13 and 15.4 nmol x mg of protein-1, respectively. The enzyme also catalysed 25-hydroxylation of vitamin D3. The ratio between the 25-hydroxylase activities towards vitamin D2 and D3 was essentially the same in the different purification steps as well as in the apparently homogeneous enzyme preparation. The two enzyme activities showed the same pH optimum and decreased in parallel upon partial denaturation of the enzyme. Cholecalciferol competitively inhibited 25-hydroxylation of vitamin D2 and vice versa. The non-steroidal cytochrome P-450 inhibitor ketoconazole inhibited both enzyme activities and the Ki values were the same. The cytochrome P-450 showed the same apparent M(r), substrate specificity and N-terminal amino acid sequence as the previously purified vitamin D3 25-hydroxylase from pig liver microsomes. A monoclonal antibody raised against the vitamin D3 25-hydroxylase also recognized the vitamin D2 25-hydroxylase. The antibody immunoprecipitated the 25-hydroxylase activity towards both vitamin D2 and D3 in the purified enzyme. Taken together, the results show that the 25-hydroxylation of vitamin D2 and D3 is catalysed by the same microsomal cytochrome P-450 in pig liver microsomes. The properties of this 25-hydroxylase are discussed in relation to present knowledge concerning previously well-characterized vitamin D3 25-hydroxylases that are not able to catalyse 25-hydroxylation of vitamin D2.

Amino Acid Sequence↗
PubMed1985

The effects of sodium fluoride, calcium phosphate, and vitamin D2 for one to two years on calcium and phosphorus metabolism in postmenopausal women with spinal crush fracture osteoporosis.

Calcium and phosphorus balances and 47Ca turnover studies were performed before and after 12-27 months of daily treatment with sodium fluoride (60 mg), calcium (30-45 mmol), phosphate (29-44 mmol), and vitamin D2 (18,000 IU) in 20 postmenopausal women with spinal crush fracture osteoporosis. Before treatment the mean calcium balance (-1.6 mmol Ca/day) was negative (P less than 0.05), whereas the mean phosphorus balance (-1.6 mmol P/day) did not differ from zero (P greater than 0.10). The treatment induced an increase in calcium absorption (P less than 0.01) with an unchanged renal excretion and dermal loss of calcium and an increase (P less than 0.02) in calcium balance, which became positive (P less than 0.01) (+3.3 mmol Ca/day). This enhancement in calcium balance was obtained by the combined effects of an increase (P less than 0.05) in bone mineralization rate and a decrease (P less than 0.05) in bone resorption rate. The observed increase in net phosphorus absorption (P less than 0.001) was more pronounced than the increase in renal excretion of phosphorus (P less than 0.001), and the phosphorus balance therefore increased (P less than 0.001) and became positive (P less than 0.001). A positive correlation was observed between net calcium and net phosphorus absorption (r = 0.065; (P less than 0.001) in the 32 studies where both calcium and phosphorus balance data were available. Furthermore, a positive correlation (r = 0.61; P less than 0.05) was found between the changes in net calcium and net phosphorus absorption during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

The effect of trauma on serum concentrations of vitamin D metabolites in patients with hip fracture.

In a previous study we observed lower serum concentrations of 25(OH)D, 24,25(OH)2D, and 1,25(OH)2D in patients with hip fracture than in aged control subjects. In order to evaluate the effect of trauma on vitamin D metabolite levels, we measured serum concentrations of vitamin D binding protein (DBP) in 118 patients with hip fracture and 71 aged control subjects. Serum DBP was lower in the patients than in the controls (mean +/- SD 315 +/- 60 vs 371 +/- 44 mg/l, P less than 0.001). Serum DBP correlated positively with serum total protein, albumin, alpha 2-globulin, and the vitamin D metabolite levels in the patients. When correcting for differences in serum DBP, serum 25(OH)D and 24,25(OH)2D still were significantly lower in patients than in controls, whereas serum 1,25(OH)2D was not. The free 1,25(OH)2D index (10(5) x molar ratio 1,25(OH)2D/DBP) was lower in patients than in controls, but the level of significance was marginal. This difference was not significant when patients and controls with impairment of renal function were excluded. It is concluded that the difference in serum 25(OH)D and 24,25(OH)2D between patients and controls is largely preexistent. However, the lower serum 1,25(OH)2D in the patients is mainly caused by the trauma. The free 1,25(OH)2D concentrations are almost similar in the two groups when renal function is normal.

25-Hydroxyvitamin D 2↗
PubMed1986

Different metabolism of vitamin D2/D3 in epileptic patients treated with phenobarbitone/phenytoin.

Serum concentrations of vitamin D metabolites were measured before and during treatment with either vitamin D2 or vitamin D3, 4000 IU per day for 24 weeks, in 22 epileptic outpatients receiving phenobarbitone/phenytoin. The serum concentration of total 1,25(OH)2D did not change during the treatment period in any of the treatment groups. On the other hand, in the vitamin D2 group, serum 25(OH)D2, total 25(OH)D, and 24,25(OH)2D increased significantly during the trial, whereas serum concentrations of the vitamin D3 metabolites were unchanged. In the vitamin D3 group, serum concentrations of the vitamin D3 metabolites increased significantly, whereas the vitamin D3 metabolite levels remained unchanged. However, vitamin D3 treatment resulted in a 2-4-fold greater increase in serum concentrations compared to vitamin D2 treatment. Treatment with vitamin D2 and vitamin D3 in the same dose in IU results in considerably different serum concentrations of the vitamin D metabolites.

24,25-Dihydroxyvitamin D 3↗
PubMed1991

Marrow space star volume in the iliac crest decreases in osteoporotic patients after continuous treatment with fluoride, calcium, and vitamin D2 for five years.

Iliac crest biopsies in osteoporotic patients were obtained before and after five years of continuous treatment with sodium fluoride (40-60 mg/d), vitamin D2 (18,000 IE/d), and calcium phosphate (45 mmol/d). Star volume of marrow space and trabeculae, mean trabecular thickness, and fractional amount of trabecular bone were estimated on so-called vertical sections before and after treatment. Results showed a significant decrease in marrow space star volume after five years of treatment (35 mm3 versus 19 mm3) (2p less than 0.02). No significant changes were observed in trabecular star volume (0.149 mm3 versus 0.104 mm3) (2p greater than 0.50) or mean trabecular thickness (85 microns versus 79 microns, 2p greater than 0.30). A slight but insignificant increase in the fractional amount of trabecular bone was found (9.7% versus 10.4%, 2p greater than 0.50). A rather close inverse correlation was obtained, however, between individual changes in trabecular bone volume fraction and marrow space star volume (r = -0.72, 2p = 0.011). The findings suggest that the large marrow "cavities" had been split into two or more "cavities" by some newly generated trabecular structures leading to increased trabecular connectivity. The strength of trabecular bone may be increased due to this beneficial effect of fluoride on trabecular bone structure.

Aged↗
PubMedDate not supplied

Marked decrease in trabecular bone quality after five years of sodium fluoride therapy--assessed by biomechanical testing of iliac crest bone biopsies in osteoporotic patients.

Sodium fluoride has for more than 2 decades been a commonly used therapeutic agent for established osteoporosis because of a repeatedly documented anabolic effect on trabecular bone mass. Recently, however, three controlled trials have failed to demonstrate any therapeutic advantage of NaF over placebo with respect to vertebral fracture rate. Also, there have been several reports of an increased incidence of nonvertebral fractures during fluoride administration. Thus, the efficacy of fluoride therapy remains a controversial issue. The aim of this longitudinal study was to investigate the effect of sodium fluoride (40-60 mg per day), calcium (45 mmol), and vitamin D2 (18,000 IU) on trabecular bone strength, assessed before and after 1 or 5 years of treatment for osteoporosis. Iliac crest biopsies were taken before and after 1 year of treatment in 12 patients, and before and after 5 years of treatment in 14 patients. Measurements were made of biomechanical competence, ash content, and bone fluoride content, and bone strength parameters were normalized for ash content, thereby obtaining a measure of trabecular bone quality. Bone fluoride content was significantly increased after both 1 and 5 years of treatment, indicating that the administered fluoride had been ingested. After 1 year of treatment, no difference was observed in iliac crest trabecular bone ash content. A general trend for decreased bone strength and bone quality was observed, but this was insignificant. After 5 years of fluoride treatment, an insignificant decrease in iliac crest trabecular bone ash content was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed2005

Effects of Vitamin D analogs on gene expression profiling in human coronary artery smooth muscle cells.

Vitamin D analogs provide survival benefit for chronic kidney disease patients with cardiovascular complications. Activation of smooth muscle cells plays a role in cardiovascular diseases. It is not known how Vitamin D analogs modulate gene expression in smooth muscle cells. In this study, DNA microarray technology was used to assess the gene expression profile in human coronary artery smooth muscle cells treated with 0.1microM 1alpha,25-dihydroxyvitamin D3 (calcitriol) or paricalcitol (an analog of calcitriol) for 30 h. The effects of calcitriol and paricalcitol were similar. A total of 176 target genes were identified with 115 up-regulated and 61 down-regulated genes in the paricalcitol group. Target genes fall into various categories including cell differentiation/proliferation. Real-time RT-PCR analysis demonstrated that paricalcitol dose- and time-dependently regulated the expression of IGF1, WT1 and TGFbeta3, three genes known to modulate cell proliferation. Paricalcitol also down-regulated the expression of natriuretic peptide precursor B and thrombospondin 1. Both drugs inhibited cell proliferation in a dose-dependent manner. This study identified genes not previously known to be regulated by VDR, providing insight into understanding the role of VDR on regulating smooth muscle cell growth, thrombogenicity, fibrinolysis and endothelial regeneration.

Calcitriol↗
PubMed2006

Evidence for the activation of 1alpha-hydroxyvitamin D2 by 25-hydroxyvitamin D-24-hydroxylase: delineation of pathways involving 1alpha,24-dihydroxyvitamin D2 and 1alpha,25-dihydroxyvitamin D2.

While current dogma argues that vitamin D prodrugs require side-chain activation by liver enzymes, recent data suggest that hydroxylation may also occur extrahepatically. We used keratinocytes and recombinant human enzyme to test if the 25-hydroxyvitamin D-24-hydroxylase (CYP24A1) is capable of target cell activation and inactivation of a model prodrug, 1alpha-hydroxyvitamin D2 (1alpha(OH)D2) in vitro. Mammalian cells stably transfected with CYP24A1 (V79-CYP24A1) converted 1alpha(OH)D2 to a series of metabolites similar to those observed in murine keratinocytes and the human cell line HPK1A-ras, confirming the central role of CYP24A1 in metabolism. Products of 1alpha(OH)D2 included the active metabolites 1alpha,24-dihydroxyvitamin D2 (1alpha,24(OH)2D2) and 1alpha,25-dihydroxyvitamin D2 (1alpha,25(OH)2D2); the formation of both indicating the existence of distinct activation pathways. A novel water-soluble metabolite, identified as 26-carboxy-1alpha,24(OH)2D2, was the presumed terminal degradation product of 1alpha(OH)D2 synthesized by CYP24A1 via successive 24-hydroxylation, 26-hydroxylation and further oxidation at C-26. This acid was absent in keratinocytes from Cyp24a1 null mice. Slower clearance rates of 1alpha(OH)D2 and 1alpha,24(OH)2D2 relative to 1alpha,25(OH)2D2 and 1alpha,25(OH)2D3 were noted, arguing for a role of 24-hydroxylated metabolites in the altered biological activity profile of 1alpha(OH)D2. Our findings suggest that CYP24A1 can activate and inactivate vitamin D prodrugs in skin and other target cells in vitro, offering the potential for treatment of hyperproliferative disorders such as psoriasis by topical administration of these prodrugs.

Animals↗
PubMed2004

Tissue distribution and activity studies of 1,24-dihydroxyvitamin D2, a metabolite of vitamin D2 with low calcemic activity in vivo.

The active vitamin D compound 1alpha,24(S)-dihydroxyvitamin D(2) (1,24(OH)(2)D(2)) is under development as a therapy for disorders including cancer and secondary hyperparathyroidism. 1,24(OH)(2)D(2) is a potent inhibitor of cell proliferation in vitro and, relative to calcitriol (1,25(OH)(2)D(3)), has reduced calcemic activity in vivo. To examine the mechanisms underlying this reduced calcemic activity, we studied the tissue distribution in rats of radiolabeled 1,24(OH)(2)D(2) or 1,25(OH)(2)D(3) over 24h. Serum levels of 1,24(OH)(2)D(2) were lower than those of 1,25(OH)(2)D(3) at all time points; however, tissue levels of radiolabeled compounds followed different patterns. In duodenum and kidney, 1,24(OH)(2)D(2) and 1,25(OH)(2)D(3) rose to similar levels at early time points; 1,24(OH)(2)D(2) levels then declined more rapidly. In bone marrow, 1,24(OH)(2)D(2) and 1,25(OH)(2)D(3) were present at similar levels at all time points. In liver, 1,24(OH)(2)D(2) levels were two-fold higher than 1,25(OH)(2)D(3) at 1h post-injection, declining to similar levels by 8h. In vitamin D-deficient rats, doses of 1,24(OH)(2)D(2) 30-fold higher than 1,25(OH)(2)D(3) were required to produce equal stimulation of intestinal calcium absorption. In the same deficient animals, 1,24(OH)(2)D(2) and 1,25(OH)(2)D(3) were nearly equipotent at stimulating bone calcium mobilization. In cultured bone cells, 1,24(OH)(2)D(2) and 1,25(OH)(2)D(3) were equipotent at stimulating osteoclast formation and bone resorption. In summary, the reduced calcemic activity of 1,24(OH)(2)D(2) may result from altered pharmacokinetics relative to 1,25(OH)(2)D(3), resulting in relatively rapid decreases in 1,24(OH)(2)D(2) levels and activity in target organs such as intestine. Further studies will be necessary to confirm these findings and to confirm the clinical utility of 1,24(OH)(2)D(2).

Animals↗
PubMed2004

1 Alpha-hydroxyvitamin D2 and 1 alpha-hydroxyvitamin D3 have anabolic effects on cortical bone, but induce intracortical remodeling at toxic doses in ovariectomized rats.

It is well established that vitamin D metabolites have anabolic properties on cancellous bone in rats. However, few data are available on cortical bone effects of vitamin D metabolites. In this study, we examined the effects of the synthetic vitamin D analogs 1alpha-hydroxyvitamin D2 (1alpha(OH)D2) and 1alpha-hydroxyvitamin D3 (1alpha(OH)D3) on cortical bone of the tibial shaft in ovariectomized (OVX) rats using bone histomorphometry. Six-month-old Fischer 344 rats were either OVX or sham-operated (SHAM). OVX rats received vehicle, 1alpha(OH)D2 or 1alpha(OH)D3 orally via the diet in a dose range from 0.025 to 0.2 microg/kg/day. All animals were killed 3 months postsurgery after in vivo fluorochrome labeling. Relative to SHAM rats, vehicle-treated OVX rats showed a reduction in cortical bone area (%) due to expansion of the marrow cavity. Treatment of OVX rats with either 1alpha(OH)D2 or 1alpha(OH)D3 dose-dependently decreased marrow area, and increased cortical area, periosteal perimeter, and periosteal and endocortical bone formation rate compared with OVX vehicle controls. Interestingly, OVX animals receiving the highest doses showed intracortical resorption cavities, a phenomenon only exceptionally observed in rats. The intracortical hole area was significantly lower in 1alpha(OH)D2-treated compared with 1alpha(OH)D3-treated rats. We conclude that 1alpha(OH)D2 and 1alpha(OH)D3 prevent cortical bone loss in OVX rats and have anabolic effects on cortical bone at higher doses. However, very high, toxic doses of both vitamin D analogs induce intracortical remodeling as an untoward side effect.

Anabolic Agents↗
PubMed2004

RETRACTED: Menatetrenone and vitamin D2 with calcium supplements prevent nonvertebral fracture in elderly women with Alzheimer's disease.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Corresponding Author, Yoshihiro Sato, and the co-authors have been informed. Dr. Sato wishes to retract this article on the grounds that it contains fabricated clinical trial data, which he was responsible for producing. In addition, Dr. Sato claims he listed all of the named co-authors without their consent. The co-authors were therefore unaware of the presence of fabricated data in this publication and their participation in the publication. This retraction was initiated by Dr. Sato, and the Editor-in-Chief of Bone was informed by the author directly.

Aged↗
PubMed2004

Hypovitaminosis D in acutely injured pediatric burn patients.

PROBLEM: The prevalence of vitamin D insufficiency, its etiology, and associated sequelae among acutely injured burn patients is unknown. OBJECTIVE: This study assessed vitamin D and endocrine status, as well as the effect of anabolic agents, in pediatric patients who had sustained burns in excess of 25% total body surface area (TBSA). SUBJECTS: Sixty-nine patients with a mean TBSA burn of 50.6+/-2.2% (range 27% to 94%) and full thickness injury of 41.3+/-3.0% (range 0% to 94%) were studied. Subjects ranged in age from 0.6 to 18 years (mean, 5.8+/-0.6 years). Main outcome measures Blood samples were obtained for serum 25-hydroxyvitamin D (D25), 1,25-dihydroxyvitamin D (D1,25), albumin, cortisol, triiodothyronine (T3), tetraiodothyronine (T(4)), thyroid stimulating hormone (TSH), and parathormone (PTH). RESULTS: Two hundred eighty morning blood samples of D25 and D1,25 demonstrated that 45% and 26.2% were low and 8.9% and 11% were very low, respectively. At least one low D25 or D1,25 level occurred in 62.3% of all subjects. Very low levels were noted in 23.2% of all patients. There was an increased incidence of hyperparathyroidism in patients with very low serum D25. Vitamin D25 and D1,25 levels were lower in subjects with larger burns or inhalation injury, as well as those treated with thyroxine or oxandrolone. Serum albumin, cortisol, T(4), and TSH were not correlated with concentration of vitamin D. CONCLUSIONS: Demonstration of a high incidence of low serum vitamin D indicates vitamin D status may be significantly compromised in burned children. It is unclear why vitamin D deficiency exists in this population. The most effective way to improve vitamin D status remains elusive at this time.

Adolescent↗
PubMed2004

Primary hyperparathyroidism and osteoporosis in 2004.

In patients with primary hyperparathyroidism, a definite diagnosis is the first step in the management strategy and relies on appropriately selected and carefully interpreted laboratory tests. Parathyroid hormone assays are being increasingly performed as part of the routine evaluation of osteoporosis. In this setting, laboratory tests are often consistent with primary hyperparathyroidism but should be interpreted with caution. Bone mineral density measurements are useful for assessing the impact of primary hyperparathyroidism. The recommended bone mineral density cutoffs for selecting patients requiring parathyroidectomy were lowered in 2003, and the number of surgically treated patients has increased as a result. Parathyroidectomy remains the treatment of choice given the low mortality associated with this procedure and the absence of pharmacological alternatives suitable for long-term use.

Bone Density↗
PubMed2006

Early response to vitamin D2 in children with calcium deficiency rickets.

OBJECTIVE: To assess the effect of vitamin D(2) administration on serum vitamin D metabolite concentrations in calcium deficiency rickets. STUDY DESIGN: We administered vitamin D(2), 50,000 IU orally to 16 Nigerian children 15 to 48 months of age with radiographically active rickets. We measured calcium and vitamin D metabolites at baseline and at 1, 3, 7, and 14 days. RESULTS: At baseline, ranges of serum 25-hydroxyvitamin D (25(OH)D) concentrations were 18 to 40 nmol/L (7-16 ng/mL), and 1,25-dihydroxyvitamin D (1,25-(OH)(2)D) concentrations were 290 to 790 pmol/L (120-330 pg/mL). After vitamin D administration, serum 25(OH)D and 1,25(OH)(2)D concentrations rapidly rose and peaked at 2.8 and 1.9 times the baseline values (P < .001), respectively, at 3 days. Positive correlations between 1,25(OH)(2)D and 25(OH)D were strongest at day 3 (r = 0.84, P < .001) and weakest at day 14 (r = 0.41, P = .11). The relationship of 1,25(OH)(2)D with 25(OH)D at baseline and the increase in 1,25(OH)(2)D in response to vitamin D were similar to those described in children with vitamin D deficiency. However, unlike the pattern in vitamin D deficiency, 1,25(OH)(2)D remained positively correlated with 25(OH)D after administration of vitamin D. CONCLUSION: Dietary calcium deficiency increases the demand for 25(OH)D above that required in vitamin D deficiency to optimize 1,25(OH)(2)D concentrations. Assessment of vitamin D sufficiency in persons or communities may need to be adjusted for habitual dietary calcium intake.

Administration, Oral↗
PubMed2004

19-Nor-1alpha,25-dihydroxyvitamin D2 (paricalcitol) exerts anticancer activity against HL-60 cells in vitro at clinically achievable concentrations.

19-Nor-1alpha,25-dihydroxyvitamin D2 (paricalcitol) is an analogue of 1,25(OH)2D3 with reduced calcemic effects that is approved in the United States for the suppression of parathyroid hormone in chronic renal failure. Paricalcitol has anticancer activity in prostate cancer cells. We tested the effects of paricalcitol on the HL-60 leukemia cells, studying cellular differentiation, cell cycle changes, apoptosis and cellular proliferation. Paricalcitol at 10(-8)M concentration induced the maturation of HL-60 cells in a time-dependent manner, as shown by increased expression of CD11b differentiation surface antigen. The ability of HL-60 cells to reduce nitroblue tetrazolium (NBT) was markedly increased after exposure to paricalcitol at 10(-8)M for 72 h. Paricalcitol inhibited colony formation of HL-60 cells in a soft agar semisolid media after 10-day incubation (estimated IC50 of 5 x 10(-9) M. Exposure to 10(-8)M paricalcitol for 72 h increased the number of cells in G0/G1 phase, and decreased the number of cells in S phase, and significantly increased the number of HL-60 cells undergoing apoptosis. The concentration required to achieve inhibition of growth of HL-60 cells is comparable to clinically achievable levels. These findings support the clinical evaluation of paricalcitol as an antileukemia agent.

Apoptosis↗
PubMed2005

Differential effects of Vitamin D analogs on bone formation and resorption.

Deficiency in Vitamin D and its metabolites leads to a failure in bone formation primarily caused by dysfunctional mineralization, suggesting that Vitamin D analogs might stimulate osteoblastic bone formation and mineralization. In this study, we compare the effect of selected Vitamin D analogs and active metabolite, 1alpha,25-dihydroxyvitamin D(3), 19-nor-1alpha, 25-dihydroxyvitamin D(2), and 1alpha-hydroxyvitamin D(2) or 1alpha,25-dihydroxyvitamin D(2) on bone formation and resorption. In a mouse calvariae bone primary organ culture system, all Vitamin D analogs and metabolite tested-stimulated collagen synthesis in a dose-dependent manner and 19-nor-1alpha, 25-dihydroxyvitamin D(2) was the most efficacious among three. 19-nor-1alpha, 25-dihydroxyvitamin D(2) and 1alpha,25-dihydroxyvitamin D(2) showed similar potencies and 1alpha,25-dihydroxyvitamin D(3) was less potent than others. Osteocalcin was also up-regulated in a dose-dependent manner, suggesting that the three Vitamin D analogs have the equal potencies on bone formation. 25-Hydroxyvitamin D-24-hydroxylase expression was induced in a dose-dependent manner and 19-nor-1alpha, 25-dihydroxyvitamin D(2) was less potent than other two compounds. In a mouse calvariae organ culture, all induced a net calcium release from calvariae in a dose-dependent manner, but the potency is in the order of 1alpha,25-dihydroxyvitamin D(2) congruent with1alpha,25-dihydroxyvitamin D(3)>19-nor-1alpha, 25-dihydroxyvitamin D(2). In a Vitamin D/calcium-restricted rat model, all caused an elevation in serum calcium in a dose-dependent manner. There is no significant difference between 1alpha,25-dihydroxyvitamin D(3) and 1alpha-hydroxyvitamin D(2) in potencies, but 19-nor-1alpha, 25-dihydroxyvitamin D(2) is at least 10-fold less potent than the other two compounds. Our results suggest that Vitamin D analogs have direct effects on bone resorption and formation, and 19-nor-1alpha, 25-dihydroxyvitamin D(2) may be more effective than 1alpha,25-dihydroxyvitamin D(3) and 1alpha-hydroxyvitamin D(2) on stimulating anabolic bone formation.

Animals↗