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At least 595 records · Page 33Linked to original sources
PubMed1995

Transcriptional control of the osteocalcin gene by 1,25-dihydroxyvitamin D-2 and its 24-epimer in rat osteosarcoma cells.

The effects of two vitamin D analogs, 1,25-dihydroxyvitamin D-2 and 24-epi-1,25-dihydroxyvitamin D-2, were examined on osteocalcin gene expression in the rat osteosarcoma cell line ROS 17/28. Our results indicate that these analogs are more transcriptionally active than 1,25-dihydroxyvitamin D-3, particularly the 24-epimer. Assessment of reporter gene chloramphenicol acetyltransferase (CAT) activity, using the vitamin D responsive element (VDRE) derived from the human osteocalcin gene promoter. revealed that both analogs stimulated CAT activity 5- to 10-fold. 1,25-Dihydroxyvitamin D-2 was slightly more active than 1,25-dihydroxyvitamin D-3, while the 24-epimer was twice as effective. 1,25-Dihydroxyvitamin D-3 also stimulated osteocalcin mRNA accumulation by 2-fold over vehicle-treated cells, 1,25-dihydroxyvitamin D-2 by 2.5-fold, and 24-epi-1,25-dihydroxyvitamin D-2 by 4-fold. Electrophoretic mobility shift assays using the osteocalcin vitamin D responsive element revealed no increase in DNA binding with either analog when compared to 1,25-(OH)2D3. Examination of CAT activity using the rat 24-hydroxylase VDRE indicated no significant difference in transcription with these compounds, suggesting that the vitamin D-2 analogs preferentially activate osteocalcin gene expression.

Animals↗
PubMed1991

Biological activity of 1 alpha, 25-dihydroxyvitamin D derivatives--24-epi-1 alpha, 25-dihydroxyvitamin D-2 and 1 alpha,25-dihydroxyvitamin D-7.

Biological activity of 24-epi-1 alpha,25-dihydroxyvitamin D-2 (24-epi-1,25(OH)2D2) and 1 alpha,25-dihydroxyvitamin D-7 (1,25(OH)2D7), the 22,23-dihydro derivative of the former compound, was investigated. Both of the vitamin D derivatives stimulated intestinal calcium transport and calcium mobilization from bones in rats; however, the effect was about 50% of that of 1 alpha,25-dihydroxyvitamin D-3 (1,25(OH)2D3). On the other hand, 24-epi-1,25(OH)2D2 and 1,25(OH)2D7 inducement of HL-60 human leukemia cell differentiation was comparable to that of 1,25(OH)2D3. Accordingly, the differentiation-inducing activity of 24-epi-1,25(OH)2D2 and 1,25(OH)2D7 was much greater than their ability to stimulate calcium metabolism. In contrast to 1,25(OH)2D3, 24-epi-1,25(OH)2D2 and 1,25(OH)2D7 exerted little hypercalcemic activity in mice. These results suggest that both vitamin D derivatives will be useful as anti-tumor agents.

Alkaline Phosphatase↗
PubMed1992

Disturbances of mineral and bone metabolism following gastric antrectomy in the rat.

In antrectomized (B-I) and control rats, bone mineralization, the fractional intestinal absorption of calcium, magnesium and phosphorus, the balances of these minerals, their serum concentration and renal excretion, together with serum gastrin, calciotropic hormones (parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D), and osteocalcin were assessed four months after surgery. B-I evoked hypogastrinemia, but no changes in the serum concentrations of minerals and calciotropic hormones, or urinary cyclic AMP. The major significant changes brought about by B-I were: (1) a decrease in bone dry weight, specific density, bone ash calcium and magnesium content; (2) a decrease in the fractional absorption and urinary excretion of calcium and magnesium; (3) an increase in urinary hydroxyproline and serum osteocalcin in the presence of normal serum bone isoenzyme of alkaline phosphatase. It is concluded that in the rat (1) B-I over the long term decreases both bone mineral content and calcium and magnesium absorption, in the absence of any counterregulation; (2) B-I rats may have attained a new equilibrium which is characterized by decreased absorption and urinary excretion of calcium and magnesium, but maintenance of normocalcemia at the expense of bone; (3) the concomitant changes of serum bone markers are contradictory, which makes their interpretation and use in the present context difficult.

Animals↗
PubMed1981

Induction of bone resorption by parathyroid hormone in congenital malignant osteopetrosis.

A male patient, afflicted with malignant congenital osteopetrosis, was studied over a 5 year period. Hypocalcemia (less than 8 mg/dl) with lack of an appropriate increase in serum immunoreactive parathyroid hormone (iPTH) prevailed at all times. Under a calcium restricted diet, a 6-hour infusion of parathyroid extract normalized serum calcium, and increased the urinary hydroxyproline excretion suggesting that bone resorption had been induced. A second attempt to induce resorption was made by infusing a synthetic amino terminal fragment of bovine PTH over a period of 3 weeks at the dose of 1.5 units/kg/hr. This infusion evoked an increase in serum calcium (8.1 to 10.5 mg/dl), urinary calcium (0.03 to 0.65 mg/g creatinine) and urinary hydroxyproline (160 to 372 mg/g creatinine); and urinary hydroxyproline (160 to 372 mg/g creatinine); increases which were reversed by calcitonin administration. Iliac crest bone biopsies were obtained before and on the last day of the 3-week infusion. Quantitative comparison of the two specimens showed that, during PTH infusion, there was a 23% decrease in bone volume due to the increase in marrow space, a 93% increase in the number of osteoclasts and 136% increment in the osteoclastic resorption surface. Electron microscopic examination of the osteoclasts in the first tissue sample showed no evidence of ruffled borders, while in the second biopsy, numerous cytoplasmic processes indicative of resorptive activity were visible at the matrix-cell interface. It is proposed that, in our patient, the osteopetrotic phenotype is the consequence of an abnormality in the interaction between PTH and osteoclasts that may be related to the synthesis of a physiologically "defective" PTH.

25-Hydroxyvitamin D 2↗
PubMedDate not supplied

Vitamin D metabolism in insulin-dependent diabetes mellitus.

A significant loss of bone has been observed in diabetes mellitus. The pathogenesis is unknown, but an impairment of vitamin D metabolism might be involved. Consequently, we have studied vitamin D metabolism in five groups of insulin-dependent diabetic patients. Significantly reduced levels of serum 25(OH)D were seen only in patients with diabetic nephropathy. The serum levels of 1,25 (OH)2D were reduced only in diabetic ketoacidosis but normalized during recovery. It is concluded that vitamin D metabolism is largely normal in adult insulin-dependent diabetes, and it seems unlikely that a disturbance of the vitamin D metabolism can explain the bone loss in the ordinarily controlled diabetics.

24,25-Dihydroxyvitamin D 3↗
PubMedDate not supplied

Serum dihydroxyvitamin D metabolite concentrations in patients on chronic anticonvulsant drug therapy: response to pharmacologic doses of vitamin D2.

We examined the effects of chronic anticonvulsant drug administration on the serum concentrations of dihydroxyvitamin D metabolites and the response of these metabolite levels to short-term treatment with pharmacologic doses of vitamin D2. Twelve patients maintained on chronic combined diphenylhydantoin and phenobarbital therapy were studied before and after the administration of vitamin D2, 75,000 units/week for 6 weeks. Prior to vitamin D2 administration, the patient group demonstrated decreased serum calcium (P less than 0.01) and increased serum iPTH (P less than 0.02) concentrations relative to 18 matched controls. Serum 25OHD and 24,25(OH)2D concentrations in the patient group were reduced by 38% and 75% (P less than 0.001), while serum 1,25(OH)2D concentration was increased by 27% (P less than 0.05) relative to control values. After vitamin D administration serum calcium and iPTH concentrations in the patient group were restored to values that were not significantly different from control levels. Serum 25OHD and 24,25(OH)2D concentrations were increased by 4.6- and 6.3-fold, respectively, to supranormal levels. Serum 1,25(OH)2D concentration exhibited an unexpected further 30% increase over pretreatment values, resulting in a return of the serum 1,25(OH)2D/24,25(OH)2D concentration ratio to a normal value. These data indicate that in patients treated chronically with anticonvulsant drugs, serum 25OHD concentration responds appropriately to vitamin D2 administration, but regulation of renal dihydroxy metabolite formation may be altered.

25-Hydroxyvitamin D 2↗
PubMed1980

Renal parathyroid hormone-dependent adenylate cyclase activity after repletion of vitamin D-deficient rats with vitamin D-2.

Rats fed a diet deficient in both vitamin D and Ca2+ exhibited a greater depression of the renal parathyroid hormone (PTH)-dependent adenylate cyclase than was observed in rats fed diets deficient in either vitamin D or calcium. Total serum Ca2+ was decreased from a control level of 11.2 mg/dl to 8.5 mg/dl in rats fed the diet deficient in calcium alone, and to 5.4 mg/dl in rats fed the diet deficient in vitamin D. Serum calcium was decreased further to 4.3 mg/dl in rats fed the diet deficient in both vitamin D and Ca2+. Serum immuno-reactive PTH was significantly elevated over control levels when rats were fed the test diets; however, there were no significant differences between the elevated levels in the three experimental groups. Repletion of rats deficient in vitamin D only with a single oral dose of 3200 I.U. vitamin D-2 resulted in restoration of serum calcium to normal levels, a return of serum PTH to the control state, and an associated increase in PTH-dependent adenylate cyclase activity to the control level by 72 h. Repletion of rats deficient in both vitamin D and Ca2+ with the same dose of vitamin D-2 raised serum Ca2+ to 7.2 mg/dl by 72 h, but did not cause a reduction in circulating PTH, nor did it result in any significant improvement in the responsiveness of the membrane adenylate cyclase to PTH. These results suggest that elevated PTH is a factor in the down regulation of the PTH-dependent adenylate cyclase, but do not rule out a role for calcium as a regulatory factor.

Adenylyl Cyclases↗
PubMed1984

Differences in the metabolism of vitamin D2 and vitamin D3 by subcellular fractions from rat liver.

The 25-hydroxylation of vitamin D2 and vitamin D3 was studied in the mitochondrial fraction from rat liver and in a reconstituted system containing cytochrome P-450 from rat liver microsomes. The mitochondrial fraction catalyzed the 25-hydroxylation of vitamin D3 at least two times more effectively than the 25-hydroxylation of vitamin D2. Microsomal cytochrome P-450 catalyzed an efficient 25-hydroxylation of vitamin D3, but no 25-hydroxylation of vitamin D2 could be detected. The present results show a difference in the 25-hydroxylation of vitamin D2 and vitamin D3 in rat liver in vitro.

Animals↗
PubMed1988

The plasma binding protein for vitamin D is a site of discrimination against vitamin D-2 compounds by the chick.

The binding of 25-hydroxy-[26,27-3H]vitamin D-3 and 25-hydroxy-[26,27-3H]vitamin D-2 to the vitamin D binding protein in the plasma of both rats and chicks has been studied. In the case of rats, sucrose density gradient analysis, competitive displacement, and Scatchard analysis demonstrate that 25-hydroxyvitamin D-3 and 25-hydroxyvitamin D-2 are bound equally well to the vitamin D binding protein. In contrast, 25-hydroxyvitamin D-2 is poorly bound, while 25-hydroxyvitamin D-3 is tightly bound to the vitamin D binding protein in chick plasma. On the other hand, the chick intestinal receptor binds 1,25-dihydroxyvitamin D-2 and 1,25-dihydroxyvitamin D-3 equally well with a KD of 7.10(-11) M for both compounds. These results strongly suggest that the failure of the plasma transport protein in chicks to bind the vitamin D-2 compounds may be responsible for their relative ineffectiveness in these animals.

25-Hydroxyvitamin D 2↗
PubMed1993

1 alpha, 25-Dihydroxyvitamin D3 and 19-nor-1 alpha, 25-dihydroxyvitamin D2 suppress immunoglobulin production and thymic lymphocyte proliferation in vivo.

BALB/CANNHSD female mice were intraperitoneally (i.p.) injected with 1,25-dihydroxyvitamin D-3 (1,25-(OH)2D3) (20 ng/day) or 19-nor-1,25-(OH)2D2 (100 ng/day) for 7 days and then given the same dose every other day thereafter until day 17 for measuring cell-mediated immunity and on day 33 for observing immunoglobulin production. To observe Ig production, the mice were immunized with an injection of hemocyanin (150 microgram/0.1 ml, i.p.) on day 8. On the day 7, 15 and 20 after immunization, the IgG1, and on day 17 and 20, the IgG3 levels in 1,25-(OH)2D3 and 19-nor-1,25-(OH)2D2 groups were significantly lower than in the control group. To measure cell-mediated immunity, mice were sensitized with dinitrofluorobenzene (DNFB) on the shaved abdominal skin. The number of thymic lymphocytes and their stimulation index were significantly reduced by 1,25-(OH)2D3 and 19-nor-1,25-(OH)2D2. These results demonstrate that 1,25-(OH)2D3 and 19-nor-1,25-(OH)2D2 can suppress immunoglobulin production and thymic lymphocyte proliferation in vivo. 19-Nor-1,25-(OH)2D2 at doses of 100 ng/day was less effective than 1,25-(OH)2D3 at doses of 20 ng/day.

25-Hydroxyvitamin D 2↗
PubMed1977

Vitamin D2 in vertebrate evolution.

1. The affinities of the specific vitamin D plasma transport proteins for 25-hydroxyergocalciferol and 25-hydroxycholecalciferol were studied in sixty three vertebrate species. 2. Fish, reptile, bird and monotreme plasma proteins bound 25-hydroxyergocalciferol considerably less efficiently than 25-hydroxycholecalciferol. 3. Vitamin D transport proteins from twenty-two placental mammals bound 25-hydroxyergocalciferol and 25-hydroxycholecalciferol with equal efficiency. 4. Proteins from nine mammals bound 25-hydroxycholecalciferol 10-30% more efficiently than 25-hydroxyergocalciferol.

Animals↗
PubMed1993

Advantages of paper chromatography as a preparative step in the assay of 1,25-dihydroxyvitamin D.

Ether extraction and paper chromatography were used to separate the main metabolites of vitamin D in plasma [25-(OH), 24,25-(OH)2 and 1,25-(OH)2 vitamin D]prior to radio receptor-assay. The overall procedural loss of the 1,25-(OH)2 vitamin D was 58 +/- 5% (n = 40), corrected for by tracer addition. The sensitivity of the assay was 0.5 fmol/tube, corresponding to 4 pmol/l, and the intra- and inter-assay coefficients of variation were 10.5% and 11.5%, respectively. The range of values measured in healthy controls was 80-200 pmol/l (n = 60), which is in agreement with findings reported in the literature. A comparison of the results of the present procedure with those obtained with a procedure employing C18 purification, disclosed a correlation coefficient of 0.92 (p < or = 0.0001), a slope of 0.89 (p < or = 0.0001) and a small non-significant intercept of 5.0 pmol/l (n = 53).

Animals↗
PubMed1986

Vitamin D deficiency in women with femoral neck fracture.

Calcium (Ca) metabolism, with particular reference to serum vitamin D metabolites, was investigated in 40 women with femoral neck fracture (mean age 77.1 +/- 8.6 yr). All the patients were ambulant before the fracture; eight were long-term geriatric in-patients. Serum total and ionised calcium and serum albumin levels were significantly lower, and serum parathormone (PTH) levels significantly higher in fracture patients than in controls. Both serum 25-OH-D and 1,25-(OH)2D were significantly lower in fracture patients than in controls. We concluded that vitamin D, serum PTH and calcium levels should be checked with greater frequency in patients at high risk for osteoporosis and osteomalacia before they reach the age of 70.

25-Hydroxyvitamin D 2↗