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PubMed1986

The action of various vitamin D3 metabolites on calcium and phosphorus metabolism in chick embryo calvariae.

Chick embryos from vitamin D-deficient hens given physiological doses of 1,25-dihydroxyvitamin D3 or 24,25-dihydroxyvitamin D3 or both become severely hypocalcemic, hyperphosphatemic and fail to hatch as compared to those derived from hens given 25-hydroxyvitamin D3 or 24,25-difluoro-25-hydroxyvitamin D3. Calvariae from the former contain less mineral and on incubation in vitro produce significantly lower calcium and higher phosphate concentration in the medium than do the calvariae derived from the embryos of hens supported on 25-hydroxyvitamin D3 or 24,24-difluoro-25-hydroxyvitamin D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1989

Prevention of glucocorticoid-induced osteopenia: effect of oral 25-hydroxyvitamin D and calcium.

Twenty-four patients (9 M and 15 F, age range 51-82) with polymyalgia rheumatica receiving 6-methylprednisolone for a period of 9 months (16 mg/daily/two weeks, 14 mg/daily/two weeks, 12 mg/daily/1 month, 10 mg/daily/1 month, 8 mg/daily/1 month, 6 mg/daily/1 month and 4 mg/daily for the last four months) were randomly assigned to receive either 250HD3 (35 mcg/day for 25 days/month) (Group A) or placebo (Group B) in a double-blind study. All patients also received 500 mg elemental calcium daily. Before and at 3, 6 and 9 months ESR, tenderness on palpation and subjective pain were evaluated. At the same times, mineral metabolism parameters (serum calcium, phosphorus, alkaline phosphatase, 24-h urinary calcium, phosphate and 24-h hydroxyproline excretion) and radial bone mineral content (BMC) were evaluated. Activity indexes (ESR and clinical parameters) improved in both groups. Furthermore, serum alkaline phosphatase and 24-h hydroxyproline excretion decreased significantly only in Group A, and BMC decreased significantly in Group B but rose slightly in Group A. No side effects were observed in any of the patients.

Administration, Oral↗
PubMed1985

25-Hydroxycholecalciferol in experimental osteoporosis.

UNLABELLED: The authors, using the experimental pattern of bone rarefaction induced by a low calcium diet, tried to determine if 25-hydroxycholecalciferol, administered at doses and according to procedures similar to those used in osteoporosis, might interfere in such a process of rarefaction. The statistical evaluation of the results concerning the size of the amount of spongy bone presented evidence for the sharp decrease in the specific bone volume in rats placed on a low calcium diet as compared to control rats. Such a difference is found even between rats treated with 25-OH-D3. Nonetheless, the authors reported a difference--although not statistically significant--that indicated an increase in the amount of bone in rats on a normal diet but treated with vitamin D as compared to control rats. IN CONCLUSION: 25-OH-D3 by itself, the diet being the same, was not able to ameliorate the amount of bone.

Animals↗
PubMed1990

Normal serum concentrations of 1,25 dihydroxyvitamin D in osteoporosis.

With the aim of evaluating the role of 1,25 dihydroxyvitamin D in the pathogenesis of osteoporosis, this hormone was studied in 90 subjects. They were divided into three groups: the first group consisted of 30 normal female subjects (aged 30 to 45); the second group comprised 30 elderly female subjects (aged 67 to 90) the third group consisted of female patients (aged 65 to 87) with clinical and radiological evidence of osteoporosis. Variations of serum 1,25 dihydroxyvitamin D, after stimulation with oral P04 (1,000 mg/day for 10 days) and stimulation with oral Ca (1,000 mg/day for 10 days), were studied in 16 osteoporotic females (10 of them received P04) and six Ca (Controls). This second study was performed to evaluate the renal 1-alpha-hydroxylation. No significant variation between serum 1,25 dihydroxyvitamin D of elderly and osteoporotic females was observed when compared with normal young healthy subjects. Moreover, a significant increase in serum 1,25(OH)2D after oral P04 was found in accordance with a significant increase in serum parathormone. These data demonstrate that changes in serum 1,25(OH)2D levels did not seem to play a significant part in the pathogenesis of osteoporosis in our population neither could a deficit of renal 1-alpha-hydroxylation be demonstrated.

Adult↗
PubMed1995

Vitamin D3 metabolism in patients with rheumatic diseases: low serum levels of 25-hydroxyvitamin D3 in patients with systemic lupus erythematosus.

1,25-dihydroxyvitamin D3 (1,25(OH)2 D3) has been shown to modulate lymphocyte activation in vitro. Through binding to specific receptors 1,25-(OH)2 D3 inhibits proliferation, immunoglobulin production and the release of cytokines. Moreover, 1,25-(OH)2 D3 is efficiently produced by activated monocytes. These findings suggest that 1,25-(OH)2 D3 may play a role as a regulator of immunological activation. Consequently, we found it of interest to study the serum levels of the two major metabolites of vitamin D3 in patients with systemic lupus erythematosus (SLE) (n = 21), rheumatoid arthritis (RA) (n = 29) and osteoarthritis (n = 12). In patients with SLE the levels of 25-OH D3 were below those of the healthy controls (p = 0.0008) and OA (p = 0.0168). The levels 1,25-(OH)2 D3 corresponded to normal levels. There were no significant correlations between 25-OH D3 levels and clinical or paraclinical disease manifestations. Further, the phenotypic distribution of Gc-globulin, which binds vitamin D3 metabolites in circulation, was normal. The serum concentrations of 1,25-(OH)2 D3 and 25-OH D3 in patients with RA and OA corresponded to those of the controls. Although the cause of the reduced 25-OH D3 levels in SLE patients is unclear, possible beneficial effects of administration of vitamin D to these patients should be considered.

Adult↗
PubMed1992

Adolescent osteoporosis disclosing familial osteopenia.

The observations of familial juvenile osteoporosis, presumably of genetic origin are exceptional. The authors report the observation of a 16-year old adolescent suffering from osteoporosis, confirmed by histomorphometry and decrease in bone density (lumbar vertebrae 0.79 g/cm2 and femoral neck 0.88 g/cm2: LUNAR DPX). We prescribed fluorine and calcium therapy. Lumbar bone density increases by 11% and bone density of the thighbone neck by 7.6%. We cannot rule out growth as a factor in the changes observed, given that the propositus is only 16. A densitometric investigation performed in 4 of his 12 brothers shows a decrease in the lumbar bone mineral content (from 61 to 94% expressed as Z score). A genotypic origin seems to be conceivable, especially since no other cause could be considered (endocrinal, alimentary...). On the other hand, there is no argument in favour of osteogenesis imperfecta disease. The bone densitometry is a useful diagnostic means to detect familial forms of osteoporosis.

Adolescent↗
PubMed1989

Effect of phototherapy on serum 25-hydroxyvitamin D in the Antarctic.

The hypothesis that sunlight may induce the enzymes involved in the vitamin D pathway has been tested by comparing the ability to synthesize vitamin D3 and its 25 hydroxy metabolite (25-OHD) in 2 groups of male volunteers resident at the British Antarctic base at Rothera Point (67 degrees 34'S.). One group endured the UV depleted winter and the other group received regular phototherapy throughout the winter. Both groups then received a course of 14 days phototherapy in October (Southern Hemisphere spring). The group receiving regular phototherapy had a trend towards a higher level of serum 25-OHD, and the October phototherapy course produced a further small increase in serum 25-OHD values. In the previously non irradiated group the October phototherapy produced a much larger increase in serum 25-OHD so that they attained the previously higher values of the pre-iradiated group. There was a negative correlation between the pre October phototherapy serum concentration of 25-OHD and the subsequent increment (r-0.78, p less than 0.01) but no relationship between the serum 25-OHD and D3 after phototherapy. These results provide evidence against the existence of enzyme induction of vitamin D 25 hydroxylase by light.

Adult↗
PubMed1983

1,25 dihydroxyvitamin D-induced inhibition of 3H-25 hydroxyvitamin D production by the rachitic rat liver in vitro.

The effect of the vitamin D metabolites 1,25 dihydroxyvitamin D (100 pg/ml) and 25-hydroxyvitamin D (30 ng/ml) on hepatic production of 3H-25 hydroxyvitamin D was investigated using rachitic liver perfusions and homogenates. 1,25 dihydroxyvitamin D inhibited hepatic 3H-25 hydroxyvitamin D production in the liver perfusion (3.6 +/- 0.4 vs 2.0 +/- 0.5 pmol/liver, P less than 0.05) and in liver homogenates (11.9 +/- 0.6 vs 10.1 +/- 0.4 pmol/g liver protein/3 h, P less than 0.02). Inhibition was time and dose dependent. 25-hydroxyvitamin D inhibited production in liver homogenates (11.9 +/- 0.6 vs 9.2 +/- 0.1 pmol/g liver protein/3 h, P less than 0.05) but not in the intact liver (3.6 +/- 0.4 vs 3.4 +/- 0.5 pmol/liver). The data indicate that 1,25 dihydroxyvitamin D is able to feedback regulate the production of its precursor, 25-hydroxyvitamin D. Although 25-hydroxyvitamin D also inhibits its own production in liver homogenates, it failed to alter total production in the intact liver, suggesting that this metabolite may require immediate access to the vitamin D 25-hydroxylase, located on the microsomes and mitochondria, to induce inhibition.

Animals↗
PubMed1983

The role of vitamin D in the medullary bone formation in egg-laying Japanese quail and in immature male chicks treated with sex hormones.

The effect of vitamin D3 on medullary bone formation was investigated in egg-laying Japanese quail and in immature male chicks treated with sex hormones. When laying quail were fed a vitamin D-deficient diet for 16 days, their eggshell weights and egg production rate were markedly reduced in a time-dependent manner with a significant decrease in plasma calcium and 25-hydroxyvitamin D3 levels. The calcium content of the medullary bone of femurs decreased markedly with the progress of vitamin D deficiency, whereas that of the cortical bone remained unchanged. Quantitative histological examination also showed that the area of the mineralized portion of medullary bone in quail that were fed the vitamin D-deficient diet markedly decreased compared with that in the control laying quail, whereas the total area of the mineralized and unmineralized portions of medullary bone in the bone marrow cavity increased moderately. Daily administration of vitamin D3 (0.75 microgram/day) to the vitamin D-deficient quail increased the mineralization of medullary bone as early as day 4. Daily administration of both estradiol (0.3 mg/day) and testosterone (0.9 mg/day) for 3 weeks to immature male chicks induced an apparent hypercalcemia and matrix formation of medullary bone, regardless of the vitamin D status of the chicks. Mineralization of medullary bone was observed only when vitamin D3 was administered together with the sex hormones. These results suggest that vitamin D3 is directly involved in the mineralization of medullary bone in birds.

Animals↗
PubMed1984

Effects of vitamin D3 metabolites on calcium fluxes in intact chicken skeletal muscle and myoblasts cultured in vitro.

25-hydroxycholecalciferol (25OHD3) and 1,25-dihydroxycholecalciferol (1,25(OH)2D3) at physiological concentrations exerted direct effects on Ca fluxes in cultured vitamin D-deficient chick soleus muscle and myoblasts. Isotopic desaturation curves of soleus muscle prelabeled with 45Ca indicated that the action of 25OHD3 is localized in a slow-exchangeable Ca pool where it stimulates net Ca uptake. On the other hand, the predominant effects of 1,25(OH)2D3 consist in an increase of the rate constant of Ca efflux of this pool and in an increase of net Ca uptake in a fast-exchangeable pool. 24,25-dihydroxycholecalciferal proved to be inactive on both Ca uptake and efflux. In addition, 1,25(OH)2D3 significantly increased 45Ca labeling of cultured chick myoblasts. These effects were accompanied by changes in the growth and differentiation of the cultures. The results suggest a direct involvement in vivo of 25OHD3 and 1,25(OH)2D3 on muscle cellular calcium.

Animals↗
PubMed1984

Vitamin D deficiency in mothers of rachitic infants.

The existence of nutritional deficiency rickets among infants in sunny Riyadh was confirmed radiologically. Most of the rachitic infants were breast-fed, some received unsupplemented infant feeding formulae, and all live in an environment that is devoid of sunlight. Their mean age at the time of onset was 10.5 months. 25-Hydroxyvitamin D (25OHD) levels were found to be low in mothers of the rachitic infants. This maternal deficiency as a factor in pathogenesis of rickets in the infant is discussed. Proposals are made to prevent the occurrence of rickets on this scale.

Breast Feeding↗
PubMed1984

Extrarenal metabolism of 25-hydroxycholecalciferol in the rat: regulation by 1,25-dihydroxycholecalciferol.

To determine the role of the kidney in regulation of 25-hydroxycholecalciferol (25OHD3, metabolism, the effects of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] on 3H-25OHD3 were compared in intact and nephrectomized vitamin D-deficient rats. Sixteen hours after the intravenous administration of 3H-25OHD3, extracts of serum and pooled small intestinal mucosa were fractionated by Sephadex LH-20 column chromatography followed by high performance liquid chromatography. In intact rats, 1,25(OH)2D3 (50 ng/day i.p. for 7 days) increased mean serum 3H-24,25-dihydroxycholecalciferol [3H-24,25(OH)2D3] from 2 +/- 2-210 +/- 80 fmol/ml (mean +/- 1 SD), increased mean serum 3H-25,26-dihydroxycholecalciferol [3H-25,26(OH)2D3] from 2 +/- 2-12 +/- 6 fmol/ml and lowered mean serum 3H-1,25(OH)2D3 from 210 +/- 40-4 +/- 4 fmol/ml. Similarly, in nephrectomized animals, 1,25(OH)2D3 increased mean serum 3H-24,25-(OH)2D3 from 6 +/- 11-115 +/- 30 fmol/ml and increased mean serum 3H-25,26(OH)2D3 from 3 +/- 3-26 +/- 10 fmol/ml. Nephrectomy increased serum 3H-25(OH)D3 in untreated (from 1450 +/- 225-2675 +/- 225 fmol/ml serum) and 1,25(OH)2D3 treated rats (from 1600 +/- 175-3075 +/- 100 fmol/ml). 3H-1,25(OH)2D3 averaged 74 +/- 16% of total radioactivity in intestinal mucosa of untreated intact rats and was not detected in either the serum or intestinal mucosa of nephrectomized animals. The results suggest that in intact animals, extrarenal synthesis can account for substantial 24,25(OH)2D3 production and for most 25,26(OH)2D3 production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Evidence for abnormal regulation of circulating 1 alpha, 25-dihydroxyvitamin D in patients with pulmonary tuberculosis and normal calcium metabolism.

Available evidence indicates that hypercalcemia in pulmonary tuberculosis results from increases in circulating 1 alpha, 25-dihydroxyvitamin D [1 alpha, 25(OH)2D]. To further characterize vitamin D metabolism in this disorder, the effects of vitamin D, 100,000 units a day for 4 days, were compared in 25 normal subjects and 11 patients with active pulmonary tuberculosis who were normocalcemic and had not had hypercalcemia. Serum calcium, phosphorus, 25-hydroxyvitamin D (25-OHD) and 1 alpha, 25(OH)2D were measured. Whereas vitamin D increased mean serum 25-OHD from 20 +/- 2 (+/- SE) to 40 +/- 5 ng/ml (P less than 0.001) and did not change mean serum 1 alpha, 25(OH)2D in the normals (33 +/- 2 vs. 31 +/- 2 pg/ml), it increased mean serum 25-OHD from 21 +/- 4 to 55 +/- 13 ng/ml (P less than 0.05) and mean serum 1 alpha, 25(OH)2D from 28 +/- 2 to 35 +/- 3 pg/ml (P less than 0.05) in the patients. Serum calcium was normal and remained within the normal range in all subjects and patients. The findings indicate that there is a modest but significant abnormality in the regulation of circulating 1 alpha, 25(OH)2D in normocalcemic patients with pulmonary tuberculosis. The results are similar to those previously reported by us in normocalcemic patients with sarcoidosis.

Adult↗
PubMed1980

A simplified technique for the measurement of intestinal absorption of calcium in the dog: effects of PO4 depletion and 25(OH)D3 in uremia.

A simplified method is described for the measurement of calcium absorption in the dog. This method uses 45Ca and takes less than 8 h to perform. Calcium absorption was measured in normal and uremic dogs on different intakes of calcium and phosphorus and compared to the results obtained in the same animal maintained on the same diet by another method using 47Ca and a double dilution procedure. The correlation coefficient between the two methods was 0.99 (P < 0.001). The advantages of the simplified method are discussed.

Animals↗
PubMed1981

Mixed-function oxidases of 25-hydroxycholecalciferol in isolated chick kidney glomeruli: evidence for nuclear localization.

Pure chick kidney glomeruli and proximal tubular fragments have been isolated by graded sieving through nylon screens. Electron micrographs revealed that, in distinct contrast to proximal epithelial cells, the glomerular epithelial and endothelial cells are essentially devoid of mitochondria. Glomeruli as well as proximal tubular fragments contain the 1 alpha- and 24R-hydroxylases of 25-hydroxycholecalciferol. The level of 1 alpha-hydroxylase activity was the same in both segments of the nephron. However, the tubular fragments contained twice the 24R-hydroxylase activity found in glomeruli. Glomerular nuclei were purified by sucrose gradient sedimentation and used to confirm the association of the 1 alpha-hydroxylase with this kidney organelle. Almost all of the glomerular 1 alpha-hydroxylase activity was found in the nuclear fraction. Two metabolites, which are produced predominantly by the nuclei, are designated N-1 and N-2. Their structural identity remains unknown. The novel presence of the 1 alpha-hydroxylase in the glomerulus may be important in defining the etiology of bone diseases in patients with glomerulonephritis and similar disorders.

24,25-Dihydroxyvitamin D 3↗