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Query: UNIPROT:P06889 (Mol)
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The response of tibial metaphyses to pharmacologic levels of vitamin D in uremic rats fed a low calcium diet was evaluated morphometrically. Uremic (5/6 nephrectomized) rats given vitamin D had increased percent metaphyseal hard tissue, trabecular surface perimeter and percent trabecular osteoid surface and reduced numbers of osteoblasts and osteoclasts per millimeter of trabecular perimeter compared to either uremic rats given placebo or sham-operated rats given vitamin D. It was concluded that the resistance of metaphyseal trabeculae in uremic rats to vitamin D was due in part to the increase in osteoid-covered surfaces which inhibited osteoclasis and subsequent remodeling. The pathogenesis of worsening osteomalacia as a consequence of vitamin D administration to uremic rats on a low calcium diet remains unclear.
Virchows Arch B Cell Pathol Incl Mol Pathol 1979 Jun 29
PMID:Morphometric analysis of skeletal response to vitamin D in uremic rats fed a low calcium diet. 4 7

1. In vitamin D-deficient chicks both vitamin D3 and 1alpha-hydroxycholecalciferol markedly decrease renal 1-hydroxylase activity and induce 24-hydroxylase activity. 2. Actinomycin D abolishes both effects. 3. These results are consistent with feedback regulation of vitamin D3 metabolism by a direct nuclear action of the vitamin or its metabolites on the kidney cells.
Clin Sci Mol Med 1975 Mar
PMID:Feedback regulation of 25-hydroxycholecalciferol metabolism by vitamin D3. 16 20

1. The metabolism of an intravenous pulse dose of double-isotope-labelled cholecalciferol has been studied in control subjects with widely differing states of vitamin D nutrition and in patients with primary disorders of parathyroid function. 2. The formation of labelled 1,25-dihydroxy-cholecalciferol [1,25-(OH)2D3] and labelled 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] has been related to the prevailing concentrations in serum of 25-hydroxycholecalciferol [25-(OH)D3], immunoreactive parathyroid hormonel, calcium and orthophosphate (Pi). 3. In control subjects with relative vitamin D deficiency [serum 25-(OH)2D3 was related inversely to the serum 25-(OH)D3 and serum calcium, and directly to serum immunoreactive parathyroid hormone. No formation of 1,25-(OH)2D3 was detectable to form labelled 24,25(OH)2D3 preferentially. 4. No control subject produced significant amounts of both labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously. 5. All subjects with primary hyperparathyroidism produced significant amounts of labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously; the renal turnover of 25-(OH)D3 was apparently greater than in nutritionally matched controls. Serum labelled 1,25-(OH)2D3 in this disease was not correlated with serum 25-(OH)D3, immunoreactive parathyroid hormone, calcium or Pi. Production of labelled 24,25-(OH)2D3 was inappropriately high for the prevailing nutritional state. 6. The indirectly estimated their concentration of 1,25-(OH)2D3 showed only a fourfold variation in control subjects (45-180 pmol/l), compatible with its having a regulated hormonal function. 7. The data suggest that the production of 1,25-(OH)2D3 from a pulse dose of cholecalciferol is normally regulated, directly or indirectly, by the parathyroid hormone.
Clin Sci Mol Med 1975 May
PMID:Vitamin D metabolism and parathyroid function in man. 16 31

1. A method for assessing cholecalciferol absorption in man is described. 2. The intestinal absorption of [3H]cholecalciferol was studied in 20 female geriatric patients, most of whom were vitamin D-depleted. 3. The plasma [3H]cholecalciferol response after oral ingestion was significantly lower than that of a group of younger female subjects. 4. The plasma response of labelled polar metabolites of cholecalciferol was also lower in the geriatric than in the younger group, suggesting that increased removal of label by conversion into more polar metabolites could not account for the reduced plasma [3H]cholecalciferol response. 5. There was no evidence that alteration in gastrointestinal motility could account for the different rate of appearance of the labelled vitamin in the plasma in the two groups. 6. It is suggested that there is a defect in intestinal absorption of cholecalciferol in the elderly.
Clin Sci Mol Med 1978 Aug
PMID:Intestinal cholecalciferol absorption in the elderly and in younger adults. 20 29

1. Chromatography measurements indicated that adult rats converted 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol at a lower rate than that reported earlier for young animals. In serum, less-polar metabolites were found which probably represented vitamin D esters and vitamin D3. 2. A low dietary intake of calcium resulted in an evident increase in the fraction corresponding to 1,25-dihydroxycholecalciferol in the kidneys and also in the intestinal mucosa and serum. 3. Inclusion of 0.67 mmol of cadmium/l of drinking water at a low dietary intake of calcium resulted in an increased accumulation of both cadmium and zinc in the kidneys and liver compared with values at a normal dietary calcium intake. 4. At a normal dietary calcium intake, cadmium exposure caused inhibited production of 1,25-dihydroxycholecalciferol by the kidneys and an increased accumulation of 24,25-dihydroxycholecalciferol, vitamin D3 and vitamin D esters in the serum. 5. The inhibitory effect of cadmium on the renal conversion of 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol was almost completely counteracted by a simultaneous low dietary calcium intake. Cadmium-exposed, calcium-deficient animals also showed a maintained accumulation of 1,25-dihydroxycholecalciferol in the intestinal mucosa.
Clin Sci Mol Med 1977 Nov
PMID:Vitamin D metabolism in adult rats at low and normal calcium intake and the effect of cadmium exposure. 58 28

1. Five patients with the osteomalacia of chronic renal failure were given 50--100 nmol of 25-hydroxy vitamin D3 intravenously per day for 24--28 days. 2. In all five patients, during administration of 25-hydroxy vitamin D3 there was a substantial rise in the plasma concentration of 25-hydroxy vitamin D from initially abnormally low values. 3. Significant improvement in bone mineralization, intestinal calcium absorption and muscle strength occurred in the three patients with the greatest rise in plasma 25-hydroxy vitamin D.
Clin Sci Mol Med 1977 May
PMID:The effect of 25-hydroxy vitamin D3 in the osteomalacia of chronic renal failure. 86 43

1. One-year-old male rats were injected intravenously with 200 pmol of 25-hydroxy[26(27)-methyl-3H]cholecalciferol per 100 g body weight and the presence of this metabolite of vitamin D, as well as other metabolites, produced during the following 8 h was examined in serum, urine and bile. 2. The chromatography data indicated an excretion of 25-hydroxycholecalciferol both in bile and urine and, in urine, also of 1,25-dihydroxycholecalciferol. In bile, fractions of labelled substances were also obtained which, according to their elution positions, might represent cholecalciferol and conjugated metabolites. 3. The excretion of active metabolites of vitamin D in normal urine might be elevated in chronic renal failure and, in conjunction with a reduced synthesis, contribute to the occurrence of renal osteodystrophy.
Clin Sci Mol Med 1977 Oct
PMID:Excretion of active metabolites of vitamin D in urine and bile of the adult rat. 91 62

1. We describe a modified competive protein-binding assay for 25-hydroxyvitamin D, which does not require the prior separation of vitamin D from 25-hydroxyvitamin D. 2. Bovine albumin was used in the buffer, at a concentration of 1mg/ml, as a protein stabilizer and lipid solubilizer. Bovine albumin from different manufactures produced very different non-specific binding of 25-(3H)hydroxycholecalciferol (ranging from 3.3 per cent to 58.9 per cent). 3. The mean concentration of 25-hydroxyvitamin D in sera from normal children in Johannesburg was 76.75 +/- 24.75 mumol/ml (30.7 +/- 9.9 ng/ml).
Clin Sci Mol Med 1976 Dec
PMID:A competitive protein-binding assay for 25-hydroxyvitamin D. 107 Apr 25

1. The bivalent cation-binding agent, cellulose phosphate, together with a low calcium diet was given for 6 days to nine patients with primary hyperparathyroidism subsequently verified at surgery. 2. Urinary calcium fell promptly by 8-4 mmol/24 h, and by 70% and reached amounts below 4-0 mmol/24 h in five of the nine patients. The magnitude of fall may have been related to increased synthesis of vitamin D by the skin in a sub-tropical environment. Plasma magnesium fell steadily and urinary magnesium fell by 80%. 3. The plasma calcium showed two types of response. In five patients there was no significant change because a reduction in calcium load was offset by a further increase in the already high tubular reabsorption of calcium. In the remaining four patients, the tubular reabsorption of calcium was at a higher level initially and failed to increase further on the experimental regime, with a corresponding fall in plasma calcium. 4. The hypercalcaemia of primary hyperparathyroidism can be explained by increased renal tubular reabsorption of calcium; net bone resorption makes only a small contribution but an additional factor dependent on the blood-bone equilibrium is not ruled out. 5. Comparison with other published data suggests that the fall in urinary calcium in response to a calcium-depleting regimen is prevented by concurrent depletion of inorganic phosphate and may be enhanced by concurrent depletion of magnesium. 6. Persistence of hypercalcaemia combined with an increase in tubular reabsorption of calcium in response to cellulose phosphate may be of diagnostic value in suspected primary hyperparathyroidism. 7. Cellulose phosphate may be of value in stone prevention in patients with primary hyperparathyroidism who are unsuitable for surgical treatment.
Clin Sci Mol Med 1975 Aug
PMID:Effect of cellulose phosphate and dietary calcium restriction in primary hyperparathyroidism. 114 6

Monocytic differentiation-inducing activity of 26,26,26,27,27,27-hexafluoro-1 alpha,25-dihydroxyvitamin D3 [26,27-F6-1 alpha,25-(OH)2D3] was re-evaluated in human promyelocytic leukemia (HL-60) cells in serum-supplemented or serum-free culture. The order of in vitro potency for reducing nitroblue tetrazolium (NBT) was 26,27-F6-1 alpha,25-(OH)2D3 greater than 1 alpha, 25-dihydroxyvitamin D3 [1 alpha,25-(OH)2D3] = 26,26,26,27,27,27-F6-1 alpha,23(S), 25-trihydroxyvitamin D3 [26,27-F6-1 alpha,23(S), 25-(OH)3D3] under serum-supplemented culture conditions, whereas the order was 1 alpha, 25-(OH)2D3 = 26,27-F6-1 alpha,25-(OH)2D3 greater than 26,27-F6-1 alpha,23(S), 25-(OH)3D3 under serum-free culture conditions. This rank order for differentiation-inducing activity under serum-free culture conditions correlated well with the binding affinity of these analogs for vitamin D3 receptor of HL-60 cells. The order of relative % binding affinity for the vitamin D-binding protein in fetal calf serum was 1 alpha,25-(OH)2D3 (100%) much greater than 26,27-F6-1 alpha,25-(OH)2D3 (5.1%) greater than 26,27-F6-1 alpha,23(S), 25-(OH)3D3 (less than 1%). These results suggest that serum vitamin D-binding proteins apparently modulate monocytic differentiation of HL-60 cells by 26,27-F6-1 alpha,25-(OH)2D3 under serum-supplemented culture conditions.
J Steroid Biochem Mol Biol 1992 Jan
PMID:Effects of vitamin D-binding proteins on HL-60 cell differentiation induced by 26,26,26,27,27,27-hexafluoro-1 alpha,25-dihydroxyvitamin D. 131 Apr 14


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