Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. 1,25-Dihydroxycholecalciferol (1,25-(OH)2-D3) was given at a dose of 5-0 nmol (2-1 mug) daily by mouth for 4-12 days to three patients with hypophosphataemic (type I), vitamin D-resistant rickets. 2. 1,25-(OH)2-D3 increased intestinal absorption and urinary excretion of calcium without significant effect on the renal handling of phosphate or its plasma concentration. 3. It is concluded that in this type of vitamin D-resistant rickets the renal phosphate abnormality is unlikely to be due to diminished endogenous production of 1,25-(OH)2-D3. 4. The difference between this condition and other hypophosphataemic states is discussed.
Clin Sci Mol Med 1975 Mar
PMID:The effect of 1,25-dihydroxycholecalciferol on renal tubular reabsorption of phosphate, intestinal absorption of calcium and bone histology in hypophosphataemic renal tubular rickets. 16 19

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. Vitamin D-deficient chicks, maintained on a diet adequate in calcium and treated with ethane-1-hydroxy-1,1-diphosphonate for 2 days before a single oral dose of cholecalciferol (vitamin D3), converted the vitamin into 24,25-dihydroxycholecalciferol instead of into the normal metabolite 1,25-dihydroxycholecalciferol. 2. This inhibition of the renal 1-hydroxylase disappeared on withdrawal of the diphosphonate. 3. Kidneys from chicks given diphosphonate for 12 days converted 25-hydroxycholecalciferol into 24,25-dihydroxycholecalciferol on incubation in vitro. 4. The inhibition of the 1-hydroxylase was markedly accelerated by treating the birds with cholecalciferol. 5. No inhibition of renal 1-hydroxylation was observed in birds maintained on a diet low in calcium. 6. A possible mechanism producing this effect is discussed.
Clin Sci Mol Med 1975 Nov
PMID:The effects of a diphosphonate and dietary calcium on the metabolism of vitamin D3 (cholecalciferol) in the chick. 17 77

1. In subjects with normal renal function there was a strong positive correlation between serum concentrations of 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol, as measured by competitive protein-binding assay. 2. The 24,25-dihydroxycholecalciferol concentration was about 7% of the prevailing 25-hydroxycholecalciferol concentration. 3. In contrast, sera from anephric patients contained very low or undetectable amounts of 24,25-dihydroxycholecalciferol even after the serum 25-hydroxycholecalciferol concentrations in these patients had been elevated by oral administration of 25-hydroxycholecalciferol. 4. In a further group of anephric patients, all having normal serum 25-hydroxycholecalciferol concentrations, no radioactively labelled 24,25-dihydroxycholecalciferol was formed from an injected pulse dose of [3H,14C]cholecalciferol. 5. These results indicate that in man the kidney is the major site of 24-hydroxylation of 25-hydroxycholecalciferol.
Clin Sci Mol Med Suppl 1978 Dec
PMID:The absence of 24,25-dihydroxycholecalciferol in anephric patients. 21 22

Removal of the thyroid in normocalcemic rats with functional parathyroid transplants was found to reduce the hepatocyte DNA synthetic activity which normally follows partial hepatectomy. This proliferative incapacitation of hepatocytes appeared to be due specifically to a calcitonin deficiency since it was overcome by a single injection of pure synthetic salmon calcitonin shortly after partial hepatectomy. Salmon calcitonin and bovine parathyroid hormone were equally able to reverse the similar proliferative incapacitation of hepatocytes in hypocalcemic rats which had both their parathyroid and thyroid glands removed one day before partial hepatectomy. However, these two hormones (individually or together) could not reverse the proliferative incapacity resulting from a more prolonged (3-day) exposure to the hypocalcemic conditions in thyroparathyroidectomized rats, but the proliferative incapacity could be reversed by simultaneous treatment with the vitamin D3 metabolite, 1 alpha,25-dihydroxycholecalciferol. We suggest that extracellular calcium ions are the actual regulators of this hormonally-controlled hepatocyte proliferative development and that parathyroid hormone and the vitamin D3 metabolite affect proliferation indirectly by determining the extracellular calcium concentration, while calcitonin directly, or indirectly, sensitizes hepatocytes to the action of calcium.
Mol Cell Endocrinol 1979 Aug
PMID:The control of liver regeneration by calcitonin, parathyroid hormone and 1 alpha,25-dihydroxycholecalciferol. 49 50

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. 1alpha,25-Dihydroxy-25-hemisuccinate cholecalciferol has been synthesized and conjugated to bovine serum albumin. 2. This conjugate is immunogenic; when injected into rabbits antibodies of high affinity for 1alpha,25-dihydroxycholecalciferol were obtained. 3. Vitamin D metabolites lacking the 1alpha-hydroxy group were of lower cross-reactivity with the antibodies. 4. By using these antibodies and 1alpha,25-[23,24-3H]dihydroxycholecalciferol as tracer a sensitive radioimmunoassay has been developed capable of detecting 20 pg of 1alpha,25-dihydroxycholecalciferol.
Clin Sci Mol Med 1978 Mar
PMID:A radioimmunoassay for 1,25-dihydroxycholecalciferol. 63 Aug 9

1. Nine-months-old male rats were divided into a normal control group and one experimental group which received eight daily intraperitoneal injections 15 pmol of 1,25-dihydroxycholecalciferol/100 g body weight. After 5 days, 20 muCi of 109CdCl2 or 20muCi of 45CaCl2 was administered by stomach tube. The intestinal absorption and tissue retention of the radioisotopes were analysed during the next 3 days, the animals being kept in metabolic cages. 2. The administration of 1,25-dihydroxycholecalciferol caused significantly increased net absorption of intestinal calcium, hypercalcaemia and increased incorporation of calcium into bone. In comparison, there was no significant effect on the intestinal absorption of trace doses of cadmium or upon the accumulation of cadmium in the liver and kidneys.
Clin Sci Mol Med 1978 Aug
PMID:Intestinal absorption and tissue retention of cadmium and calcium in normal adult rats and rats given an active metabolite of vitamin D (1,25-dihydroxycholecalciferol). 67 27

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. Ligated intestinal segments from rats treated with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) at the daily dose of 16 mumol (identical to 1 mg of phosphorus)/kg subcutaneously for 7 days show an increased rate of calcium absorption. 2. This dose of EHDP enhances the intestinal accumulation of a vitamin D3 metabolite with the chromatographic characteristics of 1,25-dihydroxycholecalciferol.
Clin Sci Mol Med 1975 Feb
PMID:Stimulation of calcium absorption and apparent increased intestinal 1,25-dihydroxycholecalciferol in rats treated with low doses of ethane-1-hydroxy-1,1-diphosphonate. 111 34


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