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At least 127 records · Page 7Linked to original sources
PubMed2001

25-hydroxy-vitamin d metabolism in human colon cancer cells during tumor progression.

RT-PCR analysis showed elevated expression of 25-hydroxyvitamin D-1alpha-hydroxylase (1alpha-OHase) and of 25-hydroxyvitamin D-24-hydroxylase (24-OHase) in well differentiated human colon carcinomas in comparison to normal mucosa. Further tumor progression is associated with a rise in 1alpha-OHase but with no significant change in 24-OHase mRNA expression. Accordingly, HPLC analysis of 25-hydroxy-vitamin D3 metabolism in freshly isolated tumor cells indicated that well to moderately differentiated colon cancers in situ are able to produce 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) and convert it through 24-OHase activity into side-chain modified metabolites, 1,24,25-(OH)3-D3 and 1,25-(OH)2- 24-oxo-D3. Likewise, 25-(OH)-D3 is metabolized into 24,25-(OH)2D3, 23,25-(OH)2D3, and 23,25-(OH)2-24-oxo-D3. Poorly-differentiated cancers expressed low levels of 1alpha-OHase mRNA, whereas 24-OHase was even over-expressed. RT-PCR and HPLC analysis of vitamin D metabolism in primary culture cell clones strongly suggested that the extent of endogenously produced 1alpha,25-(OH)2-D3 was inversely related to 24-OHase activity, which could thus limit the antimitotic efficacy of 1alpha,25-(OH)2-D3 particularly at late stages of colon cancer progression.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed2001

Ligand affinity, homodimerization, and ligand-induced secondary structural change of the human vitamin d receptor.

The intrinsic tryptophan fluorescence signal of the full-length nuclear receptor hVDR was used to directly determine the dissociation constants, K(d), of two ligands yielding K(d) = 32 nM for 1alpha,25(OH)(2)D(3) and K(d) = 322 nM for 25(OH)D(3). Ligand binding was accompanied by a conformational change in the alpha-helical part of hVDR as revealed by CD spectroscopy. In addition, the presence of calcitriol was found to be a necessary prerequisite for the homodimerisation of hVDR which was monitored using fluorescence anisotropy. We conclude that the observed ligand-induced structural change of hVDR is conditional for dimerisation of the protein.

Calcifediol↗
PubMed1993

1,25(OH)2 vitamin D3 increases ionized plasma calcium concentrations in the immature Atlantic cod Gadus morhua.

Intraperitoneal injections of 1,25(OH)2 vitamin D3 (1,25(OH)2D3) produced hypercalcemia in the marine teleost the Atlantic cod (Gadus morhua) with increased plasma concentrations of ionized calcium (CaI) while the total plasma calcium concentrations (CaT) were unaffected. A single injection of 10 micrograms kg bw-1 of 1,25(OH)2D3 increased CaI concentrations from 1.74 +/- 0.03 mM to 1.8 +/- 0.01 mM after 24 hr in Experiment 1 and from 1.67 +/- 0.03 mM to 1.82 +/- 0.06 mM after 72 hr in Experiment 2. This hypercalcemic effect was sustained by daily injections for 5 but not 7 days. Daily injections of a lower dose of 1,25(OH)2D3, 1 microgram kg bw-1, caused hypercalcemia after 5 days (CaI increased from 1.68 +/- 0.01 mM to 1.76 +/- 0.02 mM). Plasma calcium concentrations were not affected by any of the other seco-steroids (vitamin D3, (25(OH)), vitamin D3 (25(OH)D3), or 24,25(OH)2 vitamin D3 (24,25(OH)2D3), except for a decrease in CaT concentrations after 7 daily in injections of 25(OH)D3 (2 micrograms kg bw-1). Plasma phosphate concentrations were not changed by any of the seco-steroids. It is concluded that 1,25(OH)2D3 is hypercalcemic in the marine Atlantic cod.

Animals↗
PubMed1995

Effect of various vitamin D metabolites on serum calcium and inorganic phosphate in the freshwater snake Natrix piscator.

Vitamin D3 (650 pmol and 6.50 nmol/100 g body wt), 25-hydroxyvitamin D (650 pmol and 6.50 nmol/100 g body wt), and 1,25-dihydroxyvitamin D (65 pmol and 650 pmol/100 g body wt) were administered daily to the freshwater snake Natrix piscator for 15 days. Both serum calcium and inorganic phosphate levels were increased significantly in all of the treated groups. This is the first report of hypercalcemia and hyperphosphatemia in reptiles induced by 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D.

Animals↗
PubMed1999

Cholecalciferol modulates plasma phosphate but not plasma vitamin D levels and intestinal phosphate absorption in rainbow trout (Oncorhynchus mykiss).

Since the vitamin D endocrine system modulates phosphorus homeostasis and regulates inorganic phosphate (Pi) uptake by the small intestine in mammals and birds, we determined the effects of dietary cholecalciferol (vitamin D3) on Pi uptake by the small intestine, Pi concentrations in the plasma, Pi concentrations in the intestinal lumen, intestinal weights, liver weights, and concentrations of vitamin D metabolites in the plasma of rainbow trout (Oncorhynchus mykiss) fed phosphorus-sufficient (0.6 g/100 g) diets. Five groups of trout initially weighing 55.8 +/- 0.6 g were fed purified diets containing 0, 300, 2,500, 10,000, and 40,000 IU vitamin D3/kg diet over a 7- to 8-day feeding period. Plasma Pi concentration was higher in trout fed 2,500-40,000 IU/kg diet (8.26 +/- 0.27 mmol/L) than in those fed 0 and 300 IU/kg (6.99 +/- 0.30). Liver weights were 30-50% greater in fish fed 0 IU/kg than in those fed 300-40,000 IU/kg. There were no significant, diet-related differences in plasma levels of 25-hydroxycholecalciferol [25(OH)D3] and 1,25 dihydroxycholecalciferol [1,25(OH)2D3]. Increasing levels of dietary cholecalciferol also did not enhance in vitro Pi uptakes by the intestine (range of means: 0.22-0.29 nmol/mg tissue. min) and Pi concentrations in the intestinal lumen (8.5-13.5 mmol/L). Pi uptake did not differ among tissues incubated in vitamin D3, 25(OH)D3, or 1,25(OH)2D3. These results demonstrate that when fish are fed P-sufficient diets, dietary cholecalciferol increases plasma Pi concentrations but decreases liver weights, alterations which are not accompanied by changes in intestinal weight, Pi uptake by the intestine, Pi concentration in the intestinal lumen, and circulating metabolites of cholecalciferol.

Animals↗
PubMed1995

Affinity purification of human plasma vitamin D-binding protein.

During the course of our studies to probe the vitamin D ligand-binding domains of vitamin D-binding protein and vitamin D receptor, we developed a synthetic procedure to modify the 3 beta-hydroxyl group of vitamin D3 and its 25-hydroxy- and 1,25-dihydroxy metabolites with a 3'-aminopropylether group. In the present study we have coupled 25-hydroxyvitamin D3-3 beta-3'-aminopropylether to an activated Sepharose matrix. Using this stable and reusable affinity matrix we have purified human vitamin D-binding protein from human plasma to homogeneity.

Binding Sites↗
PubMed1998

Decreased serum concentrations of 1,25(OH)2-vitamin D3 in patients with gout.

We measured the serum concentrations of 1,25(OH)2-vitamin D3, 25(OH)-vitamin D3, parathyroid hormone (PTH) in 82 male patients with primary gout whose serum uric acid was significantly higher than that of 41 normal control male subjects (8.8 +/- 0.2 vs 5.6 +/- 0.2 mg/dL, p < 0.001). The serum 1,25(OH)2-vitamin D3 concentration was significantly lower in the patients with gout compared with the control subjects (39.6 +/- 1.4 vs 44.8 +/- 1.7 pg/mL, p < 0.05), while no differences were observed between the two groups in either the serum concentration of 25(OH)-vitamin D3 or PTH. The administration of uric acid lowering agent to the patients for 1 year caused a significant increase in their serum 1,25(OH)2-vitamin D3 concentration which was associated with a significant decrease in their serum uric acid concentration. In contrast, the serum concentrations of 25(OH)-vitamin D3 and PTH were not affected by these drugs. These results suggest that uric acid per se may directly decrease the serum concentration of 1,25(OH)2-vitamin D3 in patients with gout by inhibiting 1-hydroxylase activity.

Allopurinol↗
PubMed1986

Disorders of divalent ions and vitamin D metabolism in chronic alcoholism.

This chapter reviews the pathogenesis of disordered divalent mineral and bone metabolism in alcoholism, emphasizing the role of impaired vitamin D physiology. Normally, vitamin D metabolites are derived principally from cholecalciferol, which is synthesized in the skin via the energy of sunlight. Most alcoholics have subnormal levels of 25-hydroxyvitamin D [25(OH)D]. Those with Laennec's cirrhosis also have low levels of vitamin D binding protein due to impaired hepatic protein synthesis and as a result, have low serum concentrations of total, but not free, 1,25-dihydroxyvitamin D. The causes of 25(OH)D deficiency in alcoholics include reduced hepatic 25-hydroxylase activity, lack of sun exposure, inadequate dietary intake, and malabsorption. Hypomagnesemia and hypophosphatemia, which are very common in hospitalized alcoholics, result from deficient intake, malabsorption, excessive renal losses, and cellular uptake of both ions. Hypocalcemia in alcoholics is caused primarily by hypoalbuminemia but can result also from deficient intake, malabsorption, hypomagnesemia, and renal calcium wastage. Low vitamin D activity may contribute significantly to the calcium and phosphate deficiencies. Osteoporosis is extremely common in alcoholics whereas osteomalacia is exceptional. However, both bone disorders respond well to vitamin D therapy. Thus, alcoholics should be screened periodically for vitamin D deficiency and osteopenia, and when either is detected they should receive vitamin D supplements.

Alcoholism↗
PubMed2003

Extrarenal sites of calcitriol synthesis: the particular role of the skin.

Calcitriol (1alpha,25(OH)2D3), the hormonally active form of vitamin D3 (D3) is produced by a cascade of reactions, including photochemical D3 synthesis in the skin and subsequent hydroxylation at the C-25 atom in the liver and finally at C-1alpha position in the kidney. However, there is substantial evidence for additional extrarenal sites of calcitriol synthesis. In vitro, many nonrenal cells, including bone, placenta, prostata, keratinocytes, macrophages, T-lymphocytes and several cancer cells (e.g., from lung, prostata and skin) can enzymatically convert calcidiol (25OHD3) to 1alpha,25(OH)2D3. We have demonstrated that keratinocytes of the skin have unique properties in the D3 pathway; they are not only capable of producing D3 from 7-dehydrocholesterol (7-DHC), but also generate 1alpha,25(OH)2D3 from the substrates 25OHD3, lalpha-hydroxyvitamin D3 (1alpha-OHD3) and even D3. It is evident that keratinocytes possess at least 1alpha-OH-, 25OH- and 24OHase activity, which is necessary for enzymatic conversion of D3 to 1alpha,25(OH)2D3, and the 24OHase activity for initiation of catabolism of 1alpha,25(OH)2D3 to more polar metabolites. Thus, the skin is apparently the only extrarenal tissue where the complete UVB-induced pathway from 7-DHC to 1alpha,25(OH)2D3 takes place under physiological circumstances.

Animals↗
PubMed1985

Investigation of adrenal steroids and 25-hydroxy-cholecalcipherol in human gramoxone poisoning.

Serum cortisol, dehydroepiandro-sterone (DEA), dehydroepiandrosteron-sulphate (DS) and 25-hydroxy-cholecalcipherol (25-OH-D3) content were determined in 11 cases of gramoxone-poisoning by RIA method. Patients (19-21 year old men) simultaneously had ingested gramoxone 12 hours before blood samples were collected. Six of the patients died between the 5th and 8th day after the ingestion. In these cases the serum level of the adrenal steroids was markedly elevated, perhaps due to hyperreactor response of the adrenal cortex. In this group the serum 25-OH-D3 levels were decreased. On the contrary three survivors and two other patients who died on the 9th and 12th day had normal or low level of cortisol, DEA, DS and high level of 25-OH-D3. There seems to be a negative correlation between the serum levels of 25-OH-D3 and cortisol. The pathophysiological significance of the results is not clear, although this suggests that perhaps those people whose serum adrenal steroid content is lower and the 25-OH-D3 level is higher at the early stages of gramoxone poisoning have a better chance of survival.

Adrenal Cortex↗
PubMed1992

Transformation of vitamin D3 to 1 alpha,25-dihydroxyvitamin D3 via 25-hydroxyvitamin D3 using Amycolata sp. strains.

To enzymatically synthesize active metabolites of vitamin D3, we screened about 500 bacterial strains and 450 fungal strains, of which 12 strains were able to convert vitamin D3 to 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] via 25-hydroxyvitamin D3 [25(OH)D3]. The conversion activity was only detected in strains belonging to the genus Amycolata among all the organisms tested. A preparative-scale conversion of vitamin D3 to 25(OH)D3 and 1 alpha,25(OH)2D3 in a 200-1 tank fermentor using A. autotrophica FERM BP-1573 was accomplished, yielding 8.3 mg 25(OH)D3/l culture and 0.17 mg 1 alpha,25(OH)2D3/l culture. A related compound, vitamin D2, could be also converted to 25-hydroxyvitamin D2 and 1 alpha,25-dihydroxyvitamin D2 using the same strain. The cytochrome P-450 of FERM BP-1573 was detected by reduced CO difference spectra in whole-cell suspensions. Vitamin D3 in the culture induced cytochrome P-450 and the conversion activity simultaneously, suggesting that the hydroxylation at C-25 of vitamin D3 and at C-1 of 25(OH)D3 originates from cytochrome P-450.

Actinomycetales↗
PubMed1992

Disturbed calcium metabolism in subjects with elevated diastolic blood pressure.

Essential hypertension has been associated with disturbed calcium metabolism, but the available data are controversial. We measured parameters of calcium metabolism in groups of untreated male subjects (n = 78) with elevated diastolic blood pressure (101 +/- 6 mmHg, mean +/- SD) and age-matched male subjects (n = 79) with low diastolic blood pressure (62 +/- 4 mmHg). The participants of the study were drawn from a random population sample. Subjects with high diastolic blood pressure had significantly higher carboxy-terminal parathyroid hormone (PTH) plasma concentrations than controls with low diastolic blood pressure (median 114 vs. 43 pmol/l, P less than 0.01). The 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations were comparable in both groups. Individuals with high diastolic blood pressure had significantly lower total serum calcium (2.41 +/- 0.10 vs. 2.47 +/- 0.10 mmol/l, mean +/- SD; P less than 0.01). PTH concentrations were correlated with diastolic pressure (r = -0.39, P less than 0.001). The data are compatible with increased parathyroid activity despite unchanged concentrations of vitamin D metabolites in human hypertension.

Adult↗
PubMed1992

Long-term therapy with cyclosporin A does not influence serum concentrations of vitamin D metabolites in patients with multiple sclerosis.

Animal studies have shown that cyclosporin A (CyA) stimulates renal 25-hydroxyvitamin D3 [25(OH)D3]-1 alpha-hydroxylase activity; in contrast, studies in renal transplant recipients indirectly suggest that CyA reduces 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] production. To clarify the effect of CyA on vitamin D metabolite concentrations, we measured parameters of calcium metabolism in 37 CyA-treated patients (median trough whole blood levels 171-222 ng/ml) with multiple sclerosis and initially normal kidney function. The patients participated in a randomized double-blind study to assess the efficacy of CyA in multiple sclerosis. An age- and sex-matched control group (n = 39) received azathioprine (Aza). Measurements were made at the end of a 2-year treatment period. The 1,25(OH)2D3 serum concentrations were not significantly different between the two groups, although they were numerically lower in CyA-treated patients [median (range), 28.4 pg/ml (7.8-85.9) vs 41.0 pg/ml (9.2-105.1) in Aza-treated patients]. The 25(OH)D3 levels were comparable in both groups. There was no correlation between the 25(OH)D3 and 1,25(OH)2D3 concentrations. The renal function in both groups was stable in the last 6 months of the study. At the end of the study period, the endogenous creatinine clearance was significantly lower in the CyA-treated group (85 +/- 17 ml/min versus 99 +/- 22 in the Aza-treated group, P less than 0.05). The carboxyterminal parathyroid hormone (C-PTH) was within the normal range in both groups, although CyA-treated patients had significantly higher concentrations (P less than 0.01). The urinary excretion of mineral ions, cations and protein was similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗