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At least 109 records · Page 6Linked to original sources
PubMed1989

Vitamin D and vitamin-D-binding protein kinetics in patients treated with continuous ambulatory peritoneal dialysis (CAPD).

Serum and dialysate levels of 25-hydroxycholecalciferol (25-OHD3), 1,25 dihydroxycholecalciferol (1,25-(OH)2D3), and vitamin-D-binding protein (DBP) were measured in 14 patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Serum levels of 25-OHD3 and DBP were within normal range (29.1 +/- 22.9 nmol/L and 5.9 +/- 1.1 mumol/L, respectively). Serum levels of 1,25-(OH)2D3 were subnormal in all (less than 16 pmol/L) but one. In 5 patients, dialysate concentrations of 25-OHD3 were 2.3 +/- 0.9 nmol/L, the rest had levels less than 1.0 nmol/L. Small quantities of 1,25-(OH)2D3 were found in the dialysate effluents. DBP could be detected in the dialysate in all patients (0.24 +/- 0.06 mumol/L). Mass transfer (MT) of 25-OHD3 and DBP were respectively -10.4 +/- 8.3 nmol/24 h and -1.46 +/- 0.46 0.46 mumol/24 h. Peritoneal clearances of 25-OHD3 and DBP were low (0.40 +/- 0.37 mL/min and 0.18 +/- 0.06 mL/min, respectively. We conclude that CAPD leads to losses of 25-OHD3 and DBP. However, the peritoneal loss of DBP is well compensated and does not result in serum deficiency. Serum 25-OHD3 levels did not correlate with time on CAPD.

Calcifediol↗
PubMed1982

Vitamin D from skin: contribution to vitamin D status compared with oral vitamin D in normal and anticonvulsant-treated subjects.

1. The plasma 25-hydroxycholecalciferol [25-(OH)D3] response to measured u.v. irradiation applied thrice weekly for 10 weeks was investigated in normal and in anticonvulsant-treated subjects. 2. Levels of plasma 25-(OH)D3 achieved after u.v. irradiation were similar in both normal and anticonvulsant-treated subjects, suggesting that hepatic microsomal enzyme induction does not lead to low plasma 25-(OH)D3 concentrations. 3. Cholecalciferol was present in plasma of normal subjects in a very low concentrations (less than 5.0 nmol/l) and did not increase until plasma 25-(OH)D3 levels exceeded 62.5 nmol/l. 4. Cholecalciferol occurred in significant concentrations in plasma during whole body u.v. irradiation or during oral dosage of 62.5 nmol (100 i.u) or more daily. 5. Plasma 25-(OH)D3 concentrations reached a steady state after 5-6 weeks of u.v. irradiation or of oral intake within the usual intake range. 6. Cholecalciferol synthesis in skin calculated from the steady-state equation was 0.0015 +/- 0.0008 nmol/mJ. 7. Cholecalciferol synthesis in skin was also calculated from the oral dosage required to yield the same plasma 25-(OH)D3 concentration as u.v. irradiation and was 0.0024 +/- 0.0018 nmol/mJ. 8. Rates of cholecalciferol synthesis calculated from these data suggest that many of the population of England receive insufficient u.v. irradiation to maintain vitamin D status throughout the year.

Adolescent↗
PubMed1984

The effect of different vitamin D treatments on serum vitamin D levels in early postmenopausal women.

The effects of vitamin D3 and 1,25 (OH)2D3 or l alpha-OHD3 on vitamin D metabolism were studied in a 12 month placebo controlled clinical study. 29 healthy women in their early menopause were randomized for treatment with either vitamin D3 (2000 IU/day, or 1,25(OH)2D3/l alpha-OHD3(0.25 micrograms/day), or placebo for 12 months. All participants were given a calcium supplement of 0.5 g/day throughout the study. Serum and urinary calcium increased in both vitamin D groups, whereas the posttreatment values in the placebo group were exactly the same as before treatment. Changes in the vitamin D metabolites only occurred in the vitamin D3 group, where 24,25(OH)2D and 25OHD3 were significantly increased, whereas the serum concentration of 1,25(OH)2D was unchanged. In the 1,25(OH)2D3/l alpha-OHD3 group no change in the serum vitamin D was found. The present data indicate that 1,25(OH)2D is subject to a tight feedback regulation; that 1,25(OH)2D is not the only vitamin D metabolite responsible for calcium absorption from the gut, and that 1,25(OH)2D given in physiological doses does not alter the metabolism of the other vitamin D metabolites.

Calcitriol↗
PubMedDate not supplied

Comparison of low and high dose of vitamin D treatment in nutritional vitamin D deficiency rickets.

In this study, we compared three different therapy modes (150,000 IU, 300,000 IU, and 600,000 IU vitamin D p.o.) in infants with nutritional vitamin D deficiency rickets (VDR). Our purpose was to determine the most effective dosage of vitamin D with least side effects for treating VDR. The study included 56 patients, 3-36 months of age, with nutritional VDR and 20 age-matched control infants. In all infants, serum calcium, phosphorus, alkaline phosphatase, magnesium, serum 25-hydroxycholecalciferol, plasma intact parathormone levels and urinary Ca/creatine ratio were determined. Of 56 patients, 52 were able to be followed long-term. These patients were reexamined on the 3rd day, 7-10th day, and 25-30th day after treatment. On the 30th day post-treatment, we did not find any difference between the doses in the improvement of rickets. However, hypercalcemia was present in eight infants who had been administered 300,000 IU (two infants) and 600,000 IU (six infants) of vitamin D. In conclusion, our findings showed that 150,000 IU or 300,000 IU of vitamin D was adequate in the treatment of VDR, but 600,000 IU of vitamin D may carry the risk of hypercalcemia.

Administration, Oral↗
PubMed2003

Vitamin D receptor: mechanisms for vitamin D resistance in renal failure.

1,25-dihydroxyvitamin D [1,25(OH)2D3], the hormonal form of vitamin D, controls serum levels of parathyroid hormone (PTH) and parathyroid hyperplasia. Both 1,25(OH)2D3 actions involve regulation of gene transcription by the 1,25(OH)2D3/vitamin D receptor (VDR) complex. In advanced renal failure, in addition to low serum 1,25(OH)2D3 and reduced parathyroid vitamin D receptor content, several mechanisms downstream from 1,25(OH)2D3/VDR complex formation contribute to the impairment of 1,25(OH)2D3 action, including reduced levels of the retinoid X receptor, RXR, with the consequent reduction in VDR/RXR heterodimer formation, and accumulation of uremic toxins and increases in nuclear levels of calreticulin, two processes that impair the binding of the VDR/RXR complex to vitamin D responsive elements in vitamin D-regulated genes. VDR/RXR-heterodimer formation and its binding to DNA is critical for 1,25(OH)2D3 regulation of gene transcription. Early interventions with 1,25(OH)2D3 could delay the onset of vitamin D resistance by preventing both 1,25(OH)2D3 deficiency and its critical consequence, reduction in VDR content. Once established, vitamin D resistance could be counteracted by vitamin D analogs. While their less calcemic properties make higher dosing safer, their specificity to recruit co-activator molecules to the transcriptional pre-initiation complex could compensate for reduced 1,25(OH)2D3/VDR by potentiating VDR-transactivation/transrepression of genes critical for normal PTH synthesis and parathyroid cell growth.

Animals↗
PubMed2006

A 24-phenylsulfone analog of vitamin D inhibits 1alpha,25-dihydroxyvitamin D(3) degradation in vitamin D metabolism-competent cells.

The antimitotic, prodifferentiating, and proapoptotic steroid hormone, 1alpha,25-dihydroxyvitamin D(3) [1alpha,25-(OH)(2)D(3)], at supraphysiological levels has potential for tumor therapy. However, epithelial cells from tumor-prone organs such as colon, prostate, and breast express not only the vitamin D receptor, but also vitamin D hydroxylases. In contrast to normal cells, malignant cells have high basal levels of the hydroxylase 25-hydroxyvitamin D(3)-24-hydroxylase (CYP24) and, in addition, have the potential to induce CYP24 in response to 1alpha,25-(OH)(2)D(3). Because 24-hydroxylation by CYP24 would rapidly degrade the steroid hormone in the course of therapy, the enzyme activity in tumor cells should be inhibited. We demonstrate that a 24-phenylsulfone analog of 1alpha,25-(OH)(2)D(3), KRC-24SO(2)Ph-1 (S-4a), rapidly and potently inhibits 24-hydroxylase activity in human tumor cells derived from colon, prostate, and mammary gland. Although enzymatic inhibition is a consequence of direct interaction, S-4a as a vitamin D analog apparently binds to the vitamin D receptor and induces CYP24 mRNA, which, however, is not translated into increased enzymatic activity. 25-Hydroxyvitamin D(3)-1alpha-hydroxylase expression is not affected at all by S-4a. When both 1alpha,25-(OH)(2)D(3) and S-4a are added to the cell culture, transcription of CYP24 is increased, possibly because of an increase in the half-life of the hormone. The colon cell line COGA-13 has very high levels of CYP24 and is, therefore, resistant to the action of vitamin D. Yet, S-4a imparts antimitotic activity to 1alpha,25-(OH)(2)D(3) and may therefore constitute a therapeutic to stimulate the antiproliferative potential of vitamin D-based antitumor activity.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed2000

Vitamin D and autoimmunity: is vitamin D status an environmental factor affecting autoimmune disease prevalence?

The environment in which the encounter of antigen with the immune system occurs determines whether tolerance, infectious immunity, or autoimmunity results. Geographical areas with low supplies of vitamin D (for example Scandinavia) correlate with regions with high incidences of multiple sclerosis, arthritis, and diabetes. The active form of vitamin D has been shown to suppress the development of autoimmunity in experimental animal models. Furthermore, vitamin D deficiency increases the severity of at least experimental autoimmune encephalomyelitis (mouse multiple sclerosis). Targets for vitamin D in the immune system have been identified, and the mechanisms of vitamin D-mediated immunoregulation are beginning to be understood. This review discusses the possibility that vitamin D status is an environmental factor, which by shaping the immune system affects the prevalence rate for autoimmune diseases such as multiple sclerosis, arthritis, and juvenile diabetes.

Animals↗
PubMed2003

Vitamin D insufficiency in Greenlanders on a westernized fare: ethnic differences in calcitropic hormones between Greenlanders and Danes.

We studied the influence of age, gender, latitude, season, diet and ethnicity on plasma 25-hydroxyvitamin D 25 OHD, PTH, 1,25-dihydroxyvitamin D, vitamin D-binding protein, bone-specific alkaline phosphatase, and osteocalcin levels in 46 Greenlanders living in Nuuk (64 degrees N) on a traditional fare (group A), 45 Greenlanders living in Nuuk on a westernized fare (group B), 54 Greenlanders (group C), and 43 Danes (Group D) living in Denmark (55 degrees N) on a westernized fare. Blood specimens were drawn both summer and winter. Vitamin D insufficiency (plasma 25 OHD <40 nmol/l) was common in all four study groups during summer (23-74%) and winter (42-81%). Compared to groups A and D, vitamin D insufficiency was significantly more frequent in groups B and C. In all groups, summer levels of 25 OHD were above winter levels. Multiple regression analysis revealed a significant effect of ethnicity. Compared to Danes, Greenlanders had higher 1,25-dihydroxyvitamin D levels, but lower 25 OHD and PTH levels despite relatively low plasma calcium concentrations. In addition to ethnicity, 25(OH)D levels were influenced by age, season (summer > winter), and diet (a traditional Inuit diet>westernized diet). Ethnic differences exist between Greenlanders and Danes. Our results suggest that Greenlanders may have an inherent lower "set-point" for calcium-regulated PTH release or an enhanced renal 1,25(OH)(2)D production. In addition to ethnicity, age, season, and diet were important determinants of vitamin D status. Changes from a traditional to a westernized fare are associated with a reduced vitamin D status in Greenlanders. Vitamin D supplementation should be considered.

Adult↗
PubMed1983

Evaluation of 25-hydroxyvitamin D and vitamin D binding protein losses in thirteen children on continuous ambulatory peritoneal dialysis.

Thirteen children, 6 females, 7 males, aged 2 to 13 years were studied. At the time of study they were on continuous ambulatory peritoneal dialysis (CAPD) for 1 to 22 months. 25-(OH)D loss in daily dialysate fluids represented 2 to 22 micrograms/day. A significant correlation was found between 25-(OH)D plasma concentration and 25-(OH)D dialysate concentration. 25-(OH)D clearance was correlated to 25-(OH)D binding protein clearance (p less than 0.001). These findings of important 25-(OH)D losses in the dialysate fluid of children on CAPD demonstrate the necessity of carefully adapted vitamin D intakes with such a treatment.

Adolescent↗
PubMed2004

Circulating vitamin D metabolites, polymorphism in vitamin D receptor, and colorectal adenoma risk.

OBJECTIVE: Vitamin D is a potential agent for the prevention of colorectal cancer possibly through mechanisms mediated by the vitamin D receptor (VDR). We investigated the association of circulating vitamin D metabolites and a genetic variant of the VDR gene with advanced colorectal adenoma, a precursor lesion of colorectal cancer. METHODS: Cases with advanced adenoma of the distal large bowel and gender- and ethnicity-matched controls with a negative sigmoidoscopy were randomly selected from participants in the Prostate, Lung, Colorectal and Ovarian Cancer Screening trial. Genotype analysis of the VDR TaqI polymorphism was completed on 763 cases and 774 controls. Serum levels of 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] were measured in a subset of 394 cases and 397 controls. RESULTS: Serum levels of 25(OH)D were inversely associated with advanced adenoma risk in women but not in men. Comparing those in the highest quintile with those in the lowest quintile, the risk for advanced adenoma decreased by 73% in women [odds ratio (OR) = 0.27, 95% confidence interval (95% CI) = 0.11-0.69; P for trend = 0.0002], while the risk did not decrease in men (OR = 1.10, 95% CI = 0.60-2.05; P for trend = 0.85). In women, 25(OH)D levels were significantly higher in current users of hormone replacement therapy (HRT) than in former or never HRT users. Neither serum 1,25(OH)(2)D nor VDR TaqI genotype was associated with advanced adenoma risk. CONCLUSION: Higher serum 25(OH)D levels were associated with decreased adenoma risk. Serum 1,25(OH)(2)D and VDR TaqI genotype were not associated with adenoma risk.

Adenoma↗
PubMed1985

Regulation of renal vitamin D hydroxylase activity in vitamin D deficient rats.

The regulation of renal mitochondrial 1-hydroxylase activity in chronic vitamin D deficiency was studied in male rats. These rats were born of mothers who had been raised from weaning (21 days) on a vitamin D deficient diet and who had no detectable serum 1,25-dihydroxycholecalciferol (1,25-(OH)2D) at the time their offspring were weaned (28 days). In the pups, renal mitochondrial 1-hydroxylase activity was undetectable before the 3rd week of life even though the animals were severely hypocalcemic from birth. The 1-hydroxylase activity first became detectable at 26 days of age, rapidly reached a maximum at day 34, then decreased to become undetectable again by 65 days. Throughout this time serum calcium concentration was less than 5.0 mg/dL and serum parathyroid hormone (PTH) concentration, measured by a midmolecule radioimmunoassay, was two- to five-fold greater than that found in vitamin D replete rats. 1-Hydroxylase activity could be restored in the +65-day-old animals by administration of a single dose of 2.5 micrograms vitamin D3. Enzyme activity was detected within 24 h, was maximal at 72 h, and returned to undetectable levels by 96 h after administration of the vitamin. Serum 1,25-(OH)2D which was undetectable before administration of the vitamin D3, was 108 and 458 pg/mL at 16 and 40 h, respectively, after the injection. The serum concentration of this metabolite then decreased progressively to 80 pg/mL by 6 days. 24-Hydroxylase activity first became detectable 48 h after vitamin D administration, increased to a maximum at 96 h, and thereafter decreased to become undetectable by 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1981

Vitamin D metabolite concentrations in vitamin D deficiency. Are calcitriol levels normal.

The levels of vitamin D metabolites were measured in three children with a decreased dietary intake of calcium and vitamin D and sun exposure. All three children had hypocalcemia, hypophosphatemia, and elevated alkaline phosphatase activities. Two children had rickets, aminoaciduria, and elevated immunoreactive parathyroid hormone (iPTH) concentrations. The concentrations of vitamins D2 and D3, 25-hydroxyvitamins D2 and D3 (25-OH-D2 and 25-OH-D3), and 24,25-dihydroxyvitamin D (24,25-[OH]2D) were reduced. Nonetheless, the levels of calcitriol (1,25-[OH]2D) were normal. The combination of hypocalcemia, hypophosphatemia, and increased iPTH concentrations should result in supranormal calcitriol concentrations. Moreover, the ratio of PTH to calcitriol is significantly higher than in normal subjects. Accordingly, in patients with vitamin D deficiency and "normal" calcitriol values, the synthesis of this compound may be reduced. The evaluation of vitamin D deficiency should include the measurement of all metabolites.

24,25-Dihydroxyvitamin D 3↗