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PubMed1975

Response of renal calcium-binding protein. Independence of kidney vitamin D hydroxylation.

Dietary calcium and dietary phosphorus restriction were studied in chicks fed either cholecalciferol or 1alpha-hydroxycholecalciferol. Intestinal calcium absorption and calcium-binding protein of 1alpha-hydroxycholecalciferol-treated chicks remained unchanged under dietary calcium restriction, but increased under dietary phosphorus restriction. Kidney calcium-binding protein was not altered by dietary caclium restriction in chidks treated with either cholecalciferol or 1alpha-hydroxycholecalciferol, but increased under dietary phosphorus restriction independent of the vitamin D source. In contrast to the intestine, calcium-binding activity of the kidney was found to be poorly related to the calcium-binding protein concentration. It is suggested that kidney calcium-binding protein is regulated by a mechanism different from that of intestinal calcium-binding protein, and that its concentration in renal tissue is related to renal caclium excretion or plasma calcium level.

Animals↗

PubMed1976

25-Hydroxycholecalciferol inthe management of rickets associated with extrahepatic biliary atresia.

In children with extrahepatic biliary atresia, impaired hydroxylation and defective intestinal absorption of cholecalciferol may lead to a deficiency of vitamin D and rickets. The data presented herein demonstrate that in such patients serum levels of vitamin D measured as 25-hydroxycalciferol are reduced. A moderate therapeutic oral dose of 25-hydroxycholecalciferol, by circumventing the hepatic conversion of cholecalciferol to 25-hydroxycholecalciferol, will replete vitamin D stores and maintain the serum concentration of 25-hydroxycalciferol required to prevent or heal rickets in these patients.

Administration, Oral↗

PubMed2002

1,25-dihydroxyvitamin D3 receptor is upregulated in aortic smooth muscle cells during hypervitaminosis D.

Several studies have demonstrated that excess of vitamin D3 is toxic particularly to vascular tissues. A notable pathological feature is arterial calcification. The nature of the toxic metabolite in hypervitaminosis D and the pathogenesis of arterial calcification are not clearly understood. The present study was undertaken to explore whether arterial calcification is a sequel of increased calcium uptake by arterial smooth muscle mediated by up regulation of vitamin D receptor in the cells in response to elevated circulating levels of vitamin D3 in serum. The experimental study was performed in 20 New Zealand white female rabbits aged 6 months. Animals in the test group were injected 10,000 IU of cholecalciferol intramuscularly twice a week for one month. Six control animals were given intra-muscular injections of plain cottonseed oil. Animals were sacrificed and aortas were examined for pathological lesions, 1,25-dihyroxyvitamin D3 (1,25(OH)2 D3) receptor levels and 45Ca uptake in smooth muscle cells. Serum samples collected at intervals were assayed for levels of 25-OH-D3 and calcium. The results showed that in animals given injections of cholecalciferol, serum levels of 25-OH-D3 were elevated. In four of these animals calcification and aneurysmal changes were seen in the aorta. Histological lesions comprised of fragmentation of elastic fibers as well as extensive loss of elastic layers. 1,25(OH)2 D3 receptor levels were up regulated and 45Ca uptake enhanced in aortas of animals which were given excessive vitamin D3. The evidences gathered suggest that excess vitamin D is arteriotoxic and that the vitamin induces arterial calcification through up regulation of 1,25(OH)2D3 receptor and increased calcium uptake in smooth muscle cells of the arteries.

Animals↗

PubMed1977

Vitamin-D metabolism in nephrotic syndrome.

Plasma concentrations of 25-hydroxy-cholecalciferol (25-OHD3) and vitamin-D-binding globulin (V.D.B.G.) were significantly reduced in ten nephrotic subjects. V.D.B.G., which is undetectable in normal urine, was present in substantial amounts in the urine of each nephrotic subject. Administration of 3H-labelled cholecalciferol to three subjects resulted in the rapid appearance of the labelled vitamin in the urine, mainly as the 25-hydroxylated metabolite bound to V.D.B.G. in amounts which could largely account for the low plasma-25-OHD3. The plasma half-life of 25-OHD3 was substantially reduced in the nephrotic syndrome.

Adult↗

PubMed1980

Metabolites of vitamin D in human vitamin-D deficiency: effect of vitamin D3 or 1,25-dihydroxycholecalciferol.

Circulating concentrations of hydroxylated metabolites of vitamin D were measured in seven Asian patients with histologically proven osteomalacia before and during treatment with either cholecalciferol (vitamin D3) or 1,25-dihydroxycholecalciferol. All patients showed an excellent clinical and biochemical response to treatment irrespective of type of vitamin D administered. Circulating concentrations of 25-hydroxycholecalciferol and 24,25, 25,26, and 1,25 dihydroxycholecalciferols were abnormally low in the untreated patients. In five patients treated with small doses of cholecalciferol (3000 units, 75 micrograms daily) the concentration of 1,25-dihydroxycholecalciferol rose rapidly to normal and reached supra-normal levels within 72 h. Raised concentrations (up to 200 pg/ml) were sustained for several months and then started falling to normal. Serum 24,25 and 25,26 dihydroxycholecalciferols rose only gradually, after circulating 25-hydroxycholecalciferol concentration had increased to normal. In contrast, in the two patients who received 1,25-dihydroxycholecalciferol (1 microgram daily) serum concentrations of this metabolite rose to normal and only occasionally exceeded the upper limit of normal. The highest concentration observed was 80 pg/ml. Healing of osteomalacia occurred, however, in these two patients in the absence of any measurable increases in 25-hydroxycholecalciferol and 24,25 or 25,26 dihydroxycholecalciferols which all remained abnormally low. Thus, it seems that 1,25-dihydroxycholecalciferol is the most important factor for the healing of vitamin D-deficient osteomalacia and that other hydroxy metabolites are unimportant.

Adolescent↗

PubMed2006

The effects of increasing serum calcitriol on energy and fat metabolism and gene expression.

OBJECTIVE: Evidence from a number of investigations indicates that calcium intake could be inversely related to body weight through alterations in the 1,25-OH(2)-D(3) metabolism. The objective of this study was to test whether energy and substrate metabolism and adipose tissue enzyme mRNA expression can be altered by changes in serum 1,25-OH(2)-D(3) through oral cholecalciferol supplementation in non-obese human subjects. RESEARCH METHODS AND PROCEDURES: An intervention study was used with a treatment period of 7 days. During this intervention, energy expenditure (EE) and substrate metabolism were measured using indirect calorimetry at t = 0, 1, 3, and 7 days, and blood samples were obtained at t = -1, 0, 1, 2, 3, 5 and 7 days. Fat biopsies were obtained at t = 0 and 7 days for determination of expression of genes involved in lipolytic and lipogenic pathways. Subjects from the general community were studied in an ambulatory setting at a university hospital. Ten healthy young men (age, 28 +/- 3 years; BMI, 25.5 +/- 0.5 kg/m(2)) were recruited by local announcement, and all completed the study. All subjects received 2000 IU cholecalciferol/d for 7 days, and they were instructed to consume a low-cholecalciferol, low-calcium diet. EE, fat oxidation, and adipose tissue enzyme mRNA were the main outcome measures. RESULTS: Despite a significant increase in serum 1,25-OH(2)-D(3) concentration at t = 5 and 7 days, no significant differences in substrate and energy metabolism nor mRNA concentrations of different lipid metabolism-related proteins were observed. DISCUSSION: Seven-day supplementation with 2000 IU cholecalciferol/d together with a decrease in dietary calcium intake does not affect EE or substrate metabolism nor gene expression of proteins related to fat metabolism, despite a significant increase in serum 1,25-OH(2)-D(3) concentration.

Adipose Tissue↗

PubMed1968

Enzyme studies on the esterification of vitamin D in rat tissues.

1. The mechanism of vitamin D esterification in the rat was studied with liver, small-intestinal mucosa, pancreatic juice and blood plasma as enzyme sources and [1-(3)H]cholecalciferol, [U-(14)C]ergocalciferol and [4-(14)C]cholesterol as substrates. 2. No esterification of vitamin D could be detected with liver preparations nor with homogenates or acetone-dried powder extracts of intestinal mucosa. 3. Pancreatic juice esterified [1-(3)H]cholecalciferol with oleic acid, and specificity studies indicated that a cholesterol-esterifying enzyme was using vitamin D as substrate. 4. Plasma cholesterol-esterifying enzyme also esterified vitamin D. 5. The specificity of the esterification reaction is discussed in relation to (a) the molecular structure of the substrates and (b) their availability, in a micellar solution, to the enzyme. 6. It is concluded that cholesterol-esterifying enzymes esterify vitamin D in vivo during absorption from the small intestine and while it is transported in blood.

Animals↗

PubMed1978

The relationship between vitamin D-stimulated calcium transport and intestinal calcium-binding protein in the chicken.

1. The rapid stimulation of intestinal Ca(2+) transport observed in vitamin D-deficient chicks after receiving 1,25-dihydroxycholecalciferol has necessitated a re-evaluation of the correlation hitherto observed between this stimulation and the induction of calcium-binding protein synthesis. By 1h after a dose of 125ng of 1,25-dihydroxycholecalciferol, Ca(2+) transport is increased. This is at least 2h before calcium-binding protein can be detected immunologically and 1h before synthesis of the protein begins on polyribosomes, and thus the hormone stimulates Ca(2+) transport before calcium-binding-protein biosynthesis is induced. 2. The maximum increase in Ca(2+) transport observed after this dose of 1,25-dihydroxycholecalciferol (attained by 8h) is similar to that observed after 1.25-25mug of cholecalciferol, but the stimulation is only short-lived, in contrast with the effect observed after the vitamin. At later times after the hormone, however, when Ca(2+) transport has declined to its basal rate, the cellular content of calcium-binding protein remains elevated. 3. Calcium-binding protein is synthesized on free rather than membrane-bound polyribosomes, which implies that it is an intracellular protein. 4. Rachitic chicks require the presence of dietary calcium for maximum stimulation of calcium-binding protein production by cholecalciferol. 5. These results suggest that calcium-binding protein is an intracellular protein, and that its synthesis may be a consequence of the raised intracellular calcium content of the intestinal epithelial cells resulting from 1,25-dihydroxycholecalciferol-stimulated Ca(2+) transport. We propose that calcium-binding-protein synthesis is necessary for maintaining the stimulated rate of Ca(2+) transport, which is initiated by other factors.

Animals↗

PubMed1978

Vitamin D metabolism and expression in rats fed on low-calcium and low-phosphorus diets.

1. Cholecalciferol, radioactively labelled with both (14)C and (3)H, was administered weekly for 7 weeks to rats that had been depleted of vitamin D for 4 weeks before repletion with the radioactive vitamin. This permitted measurement of the steady-state effect on vitamin D metabolism of low-calcium and low-phosphorus regimens, as compared with a normal mineral intake. These dietary manoeuvres were carried out during the last 3 weeks of repletion. Cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were determined in plasma, intestine, kidney and bone. Ca(2+)-binding-protein content was measured in intestine and kidneys of comparable animals. 2. In rats on the low-calcium diets, 1,25-dihydroxycholecalciferol concentration was elevated in plasma, bone, kidney and intestine, and intestinal Ca(2+)-binding protein was increased to over twice the concentration found in the control animals. 3. The low-phosphorus regimens led to a decrease in plasma phosphate and 1,25-dihydroxycholecalciferol in all tissues studied, for the latter to the point where it was undetectable in plasma and bone. Intestinal and renal concentrations of Ca(2+)-binding protein were unchanged in the low-phosphate-intake group and decreased in the very-low-phosphate-intake group. 4. It is concluded that in the rat, unlike in the chick, hypophosphataemia is not associated with a stimulation of the production of 1,25-dihydroxycholecalciferol or its expression in the synthesis of Ca(2+)-binding protein. Therefore the plasma phosphate concentration does not appear to be directly involved in the regulation of the functional metabolism of vitamin D.

Animals↗

PubMed1978

Stimulation of intestinal calcium-binding-protein mRNA synthesis in the nucleus of vitamin D-deficient chicks by 1,25-dihydroxycholecalciferol.

Stimulation of intestinal calcium transport by the hormone 1,25-dihydroxycholecalciferol appears to involve RNA transcriptions and the synthesis of new proteins. Although one of these proteins has been identified as calcium-binding protein, no RNA molecules specifically induced by the hormone in the nucleus have been identified. Nuclear RNA from intestine of vitamin D-deficient chicks before and at various time intervals after treatment with the hormone or cholecalciferol was tested for its ability to code for calcium-binding protein in a cell-free system. Calcium-binding-protein mRNA could only just be detected in the intestinal nuclei 2h after dosing with these steroids which is the same time that it was first observed in the polyribosomes. Thus 1,25-dihydroxycholecalciferol induces the production of new calcium-binding protein by stimulating the formation and rapid release from the nucleus of new mRNA molecules for this protein. Polyribosomal translation of the mRNA continued only as long as it was being synthesized, and the maximum rate of synthesis following a pulse dose of 125ng of the hormone was the same as that observed after prolonged stimulation with cholecalciferol. The possibility that other 1,25-dihydroxycholecalciferol-dependent events may be occurring in the nucleus in the lag period between accumulation of the hormone in the intestine and the appearance of active calcium-binding-protein mRNA, and that these may ultimately control the synthesis of that mRNA, is discussed.

Animals↗

PubMed1988

Receptor-mediated rapid action of 1 alpha,25-dihydroxycholecalciferol: increase of intracellular cGMP in human skin fibroblasts.

The intracellular cGMP concentration in normal human cultured fibroblasts was increased 2- to 3-fold by 1 alpha,25-dihydroxycholecalciferol [1 alpha,25-(OH)2D3] in a dose-dependent manner between 0.01 nM and 1 microM. The response was detectable within 1 min, reached a maximum (225% +/- 8% of baseline) at 6-8 min, and was no longer detectable at 30 min. The half-maximal effect of 1 alpha,25-(OH)2D3 was at 1.8 nM, and 24,25-dihydroxycholecalciferol showed an estimated EC50 100-fold higher. 1 beta,25-Dihydroxycholecalciferol, 25-hydroxycholecalciferol, and cholecalciferol had no detectable effect. Human skin fibroblasts with three different types of 1 alpha,25-(OH)2D3 receptor defect did not respond to 1 alpha,25-(OH)2D3 exposure with cGMP increase; however, the same cells (like normal cells) responded to testosterone or sodium nitroprusside with a rapid rise of cGMP. We conclude that the rapid rise of cGMP in response to calciferols shows an EC50 for 1 alpha,25-(OH)2D3, a cholecalciferol analog specificity, and a cell line dependency that are all suggestive of mediation through a specific 1 alpha,25-(OH)2D3 receptor.

Calcitriol↗

PubMed1977

Maternal nutrition in early pregnancy.

1. Mean daily nutrient intakes of 195 women in the first trimester of pregnancy were assessed by weighed dietary records. 2. In comparsion with recommended intakes for non-pregnant women aged 18-55 years (Department of Health and Social Security, 1969), more than two-thirds of the subjects were having insufficient energy, iron and cholecalciferol. Unsatisfactory intakes of other nutrients were not uncommon. In relation to recommended intakes for the second trimester (Department of Health and Social Security, 1969), all mothers were having insufficient cholecalciferol and more than 80% of mothers had unsatisfactory intakes of energy and Fe. 3. Intakes appreciably lower than those recommended were associated with the following factors: social classes III, IV and V; maternal age under 20 years; smoking ten or more cigarettes daily; vomiting on more than 3 d/week.

Adult↗

PubMed1980

The response of serum 25-hydroxyvitamin D concentrations to vitamin D intake and insolation in sheep.

1. Vitamin D-depleted, housed sheep were given diets providing fixed intakes of cholecalciferol ranging from 0.0 to 0.8 microgram/kg body-wt per d for 220 d. Thereafter they were shorn, deprived of dietary cholecalciferol and turned out from 30 June to 30 November. The concentration of 25-hydroxyvitamin D (25-OHD) in serum was determined at frequent intervals. 2. The serum concentrations of 25-OHD took approximately 10 weeks to stabilize after which they reflected dietary intake over 0.1--0.4 microgram/kg body-wt per d. For intakes of 0.4 and 0.8 microgram/kg body-wt per d the mean maximum concentrations were similar, but the rates of increase differed. The latter was proportional to the logarithm of intake over the range studied. 3. Changes in serum 25-OHD due to insolation were similar in all sheep regardless of their starting values, and consequently in some animals reached levels considerably greater than from the dietary source. 4. Although the response of serum 25-OHD to the higher dietary intakes appeared to be limited there was no evidence of any such control over the response ot endogenously-synthesized vitamin.

Animal Nutritional Physiological Phenomena↗

PubMed1986

Absorption, deposition and distribution of dietary aluminium in immature rats: effects of dietary vitamin D3 and food-borne chelating agent.

We report the levels of aluminium, calcium and potassium in selected tissues of growing rats administered dietary or subcutaneous aluminium, and also the effect of dietary aluminium in combination with cholecalciferol, or with lactose plus a dietary chelating agent. Dietary aluminium decreased the growth rate of normal rats and increased the deposition of aluminium in the tissues. Animals given lactose with a dietary chelator showed a 17 - 100% increase in brain, heart, and muscle aluminium concentration in comparison with those fed aluminium alone. Animals fed both aluminium with cholecalciferol also showed increased levels (12-39%) of aluminium, chiefly in muscle and heart in comparison with those fed aluminium alone. Aluminium deposition was correlated positively with Ca2+ and K+ levels among each of these tissues. We conclude that in normal growing rats aluminium deposition is increased in heart and muscle in the presence of vitamin D3 and in brain, heart and muscle in the presence of lactose and a dietary chelating agent.

Aging↗

PubMed1982

The biological activity of 25-hydroxycholecalciferol and 1,25--dihydroxycholecalciferol for rainbow trout (Salmo gairdneri).

Dietary 25-hydroxycholecalciferol (25-hydroxycholecalciferol (25-OH-D3) and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] showed vitamin D activity in rainbow trout. However, inclusion of dietary cholecalciferol (vitamin D3 or D3), ergocalciferol (vitamin D2 or D2), 25-OH-D3 or 1,25-(OH)2D3 did not result in the presence of detectable levels of vitamin D or 25-OH-D in the blood plasma of the fish. Fish fed the diet devoid of vitamin D over an extended period of time showed symptoms of a droopy-tail or "lordosis-like" syndrome that appeared to be related to muscle weakness since x-ray examination indicated no abnormality in vertebral development. The requirement for vitamin D as cholecalciferol was in excess of 1600 IU/kg diet and may be as high as, or higher than 2400 IU/kg diet.

Animals↗

PubMed2005

A controlled study of vitamin D3 to prevent bone loss in renal-transplant patients receiving low doses of steroids.

BACKGROUND: New and potent immunosuppressive regimens allow for reduced doses of corticosteroids after renal transplantation. The aims of our study were to investigate whether the use of low-dose corticosteroids is associated with a reduction in posttransplant bone loss and to assess the ability of cholecalciferol supplementation to further decrease bone loss in this setting. METHODS: Ninety patients admitted for renal transplantation and scheduled to be treated per protocol with low doses of prednisolone were randomized to receive either 400 mg daily oral calcium (Ca group, n=44) or the same dose of calcium in association with a monthly dose of 25,000 IU of vitamin D3 (CaVitD group, n=46). Bone mineral density (BMD) was measured by dual energy absorptiometry at baseline and at 1 year. RESULTS: The overall population experienced a moderate but significant -2.3+/-0.9% loss of lumbar spine BMD (P<0.01) but no bone loss at the femoral neck and shaft during the first posttransplant year. Bone loss tended to be slightly higher in the CaVitD group, but the difference did not reach statistical significance. Patients in the CaVitD group had significantly higher 25(OH) but not 1,25(OH)2 vitamin D levels. We observed a highly significant negative correlation between 25(OH) vitamin D and intact parathyroid hormone (iPTH) serum levels. CONCLUSIONS: Kidney-transplant recipients receiving modern immunosuppressive regimens with low doses of corticosteroids experience only minimal loss of BMD during the first posttransplant year. Cholecalciferol supplementation did not prevent posttransplant bone loss but contributed to the normalization of iPTH levels after renal transplantation.

Adult↗

PubMed1999

Regulation of small intestinal Na-P(i) type IIb cotransporter by dietary phosphate intake.

Dietary restriction of phosphate is a well-known stimulator (acting indirectly via vitamin D(3)) of small intestinal apical Na-P(i) cotransport. In the present study, we document by Western blots and immunohistochemistry that, in mice, a low-P(i) diet given for several days leads (in parallel to a stimulation of Na-P(i) cotransport) to an increase of the abundance of the type IIb Na-P(i) cotransporter in the brush-border membrane of mouse enterocytes. Similar results were also obtained by an injection of cholecalciferol. The abundance of the type IIb transcript was investigated by Northern blots. These results indicated that the amount of the type IIb transcript was not changed by either low-P(i) diet or cholecalciferol. It is concluded that stimulation of intestinal Na-P(i) cotransport by low-P(i) diet and vitamin D(3) can be explained by an increased amount of type IIb Na-P(i) cotransporters in the brush-border membrane and that augmentation of type IIb Na-P(i) cotransporters is not related to an increased rate of transcription of the type IIb gene.

Animals↗

PubMed2006

Female asylum seekers with musculoskeletal pain: the importance of diagnosis and treatment of hypovitaminosis D.

BACKGROUND: Hypovitaminosis D is well known in different populations, but may be under diagnosed in certain populations. We aim to determine the first diagnosis considered, the duration and resolution of symptoms, and the predictors of response to treatment in female asylum seekers suffering from hypovitaminosis D. METHODS DESIGN: A pre- and post-intervention observational study. SETTING: A network comprising an academic primary care centre and nurse practitioners. PARTICIPANTS: Consecutive records of 33 female asylum seekers with complaints compatible with osteomalacia and with hypovitaminosis D (serum 25-(OH) vitamin D < 21 nmol/l). Treatment intervention: The patients received either two doses of 300,000 IU intramuscular cholecalciferol as well as 800 IU of cholecalciferol with 1000 mg of calcium orally, or the oral treatment only. MAIN OUTCOME MEASURES: We recorded the first diagnosis made by the physicians before the correct diagnosis of hypovitaminosis D, the duration of symptoms before diagnosis, the responders and non-responders to treatment, the duration of symptoms after treatment, and the number of medical visits and analgesic drugs prescribed 6 months before and 6 months after diagnosis. TESTS: Two-sample t-tests, chi-squared tests, and logistic regression analyses were performed. Analyses were performed using SPSS 10.0. RESULTS: Prior to the discovery of hypovitaminosis D, diagnoses related to somatisation were evoked in 30 patients (90.9%). The mean duration of symptoms before diagnosis was 2.53 years (SD 3.20). Twenty-two patients (66.7%) responded completely to treatment; the remaining patients were considered to be non-responders. After treatment was initiated, the responders' symptoms disappeared completely after 2.84 months. The mean number of emergency medical visits fell from 0.88 (SD 1.08) six months before diagnosis to 0.39 (SD 0.83) after (P = 0.027). The mean number of analgesic drugs that were prescribed also decreased from 1.67 (SD 1.5) to 0.85 (SD 1) (P = 0.001). CONCLUSION: Hypovitaminosis D in female asylum seekers may remain undiagnosed, with a prolonged duration of chronic symptoms. The potential pitfall is a diagnosis of somatisation. Treatment leads to a rapid resolution of symptoms, a reduction in the use of medical services, and the prescription of analgesic drugs in this vulnerable population.

25-Hydroxyvitamin D 2↗