Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CHOLECALCIFEROL”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources
PubMed2002

Nutritional interventions related to bone turnover in European space missions and simulation models.

Low energy intake, low calcium intake, low plasma 25-hydroxy-vitamin D or low calcitriol levels, and high salt intake might support the development of space osteoporosis. Therefore, my colleagues and I monitored the daily energy and calcium intakes in eight astronauts during their respective space missions (Spacelab D2, Euromir 94, Euromir 95). In most of these astronauts, energy intake was reduced by more than 20% compared with their calculated energy expenditure. In all three missions, the average daily calcium intake of the eight astronauts was 25% lower than the German recommended daily allowances of 900 mg/d for healthy people without osteoporosis risk. In some astronauts, the calcium intake was extremely low at 53 and 74 mg/d. Sodium intake in these astronauts varied from 39 mEq/d to a very high intake of 462 mEq/d. As a consequence of these results, we examined in the 21-d Mir 97 mission a preventative dietary approach of high calcium intake of at least 1000 mg/d with vitamin D supplementation (650 IU/d of Ergocalciferol) and constant sodium intake (180 mEq/d). Total serum calcium concentration and urinary calcium excretion significantly increased during this mission. Synthesis of 25-OH-cholecalciferol synthesis was markedly reduced because of inadequate ultraviolet light, whereas total 25-OH-Vitamin D levels were unchanged. However, parathyroid hormone and calcitriol levels decreased significantly. Sodium excretion decreased significantly, resulting in positive sodium balances. Based on these results, dietary calcium and vitamin D do not stabilize bone turnover because markers of bone formation were reduced and markers of bone resorption were increased. We concluded that, in contrast to terrestrial conditions, adequate or even high calcium and vitamin D intakes during microgravity do not efficiently counteract the development of space osteoporosis. Conversely, vitamin K (Konakion) seemed to counteract microgravity-induced reduction of bone formation markers. In the 179-d Euromir 95 mission, investigators administered 10 mg of vitamin K from inflight day 86 to day 136 in one astronaut. During and after supplementation, bone formation markers increased significantly during this part of the mission. Therefore, vitamin K seems to play a significant role in bone turnover during space flight.

Aerospace Medicine↗
PubMed2002

[Current topics in pediatric nutrition].

As main current topics in pediatric nutrition we have considered the results of the continuing research on the long term consequences of fetal malnutrition and intra-uterine growth retardation with the concept of metabolic imprinting leading to chronic disease in adulthood, the progresses of knowledge in the fields of iron metabolism and regulatory mechanisms of satiety, hunger and energetic balance, a better determination of recommended docosahexanoic and arachidonic acids intake in the first months of life for premature and term infants, and the studies on probiotics and prebiotics utilization for preventive and curative purposes. The concerns about vitamin D insufficiency in France have markedly decreased with the generalization ten years ago of cholecalciferol supplementation of infant formula, and more recently the authorization of dairy products supplementation. On the contrary the problem of iron deficiency in young children remains, as well as two major nutritional concerns: the very low percentage of breast-fed infants and the dramatic increase of childhood obesity which affects presently 14% of 10 year old children versus 5% in 1980.

Adolescent↗
PubMed1998

In vivo and in vitro effects of boron and boronated compounds.

Boron is ubiquitously present in soils and water. Associated with pectin it is essential for vascular plants as a component of cell walls, and it stabilizes cell membranes. It is required for the growth of pollen tubes and is involved in membrane transport, stimulating H(+)-pumping ATPase activity and K+ uptake. However, a high boron concentration in the soils is toxic to plants and some boronated derivatives are used as herbicides. An absolute requirement for boron has not been definitively demonstrated in animals and humans. However, experiments with boron supplementation or deprivation show that boron is involved in calcium and bone metabolism, and its effects are more marked when other nutrients (cholecalciferol, magnesium) are deficient. Boron supplementation increases the serum concentration of 17 beta-estradiol and testosterone but boron excess has toxic effects on reproductive function. Boron may be involved in cerebral function via its effects on the transport across membranes. It affects the synthesis of the extracellular matrix and is beneficial in wound healing. Usual dietary boron consumption in humans is 1-2 mg/day for adults. As boron has been shown to have biological activity, research into the chemistry of boronated compounds has increased. Boronated compounds have been shown to be potent anti-osteoporotic, anti-inflammatory, hypolipemic, anti-coagulant and anti-neoplastic agents both in vitro and in vivo in animals.

Adult↗
PubMed2002

Effect of high intensity pulsed electric fields and heat treatments on vitamins of milk.

The effects of high intensity pulsed electric field (HIPEF) treatments at room or moderate temperature on water-soluble (thiamine, riboflavin, ascorbic acid) and fat-soluble vitamins (cholecalciferol and tocopherol) were evaluated and compared with conventional thermal treatments. Vitamin retention was determined in two different substrates, milk and simulated skim milk ultrafiltrate (SMUF). Samples were subjected to HIPEF treatments of up to 400 micros at field strengths from 18.3 to 27.1 kV/cm and to heat treatments of up to 60 min at temperatures from 50 to 90 degrees C. No changes in vitamin content were observed after HIPEF or thermal treatments except for ascorbic acid. Milk retained more ascorbic acid after a 400 microstreatment at 22.6 kV/cm (93.4%) than after low (63 degrees C-30 min; 49.7% retained) or high (75 degrees C-15s; 86.7% retained) heat pasteurisation treatments. Retention of ascorbic acid fitted a first-order kinetic model for both HIPEF and thermal processes. First-order constant values varied from 1.8 x 10.4 to 1.27 x 10(-3) micros(-1) for the HIPEF treatments (18.3-27.1 kV/cm) and, for thermal processing ranged from 5 x 10(-3) to 8 x 10(-2) min(-1) (50-90 degrees C). No significant differences were found between the results obtained after applying HIPEF treatments at room or moderate temperature. However, results depended on the treatment media. A beneficial effect of natural skim milk components, mainly proteins, was observed on the preservation of ascorbic acid, since skim milk retained more ascorbic acid than SMUF after HIPEF treatments.

Animals↗
PubMed2004

Mineral water fortified with folic acid, vitamins B6, B12, D and calcium improves folate status and decreases plasma homocysteine concentration in men and women.

OBJECTIVE: We investigated the effects of mineral water fortified with folic acid, vitamins B(6), B(12), D and calcium on folate concentrations in serum and erythrocytes, serum vitamin B(12) and plasma homocysteine concentrations in free-living subjects. In addition, we investigated the bioavailability of calcium added to mineral water by measuring urinary calcium excretion and serum alkaline phosphatase activity. DESIGN: Randomized, controlled, double-blinded, parallel design. SETTING: Outpatient dietary intervention with free-living subjects in Eastern Finland. SUBJECTS: Altogether, 66 subjects were recruited for the study. In all, 60 subjects completed the study. INTERVENTIONS: The study began with a 2-week run-in period followed by an 8-week intervention period. During the intervention study, subjects consumed mineral water fortified with folic acid (563 microg/day), vitamins B(6) (1 mg/day), B(12) (7.5 microg/day), cholecalciferol (0.6 microg/day) and calcium (563 mg/day) or placebo mineral water. RESULTS: The fortified mineral water increased serum and erythrocyte folate concentrations by 16.1+/-5.6 nmol/l (P<0.001) and 199+/-76 nmol/l (P<0.001), respectively, and decreased plasma homocysteine concentration by 1.6 micromol/l (P<0.001). Urinary calcium excretion and serum alkaline phosphatase activity for 24 h increased significantly (P<0.001 and P=0.01 respectively) in the intervention group. CONCLUSIONS: Mineral water fortified with folic acid, vitamins B(6), B(12) and D and calcium enhanced folate status and reduced plasma homocysteine concentration in normohomocysteinemic subjects without folate deficiency. Indirect measures of calcium and bone metabolism indicated that the calcium used in the fortification of the mineral water was bioavailable.

Adult↗
PubMed2000

Direct detection of large fat-soluble biomolecules in solution using membrane inlet mass spectrometry and desorption chemical ionization.

This paper presents the first membrane inlet mass spectrometry system capable of detecting large biomolecules, such as testosterone (M(r) 288), testosterone acetate (M(r) 330) and alpha-tocopherol (M(r) 430, vitamin E). The result was obtained using a home-made chemical ionization ion source with a thermostated tubular silicone membrane mounted right in the centre of a methane CI plasma. The liquid sample was flushed through the inside of the membrane for a period of 20-25 min, where the analyte diffused into the membrane. Following this trapping period the analyte was released from the membrane into the mass spectrometer by the combined action of heat radiation from the filament and charge transfer from the chemical ionization plasma. As a result of this stimulated desorption a good desorption peak was obtained as the analyte vaporized out of the membrane. Retinol (M(r) 286, vitamin A), cholecalciferol (M(r) 384, vitamin D3) and cholesterol (M(r) 386) were also detected. However, these compounds (all containing a long hydrocarbon chain and being aliphatic alcohols) did not give a protonated molecule. They gave a series of cluster ions with the dominant located 20 mass units below the molecular ion. The detection limits of the new desorption chemical ionization MIMS technique were at low or sub-micromolar concentrations (high ppb levels) and the reproducibility was within 20%, when the area of the desorption peak was used for quantitation.

Humans↗
PubMed1976

The transport of vitamin D in the serum of primates.

"Transcalciferin" (the serum transport protein for cholecalciferol and related substances) of two New World monkeys, Cebus apella and Cebus albifrons, was found to be immunologically identical with the transcalciferin of other monkeys and partially with that of man. In contrast with the alpha-globulin mobility of the transcalciferin of other primates, the transcalciferin of cebus monkey has the electrophoretic mobility of albumin. Most of the serum 25-hydroxycholecalciferol was precipitable with isolated monospecific anti-(human transcalciferin) gamma-globulins but not with anti-(human albumin) gamma-globulins. These results indicate that the transport of 25-hydroxycholecalciferol in the cebus monkey is not due to albumin itself but to transcalciferin with the electrophoretic mobility of albumin. Similar variants of transcalciferin also exist in man.

Animals↗
PubMed1981

Vitamin D metabolism and its possible role in the developing chick embryo.

The relationship between bone formation and vitamin D metabolism was investigated in the developing chick embryo. Fertilized White Leghorn eggs were incubated at 38 degrees C in an incubator for 21 days. The fresh weight and calcium content of embryonic tibiae began to increase at day 12 and attained maximal values at day 19. Bone alkaline phosphatase and citrate decarboxylation activities, both of which represent osteoblastic activity, also began to increase at days 10-12, reached maximal values at day 19 and sharply declined thereafter. Both bone enzyme activities were highly correlated with CA2+-binding activity in the chorioallantoic membrane measured by the Chelex 100 assay. When mesonephric and metanephric homogenates were incubated with 25-hydroxy[3H]cholecalciferol, a marked and concomitant increase occurred in the metanephric 1 alpha- and 24-hydroxylase activity after day 14. The production of 1 alpha, 25-dihydroxycholecalciferol attained a maximal value at day 19 and decreased thereafter, whereas that of 24,25-dihydroxycholecalciferol continued to increase until hatching. The production rate of 1 alpha, 25-dihydroxycholecalciferol by the metanephros coincided with the changes in Ca2+-binding activity in the chorioallantoic membrane and osteoblastic activity. Since both intestinal calcium absorption and bone mineral mobilization do not occur in embryonic life, these results support the idea that 1 alpha, 25-dihydroxycholecalciferol may be involved directly in bone formation or induction of a calcium-binding protein in the chorioallantoic membrane.

Allantois↗
PubMed1983

The effects of 24R,25-dihydroxycholecalciferol and of 1 alpha,25-dihydroxycholecalciferol on ornithine decarboxylase activity and on DNA synthesis in the epiphysis and diaphysis of rat bone and in the duodenum.

The effect of cholecalciferol metabolites on ornithine decarboxylase activity and on DNA synthesis in developing long bones was investigated in vitamin D-depleted rats. In the epiphysis there was a 6.4-fold increase in ornithine decarboxylase activity 5 h after a single injection of 24R,25-dihydroxycholecalciferol but not of 24S,25-dihydroxycholecalciferol or other vitamin D metabolites. In comparison, in the diaphysis and duodenum, 1 alpha,25-dihydroxycholecalciferol, but not other vitamin D metabolites, caused a 3-3.5-fold increase in the enzyme activity. The enzyme activity in the tissues examined attained a maximal value at 5 h after the injection of the metabolites. The activity of ornithine decarboxylase in the epiphysial region increased dose-dependently as the result of a single injection of 24R,25-dihydroxycholecalciferol and attained a maximal value at a dose between 30 and 3000 ng. In addition, administration of 24R,25-dihydroxycholecalciferol, but not 24S,25-dihydroxycholecalciferol or other metabolites, caused within 24 h a 1.7-2.0-fold increase in [3H]thymidine incorporation into DNA of the epiphyses of tibial bones. In comparison, 1 alpha,25-dihydroxycholecalciferol caused a 1.5-fold increase in [3H]thymidine incorporation into DNA of the diaphyses and of the duodenum. The present data indicate that 24R,25-dihydroxycholecalciferol is involved in the regulation of epiphyseal growth, whereas 1 alpha,25,dihydroxycholecalciferol stimulates the proliferation of cells in the diaphysis of long bones and in the intestinal mucosa.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Actin affinity chromatography in the purification of human, avian and other mammalian plasma proteins binding vitamin D and its metabolites (Gc globulins).

The human plasma protein binding vitamin D and its metabolites (Gc globulin; group-specific component) has been isolated from human plasma by column affinity chromatography on gels to which monomeric actin was covalently attached. Rabbit skeletal-muscle G-actin was covalently coupled to amino-agarose gels before the application of human plasma. At actin/protein molar ratios of 4-8:1, excellent recovery (approximately 58%) of purified binding protein was achieved. After 0.75 M-NaCl washes, the binding protein was eluted from the columns in 3 M-guanidinium chloride, dialysed and analysed. These eluates contained the binding protein as 34-100% of the total protein, reflecting a 130-fold average purification in this single step. In the presence of Ca2+, gelsolin (another plasma protein that binds actin) was apparently retained by the affinity column, but this was prevented by chelation of plasma Ca2+. The actin affinity step also was effective in the isolation of the binding protein from rat, rabbit and chicken plasma, as indicated by autoradiographs of purified fractions analysed by gel electrophoresis after incubation with 25-hydroxy[26,27-3H]cholecalciferol. Further isolation by hydroxyapatite chromatography yielded a purified binding protein which displayed characteristic binding activity toward vitamin D metabolites and G-actin, and retained its physicochemical features. This brief purification sequence is relatively simple and efficient, and should prove to be useful to investigators studying this interesting plasma protein.

Actins↗
PubMed1987

Synthesis of 1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol by calvarial cells. Characterization of the enzyme systems.

The synthesis of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and 24,25-dihydroxycholecalciferol [24,25(OH)2D3] from 25-hydroxycholecalciferol [25(OH)D3] has previously been shown to occur in cells isolated from bone. The main findings of the present study are that the enzyme systems which catalyse these syntheses are: (1) active at 'in vitro' substrate concentrations over the range of 2-50 nM; (2) regulatable in a complex way by 1,25(OH)2D3, 24,25(OH)2D3, 25,26-dihydroxycholecalciferol and 25(OH)D3, but not by cholecalciferol ('vitamin D3'); and (3) have relatively short half-lives (approx. 5 h).

24,25-Dihydroxyvitamin D 3↗
PubMed1996

Genomic mechanisms involved in the pleiotropic actions of 1,25-dihydroxyvitamin D3.

The biologically active metabolite of vitamin D (cholecalciferol), i.e. 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], is a secosteroid hormone whose mode of action involves stereospecific interaction with an intracellular receptor protein (vitamin D receptor; VDR). 1,25(OH)2D3 is known to be a principal regulator of calcium homeostasis, and it has numerous other physiological functions including inhibition of proliferation of cancer cells, effects on hormone secretion and suppression of T-cell proliferation and cytokine production. Although the exact mechanisms involved in mediating many of the different effects of 1,25(OH)2D3 are not completely defined, genomic actions involving the VDR are clearly of major importance. Similar to other steroid receptors, the VDR is phosphorylated; however, the exact functional role of the phosphorylation of the VDR remains to be determined. The VDR has been reported to be regulated by 1,25(OH)2D3 and also by activation of protein kinases A and C, suggesting co-operativity between signal transduction pathways and 1,25(OH)2D3 action. The VDR binds to vitamin D-responsive elements (VDREs) in the 5' flanking region of target genes. It has been suggested that VDR homodimerization can occur upon binding to certain VDREs but that the VDR/retinoid X receptor (RXR) heterodimer is the functional transactivating species. Other factors reported to be involved in VDR-mediated transcription include chicken ovalbumin upstream promoter (COUP) transcription factor, which is involved in active silencing of transcription, and transcription factor IIB, which has been suggested to play a major role following VDR/RXR heterodimerization. Newly identified vitamin D-dependent target genes include those for Ca2+/Mg(2+)-ATPase in the intestine and p21 in the myelomonocytic U937 cell line. Elucidation of the mechanisms involved in the multiple actions of 1,25(OH)2D3 will be an active area of future research.

Amino Acid Sequence↗
PubMed1996

Ligand-dependent enhancement of human antithrombin gene expression by retinoid X receptor alpha and thyroid hormone receptor beta.

We studied potential modulators of antithrombin gene expression. A putative hormone response element (HRE) was identified by sequence similarity analysis of the antithrombin promoter, situated between nucleotides -92 and -54 relative to the transcription start site. This HRE contains three hexa-nucleotide motifs with an AGGTCA consensus, which are potential targets of members of the steroid/thyroid superfamily of nuclear receptors. Stimulation of the hepatoma cell line HepG2 with the receptor ligands L-3,5,3'-tri-iodothyronine, all-trans retinoic acid, or their combination, increased production of antithrombin into the culture medium by 1.3-, 1.6-, and 2.0-fold, respectively. In contrast, the receptor ligand 1,25-dihydroxy-cholecalciferol[1,25-(OH)2VitD3] did not influence antithrombin production. Analysis of promoter chloramphenicol acetyl-transferase (CAT) constructs, showed that the first 86 bp of the antithrombin promoter region are sufficient for basal transcription. The DNA length polymorphism of 32 bp or 108 bp, located upstream of position -276, did not influence anti-thrombin promoter activity. The antithrombin promoter activity dropped to background values when deleting the region -97/-49 of promoter fragment -453/+57. Transactivation of the antithrombin promoter by retinoid X receptor alpha (RXR alpha) (5-7-fold) or thyroid hormone receptor beta (TR beta) (4-5-fold) was only observed when at least -167/+57 bp of the promoter region is present in CAT constructs, and when the appropriate ligand of the nuclear receptor was added. This transactivation was not observed upon deletion of the antithrombin promoter region -97/-49. With three copies of the antithrombin promoter fragment -109/-42 in front of the thymidine kinase minimal promoter, transactivation was only obtained with RXR alpha, and not with TR beta. In conclusion, these results indicate that the ligand-dependent enhancement of antithrombin gene expression is regulated by RXR alpha as well as by TR beta. Transactivation of antithrombin gene expression by RXR alpha and TR beta appears to be dependent upon the presence of promoter region up to nucleotide -167. The HRE segment (-109/-42) only confers RXR alpha responsiveness to a heterologous promoter. Further study is needed to unravel the exact nature of this HRE and its 5'-flanking sequences.

Antithrombin III↗
PubMed2004

Adipocyte cholesterol balance in obesity.

Adipose tissue is specialized in the storage of energy in the form of triacylglycerol. Within the fat cell, triacylglycerols are found in a well-defined structural compartment called the lipid droplet, which occupies the vast majority of the fat cell volume. However, many other lipids are present in the lipid droplet. These include sterols, carotenoids, cholecalciferol and lipophilic toxic pollutants of the environment such as dioxins and tocopherols. The topic of this article is the role of fat cell cholesterol in adipose tissue physiology and its potential implication in pathological states such as obesity.

Adipose Tissue↗
PubMed1978

A radioimmunoassay for 1,25-dihydroxycholecalciferol.

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.

Animals↗
PubMed2001

1Alpha,25-dihydroxyvitamin D3 protects human keratinocytes from apoptosis by the formation of sphingosine-1-phosphate.

Owing to its ability to induce growth arrest and differentiation of keratinocytes, 1alpha,25-dihydroxyvitamin D3 and its analogs are useful for the treatment of hyperproliferative skin diseases, such as psoriasis vulgaris. It has been implicated that the 1alpha,25-dihydroxyvitamin D3-induced differentiation of keratinocytes is mediated, at least in part, by the formation of ceramides; however, ceramides have also been identified to induce apoptosis in many cells, including keratinocytes. Therefore, it was of interest to investigate the influence of 1alpha,25-dihydroxyvitamin D3 on apoptosis in keratinocytes. Most interestingly, physiological concentrations of 1alpha,25-dihydroxyvitamin D3 did not induce apoptosis in keratinocytes, despite the formation of ceramides. Moreover, 1alpha,25-dihydroxyvitamin D3 appeared cytoprotective and made keratinocytes resistant to apoptosis induced by ceramides, ultraviolet irradiation, or tumor necrosis factor-alpha. The cytoprotective effect was accompanied by the formation of the sphingolipid breakdown product sphingosine-1-phosphate, which prevented apoptosis in analogy to 1alpha,25-dihydroxyvitamin D3. The effect of 1alpha,25-dihydroxyvitamin D3 was specific as the almost inactive precursor cholecalciferol neither induced sphingosine-1-phosphate formation nor prevented cells from apoptosis. Besides this, the cytoprotective aptitude of 1alpha,25-dihydroxyvitamin D3 was completely abolished by the sphingosine kinase inhibitor N,N-dimethylsphingosine, which blocked sphingosine-1-phosphate formation. Moreover, sphingosine-1-phosphate was able to restore the cytoprotective effect of 1alpha,25-dihydroxyvitamin D3 in the presence of N,N-dimethylsphingosine. Taken together, here we report for the first time that 1alpha,25-dihydroxyvitamin D3 protects keratinocytes from apoptosis and additionally this cytoprotection is mediated via the formation of sphingosine-1-phosphate.

Apoptosis↗
PubMed1996

Acute biochemical effects of growth hormone treatment compared with conventional treatment in familial hypophosphataemic rickets.

OBJECTIVE: Conventional treatment of familial hypophosphaiaemic rickets with oral phosphate and 1 alpha-hydroxycholecalciferol (1 alpha HCC) does not satisfactorily correct the metabolic or physical defects of the disease and can have adverse effects, such as nephrocalcinosis. Hyperoxaluria from increased oral phosphate intake may contribute to nephrocalcinosis. Growth hormone enhances renal tubular phosphate reabsorption and 1,25-dihydroxy-cholecalciferol production in normal and in GH deficient individuals, and may thus be of benefit to patients with familial hypophosphataemic rickets. PATIENTS: We have assessed the acute effects of GH on phosphate and calcium metabolism in 6 children (age 4-14 years) with familial hypophosphataemic rickets. DESIGN: Each patient served as his/her own control and received the following in a sequential non-randomized design: conventional treatment with oral phosphate 1.0-3.4 mmol/kg/day in 3-6 divided doses and 1 alpha HCC 18-31 ng/kg/day-no treatment-GH 0.05 mg/kg daily-GH and 1 alpha HCC-and GH with phosphate and 1 alpha HCC. Each treatment was given for 7 days with 7 day periods of no treatment in between. MEASUREMENTS AND RESULTS: Glomerular filtration rate, tubular maximum rate of phosphate reabsorption per litre of glomerular filtrate (TmP/GFR) and serum 1,25-dihydroxycholecalciferol increased with GH. Mean 24-hour plasma phosphate concentrations did not increase with GH but were higher in the treatment phases which included phosphate and 1 alpha HCC (P = 0.002). Serum PTH was higher when GH was given in combination with phosphate and 1 alpha HCC compared to other phases. Urine oxalate excretion did not differ between the treatment phases. CONCLUSIONS: GH seemed to partially correct the defects in renal tubular phosphate transport and 1 alpha-hydroxylation of 25-hydroxycholecalciferol. We speculate that the net effect of GH treatment was an increase in body phosphate, although this was not reflected in a change in plasma phosphate. Therefore, GH in combination with 1 alpha HCC may act as a phosphate sparing agent, permitting treatment with lower and less frequent doses of oral phosphate and reducing adverse effects such as nephrocalcinosis.

Adolescent↗
PubMed1999

Expression of genes involved in calcium absorption in human duodenum.

BACKGROUND: The role of vitamin D metabolites in the regulation of expression of genes involved in dietary calcium absorption by the human intestine remains poorly understood despite much work in animals. MATERIALS AND METHODS: To investigate this, we measured the expression of transcripts for two of these genes, calbindin-D9k and the basolateral membrane calcium pumping ATPase, PMCA1, in duodenal endoscopic biopsies from 40 subjects. Northern blots were hybridized with previously characterized probes, and the signal was quantified by phosphor imaging. These transcript levels were related to circulating vitamin D metabolites and also analysed according to the vitamin D receptor gene TaqI polymorphism determined in DNA from blood. RESULTS: Plasma 1,25-dihydroxycholecalciferol correlated significantly with calbindin-D9k RNA (r = 0.4, P < 0.02) but not with PMCA1. Plasma 25-OH-cholecalciferol was not correlated with transcripts for either gene and, furthermore, the mean levels of these transcripts did not differ significantly when grouped by vitamin D receptor genotype. CONCLUSION: In normal humans, 1, 25-dihydroxycholecalciferol has a small but significant relationship to duodenal expression of calbindin-D9k, but not to PMCA1 expression.

Calbindins↗