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At least 631 records · Page 35Linked to original sources
PubMed1989

Vitamin D3 administration increases the membrane fluidity of intestinal mitochondria.

The fluorescence anisotropy in the mitochondria from vitamin D-treated chicks is significantly lower than that from the vitamin D-deficient animals with the inner core probe DPH. Surface membrane fluidity, measured with the probe TMA-DPH, shows no differences between the organelles of both groups. The fluorescence studies performed in mitochondrial subfractions revealed that cholecalciferol treatment induces a decrease of lipid order parameter S (DPH) in the mitochondrial inner membrane. These results pose the question of whether vitamin D3 participates in the regulation of physiological function of the intestinal mitochondria through changes in the physical properties of the membranes.

Animals↗
PubMed1988

Hypercalcemia associated with rodenticide poisoning in three cats.

Hypercalcemia (12.0 to 18.3 mg/dl) was detected in 3 cats that had eaten a rodenticide that contained cholecalciferol. Clinical signs included lethargy, anorexia, vomiting, and polydipsia. Treatment with furosemide and fluids administered IV resulted in normalization of the serum calcium concentration and in remission of the clinical signs in 2 cats. One cat with a serum calcium concentration of 18.3 mg/dl did not have clinical signs, was not treated, and was reportedly normal 9 months after initial examination. We attributed the uniformly favorable outcome of exposure to the rodenticide in these cats to the small quantity of the toxin ingested.

Animals↗
PubMed1986

[Effect of bile on intestinal calcium and vitamin D absorption. Animal experiment studies in swine].

In the human system calcium is the major constituent of bone and the regulator of important bioelectric and biochemical effects. Calcium homeostasis is underlying exact control mechanisms in which vitamin D is a predominant factor. Cholecalciferol (VD3) is metabolized and the active form 1 alpha, 25-dihydroxycholecalciferol (1,25(OH)2D3) is formed by the kidney. 1,25(OH)2D3 acts on the cell nuclei and on the luminal membrane of the intestinal mucosal cell. It enhances intestinal Ca absorption and the Ca transport to the blood system. VD3 metabolism and mechanisms of action are reported in the introduction. Early reports have described the important influence of bile for the intestinal Ca absorption. Up to now conclusive investigations are missing and became major topics as new regulator mechanisms were described recently. One of the main questions arising is, whether VD3 and other vitamin D metabolites can be absorbed in the absence of the biliary system and which effect on the enterocyte can be observed. Intestinal Ca absorption and transport was estimated in piglets using triple lumen tube system and duodenal perfusion. 4 untreated animals and 3 experimental animals with bile deprivation for a period of 5 (7) days were studied. Ductus choledochus ligation and concommittant cholecysto-colic anastomosis was applied for this purpose. The effect of vitamin D metabolites was estimated on 3 experimental animals applying a daily dosage of 600.000 I.E. VD3 orally, measuring Ca absorption 5 days afterwards; 3 animals in addition were administered a daily dosage of 2 micrograms 1,25(OH)2D3, measuring the Ca absorption 5 (7) days afterwards. Electrolytes, bilirubin, transaminases, total protein, albumin, triglycerides, Ca, phosphate, alkaline phosphatase, parathormone (PTH), 25 hydroxycholecalciferol (25OHD3) and 1,25(OH)2D3 were measured in all the animals before and after the experimental procedure. Data were calculated statistically. VD3 absorption was measured in 3 untreated control animals and 3 animals with bile deprivation, absorption of 1,25(OH)2D3 in 2 animals with bile deprivation. The basis for the evaluation of the experimental model was given by the laboratory values after bile deprivation. Changes in electrolyte and intermediary metabolism were observed postoperatively only and are assigned to the surgical treatment, thus ruling out severe metabolic disorders, which means that the experimental model should be appropriate for our purpose to look for Ca homeostasis.(ABSTRACT TRUNCATED AT 400 WORDS)

Alanine Transaminase↗
PubMed1986

[Comparative studies of calcium resorption modified by vitamin D2 and D3 in patients with chronic renal failure and dialysis patients].

In 16 patients with a chronic renal insufficiency at the stage of the compensated retention and 13 test persons of the chronic haemodialysis programme determinations of the total calcium and of the ionized calcium fraction as well as investigation of the intestinal calcium absorption by means of the isotope 47Ca were performed. In these cases the influence of vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) on these parameters of the calcium metabolism was compared. Under the treatment with vitamin D a normalization of the serum calcium levels concerning the total calcium concentration as well as with regard to the ionized calcium fraction was achieved; this effect took place parallel to the improvement of the intestinal calcium absorption. Vitamin D3, had a more favourable effect than vitamin D2. The necessary doses are below 40,000 U a day.

Blood Urea Nitrogen↗
PubMedDate not supplied

[Effect of combined vitamin D and E deficiencies on calcium metabolism and bone tissue of the rat].

In experiments on young rats a study was made of the influence of combined vitamin D and E deficiency on biochemical signs of rickets. It was shown that in intact animals vitamin E deficiency induced moderate hypocalcemia, a tendency to decreased Ca active transport in the small intestine and mineral saturation of the bone tissue, as well as a significantly increased Ca content in the skeletal muscles and heart. The concentration of 25-oxyvitamin D (25-OVD) in the blood serum of these animals was not changed. Combined vitamin D and E deficiency intensified disorders typical for rickets; sometimes synergy of such a negative effect was recorded. A delay in the recovery of Ca metabolism parameters, bone tissue condition and 25-OVD circulating concentration persisted, when the animals with vitamin D and E deficiency were injected cholecalciferol during 6 days. The data obtained have evidenced a possible role of vitamin E deficiency in the rickets development, that is, probably, mediated, to a certain extent, by its influence on metabolism and (or) biochemical function of vitamin D.

Animals↗
PubMed1984

[Does calcifediol replace vitamin D as a preventive and therapeutic agent?].

Cholecalciferol (CC) given orally is not utilized as efficiently as the CC produced by cutaneous UV light. The infant receives only minute amounts of CC by breast feeding, abolishing therefore the role of a vitamin for CC. The most important D-metabolite of human milk, the calcifediol (CF), however, has transient vitamin character. CF is both resorbed more efficiently by the intestine and it effects mineral metabolism faster via kidney than CC, which needs hydroxylation in the liver first. Thus CF shows advantages in prophylaxis and therapy. However, different (lower) dosages and the danger of hypercalcemia should be kept in mind using CF.

Breast Feeding↗
PubMed1980

[Osteomalacia due to vitamin D deficiency. Part One: mechanisms (author's transl)].

Vitamin D deficiency is in most cases subclinical and can only be detected by blood vitamin assays or biochemical changes in phosphorus and calcium metabolism. Clinical and radiological osteomalacia is much less common. It is due to prolonged and profound hypovitaminaemia, which in turn depends upon a variety of factors, the main one being defective photosynthesis. Low vitamin D dietary intake apparently does not result in osteomalacia unless it is accompanied by insufficient exposure to sun. Malabsorption of cholecalciferol results from steatorrhoea of various origina. Disorders in hepatic 25-hydroxylation are due to drug enzymatic induction and seem to be unrelated to the state of the renal function. Disorders in renal 1,25-hydroxylation may be consecutive to reduced renal tissue, impaired stimulation, or inhibiton or even congenital lack of 1-alpha hydroxylase.

Adult↗
PubMed1981

[Nutrition and bone metabolism (author's transl)].

Calcium and phosphate metabolism as well as those substances which are essential in regulating this metabolism (parathyroid hormone, thyrocalcitonin and cholecalciferol) are briefly discussed. Of three known forms of bone disease (nutritional secondary hyperparathyroidism, rickets and hypervitaminosis A), the clinical symptoms, radiological changes, (histo)pathological findings, therapeutic procedures as well as the aetiological, pathogenic and pathophysiological features will be reviewed.

Animal Nutritional Physiological Phenomena↗
PubMedDate not supplied

Secondary hyperparathyroidism in chronic renal failure.

The metabolic bone disease associated with chronic renal failure has been described collectively by the terms "renal osteodystrophy" or "renal-glomerular-osteodystrophy" and consists of osteomalacia, osteitis fibrosa, and osteosclerosis. The skeletal abnormalities may occur either alone or in combination with one another. An increased concentration of circulating immunoreactive-parathyroid hormone (i-PTH) is a recognized feature of patients with chronic renal failure, and the values are usually much higher than those found in patients with primary hyperparathyroidism associated with a parathyroid adenoma. It must, however, be recognized that the high circulatory concentrations of parathyroid hormone found in patients with chronic renal failure are of immunoassayable material which may or may not be of biological significance in respect of activity. A disturbance in the homeostatic control mechanism governing parathyroid hormone, the secretion rate, its metabolism, and target organ resistance to its action are of major importance in the pathogenesis of some aspects of the metabolic bone disease in patients with chronic renal failure. The pathogenesis of the secondary hyperparathyroidism of chronic renal failure, however, also involves disturbances in cholecalciferol metabolism, phosphate retention, and the uremic state per se.

Calcium↗
PubMed1995

Effect of winter oral vitamin D3 supplementation on cardiovascular risk factors in elderly adults.

OBJECTIVE: A possible role for vitamin D deficiency in contributing to the winter increase in cardiovascular disease mortality was investigated by testing the effect of vitamin D supplementation on blood pressure and other cardiovascular risk factors during winter. DESIGN: Randomised double-blind trial of vitamin D supplementation in winter. SUBJECTS: Men and women, mean age 70 years (range 63-76) recruited from general practitioner age-sex registers in Cambridge (UK). INTERVENTION: 95 people received a single oral dose of 2.5 mg cholecalciferol and 94 received the placebo at baseline interviews during December 1991. Follow-up assessment was 5 weeks later during January 1992. RESULTS: Comparing follow-up with baseline assessment, serum 25-hydroxyvitamin D increased in the treated group and decreased slightly in the placebo group [mean (s.d.) change: 7.2 (+/- 3.8) vs -1.4 (+/- 1.1) ng/ml, P = 0.0001]; while parathyroid hormone decreased in the treated, and increased in the placebo, group [-0.27 (+/- 0.78) vs 0.13 (+/- 0.75) pmol/l, P = 0.0004]. However, the mean change in blood pressure was similar in both groups: systolic -5 (+/- 13) vs -5 (+/- 16) mmHg, P = 0.81; diastolic -1 (+/- 9) vs -1 (+/- 9), P = 0.92; as was the mean change in serum cholesterol [-0.07 (+/- 0.52) vs -0.05 (+/- 0.60) mmol/l, P = 0.81]. In contrast, the mean change in radial pulse was significantly decreased in the treated group compared with placebo [-2 (+/- 9) vs 1 (+/- 7) beats per min, P = 0.030]. CONCLUSIONS: The failure of vitamin D supplementation to change blood pressure or serum cholesterol suggests that the winter increase in these factors is not caused by decreased vitamin D levels.

Aged↗
PubMedDate not supplied

[Vitamin D3 metabolism in the liver of pregnant rats].

The exchange of vitamin D3 in the liver of pregnant rats has been studied. Incorporation of (3H)-vitamin D3 into the liver of pregnant rats on the 13th and 21st day of pregnancy made up 85% and 90% respectively of the intensity of absorption of the summary label by controlled animals. It is found that the period of exchange of (3H)-cholecalciferol in these animals increases with prolongation of pregnancy. The 25-hydroxylation of vitamin D3 in the liver of rats on the 13th and 21st day of pregnancy significantly decreases and makes up 30% and 50% of its hydroxylation in the nonpregnant rats.

Animals↗
PubMed1995

CD49f (alpha 6 integrin) and CD66a (BGP) are specifically induced by retinoids during human monocytic differentiation.

Retinoic acid (RA) and 1,25(OH)2-cholecalciferol (VitD3) are potent regulators of normal and malignant myeloid cells. In the human monoblast cell line U-937 they induce terminal differentiation, and the resulting phenotypes display both common and distinct, inducer-specific, properties. This paper shows that in U-937 cells the two retinoids, all-trans and 9-cis RA, induced the expression of CD49f (alpha 6 integrin subunit) and CD66a (biliary glycoprotein, BGP) mRNA and protein. In contrast, expression of CD49f and CD66a was not found in untreated or VitD3-induced cells. Cytokine-induced modulation of CD49f and CD66a expression was restricted to the retinoid-induced U-937 cells. The retinoid specific induction of CD49f and CD66a was confirmed in the related monoblastic cell line THP-1. Human blood monocytes and the monocytic cell line Mono Mac 6 responded poorly to RA, with respect to the regulation of CD49f and CD66a expression, indicating that early monocytic precursors were targets for the retinoid-specific regulation. Thus, the expression of CD49f and CD66a is developmentally regulated and specifically induced by all-trans and 9-cis Ra in human monocytic cells.

Antigens, CD↗
PubMed1995

Evaluation of a radioimmunoassay for determination of calcitriol in human sera employing a 125I-labelled tracer.

The performance characteristics of a radioimmunoassay employing a 125I-labelled tracer for determination of calcitriol in human sera are reported. The assay is based on an immunoextraction step employing a monoclonal antibody against calcitriol followed by a radioimmunoassay (using 125I-labelled calcitriol and sheep antiserum against calcitriol). Bound/free separation is performed with an anti-sheep IgG antibody bound to cellulose. Within-run imprecision (n = 20) was 12.8% (mean = 9.4 ng/l) and 11.1% (mean = 48.8 ng/l), between-day imprecision (n = 11) was 27.1% (mean = 9.6 ng/l) and 17.2% (mean = 47.2 ng/l). Linearity of dilution as investigated by mixing pooled sera containing 62.0 ng/l and 4.7 ng/l calcitriol, respectively. The relationship between measured and expected concentrations was characterized by a linear correlation coefficient of r = +0.990. The values obtained with the 125I-based radioimmunoassay were compared with those obtained with a radioreceptor-assay using a 3H-labelled tracer; the regression line was y = 1.091 x -4.545 (n = 84; r = +0.935), where y = calcitriol [125I] [ng/l] and x = calcitriol [3H] [ng/l]. Mixing 9 volumes of sera from patients with renal insufficiency (n = 7) with 1 volume of 'calibrator F' (assigned value: 227 ng/l) yielded recovery rates of 90 +/- 8% (mean +/- SD). The detection limit was 3.0 ng/l. The cross-reactivity of cholecalciferol metabolites was found to be < 0.00003 for 25-hydroxycholecalciferol, 24R,25-dihydroxycholecalciferol and 25S,26-dihydroxycholecalciferol. A preliminary reference interval (5th to 95th percentile) was established in 40 apparently healthy persons (17 males and 23 females; age range: 20-61 [mean: 32] years) (19-74 ng/l). The method presented shows high practicability and may therefore be considered as a useful alternative to cumbersome assays using 3H-labelled tracers.

Adult↗
PubMedDate not supplied

[Interaction of C27-sterols with erythrocyte membranes].

It is established in the in vitro experiments that the interaction of natural C27-sterols: cholesterol, 7-dehydrocholesterol, cholecalciferol (vitamin D3), calcitriol (1 alpha, 25-dihydroxyvitamin D3), ecdysterone (20-hydroxyecdysone) and 2-deoxyecdysterone modulate both lipid and protein phases of human erythrocyte membrane at the concentration range 10(-6)-10(-12) M. These effects depend on the sterols concentration and on the number and position of hydroxy groups in the sterol molecules.

Calcitriol↗
PubMed1998

Low-molecular-weight hormonal factors that affect head formation in Hydra.

Support or inhibition of DAG-induced head formation: Hydra magnipapillata can be caused to form ectopic head structures by periodictreatmentwith PKC activators such as diacylglycerol (DAG). This ectopic head formation is supported by an extract from the ovine pineal gland that contains low-molecular-weight compounds. The frequency of ectopic head formation is also increased when DAG is paired with one of several lipophilic hormonal factors: (1) pinoline, a putative pineal hormone derived from tryptophan, (2) 12-S-HETE, a paracrine derivative of arachidonic acid, or (3) 1alpha, 25 dihydroxyvitamine D3, a hormonal factor also known as calcitriol. Dose-response curves were non-monotonic passing a maximum at low dosages. By contrast, DAG lost its capacity to induce ectopic head structures when it was paired with the provitamin D3, cholecalciferol. Patterning the head: one eicosanoid was found which influences patterning without being combined with DAG: 12-R-HETE caused growth-based elongation of the tentacles and an increase in the number of tentacles without affecting the longitudinal body pattern. Similar effects are brought about by substances that interfere with tyrosine phosphorylation, most potently bythe phosphotyrosine phosphatase inhibitor bisperoxo-(1,10-phenanthroline)-oxovanadate (V). The results speak for the existence of head-inducing hormonal factors, underline the significance of content protein kinases to pattern formation and point to a negative influence of the vitamin D3 content of the food on the capacity of the animals to develop head structures.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1998

Growth inhibitory effects of 1,25-dihydroxyvitamin D3 and its synthetic analogue, 1alpha,25-dihydroxy-16-ene-23yne-26,27-hexafluoro-19-nor-cholecalcifero l (Ro 25-6760), on a human colon cancer xenograft.

The effect of 1,25-dihydroxyvitamin D3 and its synthetic analogue, 1alpha,25-dihydroxy-16-ene-23yne-26,27-hexafluoro-19-n or-cholecalciferol (Ro 25-6760), have been evaluated both in vitro and in vivo in human colorectal cancer cell lines expressing high (HT-29) and low (SW-620) levels of vitamin D receptor. 1,25-Dihydroxyvitamin D3 caused significant dose-dependent growth inhibition of HT-29 cells at concentrations ranging from 10(-11) to 10(-6). The antiproliferative effect of Ro 25-6760 on HT-29 cells was also dose-dependent with cell counts on day 6, ranging from 98% of control at 10(-11) M to 14% of control at 10(-6) M. However, 1,25-dihydroxyvitamin D3 and Ro 25-6760 did not have any growth inhibitory effect on SW-620 at all concentrations. In mice with HT-29 tumor xenografts, administration of vitamin D at 0.1 and 0.2 microg/injection i.p. three times/week did not cause any significant tumor growth delay, whereas synthetic analogue Ro 25-6760, at both concentrations, caused a significant tumor growth inhibition in comparison with the control arm. In 30% of mice treated by R0 25-6760 the tumors disappeared on average after the second injection, and tumor growth did not resume after drug withdrawal. However, both 1,25-dihydroxyvitamin D3 or Ro 25-6760 had no growth inhibitory effect at all applied concentrations in mice with the SW-620 tumor xenografts. The mechanism for this impressive growth inhibition is not yet elucidated and warrants further investigation.

Animals↗
PubMed1998

[Pharmacological prevention of osteoporosis in patients on corticosteroid medication].

Twenty-five per cent of the patients using corticosteroids for long periods of time develops at least one fracture. Corticosteroids lead to osteoporosis through increase of renal calcium excretion and decrease of intestinal calcium absorption, bone formation by osteoblasts and serum levels of sex hormones. In spite of guidelines according to which patients protractedly using corticosteroids should take sufficient calcium and cholecalciferol, only about one-tenth of them takes any form of medication to prevent osteoporosis. It seems advisable to prescribe additional anti-osteoporosis medication for patients using > or = 7.5 mg prednisone during at least 3 months and who have a low mineral density of bone; only of biphosphonates a preventive effect clearly has been demonstrated. For postmenopausal women, hormonal supplementation therapy may offer additional benefit, reducing the risk of cardiovascular disease.

Adrenal Cortex Hormones↗
PubMed2002

Alveolar and postcranial bone density in postmenopausal women receiving hormone/estrogen replacement therapy: a randomized, double-blind, placebo-controlled trial.

BACKGROUND: We conducted a 3-year, double-blind, randomized, placebo-controlled study to determine whether the positive effects of hormone/estrogen replacement therapy (H/ERT) on postcranial bone density are accompanied by similar positive effects on oral bone mass. METHODS: A total of 135 postmenopausal women (aged 41-70 years) with no evidence of moderate or severe periodontal disease were randomized to receive daily oral conjugated estrogen (Premarin; 0.625 mg) alone or in combination with medroxyprogesterone acetate (Prempro; 0.625 and 2.5 mg, respectively) or placebo. All subjects received calcium carbonate (1000 mg/d) and cholecalciferol (400 [corrected] IU/d) supplements. The primary efficacy end points were the changes in alveolar crest height and alveolar bone density. Alveolar crest height was measured on bite-wing radiographs, and changes in alveolar bone mass were assessed by means of digital-subtraction radiography. Postcranial bone density was measured in the lumbar spine and left proximal femur by means of dual-energy x-ray absorptiometry. RESULTS: Hormone/estrogen replacement therapy significantly increased alveolar bone mass compared with placebo (+1.84% vs +0.95% [P =.04]), and tended to improve alveolar crest height (+4.83% vs +3.46% [P =.34]). Bone mineral density of the proximal femur significantly increased in the H/ERT compared with the placebo group (total proximal femur, +3.59% vs +0.22% [P =.001]; neck, +2.05% vs -0.34% [P =.02]; trochanter, +3.49% vs +0.08% [P<.001]), but not the lumbar spine (+1.01% vs +0.17% [P =.39]). Changes in alveolar bone mass correlated with bone density changes in the total femur (r = 0.28 [P =.02]) and femoral trochanter (r = 0.25 [P =.04]) in the H/ERT but not in the placebo group. CONCLUSIONS: Postcranial and oral bone mass were increased in postmenopausal women receiving H/ERT. Improvement in oral bone health constitutes an additional benefit of H/ERT.

Absorptiometry, Photon↗