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PubMed1997

The effects of ultraviolet light and cholecalciferol and its metabolites on the development of leg abnormalities in chickens genetically selected for a high and low incidence of tibial dyschondroplasia.

Four experiments were conducted to investigate the effects of ultraviolet (UV) light exposure and several cholecalciferol metabolites on the development of tibial dyschondroplasia (TD) and other parameters associated with vitamin D metabolism in chickens selected for high (HTD) and low (LTD) incidence of TD. In Experiment 1, exposure of chickens to UV light reduced the incidence and severity of TD more in LTD chickens than in HTD chickens, as evident by the significant interactions (P < 0.10 and 0.04). In Experiment 2, the addition of cholecalciferol to diets that were deficient in cholecalciferol linearly decreased the incidence of vitamin D rickets and increased bone ash, but increased the incidence of severe TD. The LTD chickens had a higher maximal bone ash of 40.0 +/- 0.7% than did the HTD chickens, which had a maximal bone ash of 37.0 +/- 0.7%. In Experiment 3, the addition of 5 micrograms/kg of 25-hydroxycholecalciferol [25-(OH)D3], 1-alpha-hydroxycholecalciferol, or 1,25- dihydroxycholecalciferol decreased the incidence and severity of TD in the LTD chickens and had no effect on TD in HTD chickens. In Experiment 4, increasing dietary 25-(OH)D3 increased plasma 25-(OH)D3 levels in both lines, but HTD chickens had higher plasma 25-(OH)D3 levels at 20 and 40 micrograms/kg of dietary 25-(OH)D3. The incidence and severity of TD were reduced in the LTD chickens by dietary 25-(OH)D3, but little effect was noted in HTD chickens. The LTD chickens reached a maximal bone ash at 9.7 +/- 1.9 micrograms/kg and HTD chickens reached the same bone ash at 33.0 +/- 7.0 micrograms/kg. These results indicate that UV light and vitamin D metabolites are not effective in preventing TD in HTD chickens, but that altered vitamin D metabolism does exist between HTD and LTD chickens.

Analysis of Variance↗

PubMed1995

Copper malabsorption after intestinal resection in rats. Effects of cholecalciferol and ascorbic acid.

Dietary modifications can partly compensate for the alterations in copper homeostasis caused by distal intestinal resection, by improving biliary function. We studied the effects of resecting 50% of the distal small intestine (DSI) on copper status in rats fed three semisynthetic diets (basal diet, and basal diet with cholecalciferol or ascorbic acid). Intestinal resection significantly decreased the digestive (apparent digestibility coefficient; ADC) and metabolic utilization (balance) of copper 1 month after surgery. However, the supplementation of the basal diet with cholecalciferol attenuated the negative impact of surgery, leading to small differences in Cu ADC and Cu balance between transected and resected rats. Ascorbic acid also enhanced copper retention. Copper status was not as markedly affected by intestinal resection as digestive utilization 1 month after the operation. The beneficial effects of cholecalciferol and ascorbic acid at the digestive and metabolic levels suggest ways to lessen the impact of intestinal resection, and to avoid possible long-term postabsorptive alterations in copper distribution.

Animals↗

PubMed1984

Fecal loss of cholecalciferol in gastrectomized rats.

Rats were gastrectomized, and the intestinal absorption and fecal excretion of cholecalciferol were studied following the administration of radioactive cholecalciferol, either by subcutaneous injection or with the aid of a gastric tube. From measurements of radioactivity in feces and sera it has been possible to establish that gastrectomy in rats results in impaired intestinal absorption and increased fecal excretion of cholecalciferol. These findings indicate that gastrectomy alters the nutritional status of vitamin D, and may explain the high incidence of osteomalacia as a complication of gastrectomy.

Animals↗

PubMedDate not supplied

Prophylaxis and treatment of childhood rickets with parenteral cholecalciferol.

The safety and efficacy of parenteral cholecalciferol was evaluated in the treatment and prevention of childhood rickets. Children with active disease, and those at high risk for developing rickets were treated either with intravenous or intramuscular cholecalciferol in dosages of 1000 to 1500 IU daily, for periods of 28 to 450 days. All children with rickets responded with radiographic evidence of healing. No child in the prophylaxis group developed bone disease. Side effects were minimal. Parenteral cholecalciferol is a safe and effective therapy for the treatment and prevention of childhood rickets.

Alkaline Phosphatase↗

PubMed2006

Alendronate with and without cholecalciferol for osteoporosis: results of a 15-week randomized controlled trial.

OBJECTIVE: Many osteoporosis patients have low 25-hydroxyvitamin D (25OHD) and do not take recommended vitamin D amounts. A single tablet containing both cholecalciferol (vitamin D3) and alendronate would improve vitamin D status concurrently, with a drug shown to reduce fracture risk. This study assessed the efficacy, safety, and tolerability of a once-weekly tablet containing alendronate 70 mg and cholecalciferol 70 microg (2800 IU) (ALN + D) versus alendronate 70 mg alone (ALN). METHODS: This 15-week, randomized, double-blind, multi-center, active-controlled study was conducted during a season when 25OHD levels are declining, and patients were required to avoid sunlight and vitamin D supplements for the duration of the study. Men (n = 35) and postmenopausal women (n = 682) with osteoporosis and 25OHD >or= 9 ng/mL were randomized to ALN + D (n = 360) or ALN (n = 357). MAIN OUTCOME MEASURES: Serum 25OHD, parathyroid hormone, bone-specific alkaline phosphatase (BSAP), and urinary N-telopeptide collagen cross-links (NTX). RESULTS: Serum 25OHD declined from 22.2 to 18.6 ng/mL with ALN (adjusted mean change = -3.4; 95% confidence interval [CI]: -4.0 to -2.8), and increased from 22.1 to 23.1 ng/mL with ALN + D (adjusted mean change = 1.2; 95% CI: 0.6 to 1.8). At 15 weeks, adjusted mean 25OHD was 26% higher (p < 0.001, ALN + D versus ALN), the adjusted relative risk (RR) of 25OHD < 15 ng/mL (primary endpoint) was reduced by 64% (incidence 11% vs. 32%; RR = 0.36; 95% CI: 0.27 to 0.48 [p < 0.001]), and the RR of 25OHD < 9 ng/mL (a secondary endpoint) was reduced by 91% (1% vs. 13%; RR = 0.09; 95% CI: 0.03 to 0.23 [p < 0.001]). Antiresorptive efficacy was unaltered, as measured by reduction in bone turnover (BSAP and NTX). CONCLUSION: In osteoporosis patients who avoided sunlight and vitamin D supplements, this once-weekly tablet containing alendronate and cholecalciferol provided equivalent antiresorptive efficacy, reduced the risk of low serum 25OHD, improved vitamin D status over 15 weeks, and was not associated with hypercalcemia, hypercalciuria or other adverse findings, versus alendronate alone.

Aged↗

PubMed2005

Body fat and cholecalciferol supplementation in elderly homebound individuals.

Vitamin D deficiency, observed mainly in the geriatric population, is responsible for loss of bone mass and increased risk of bone fractures. Currently, recommended doses of cholecalciferol are advised, but since there are few studies evaluating the factors that influence the serum levels of 25-hydroxyvitamin D (25(OH)D) following supplementation, we analyzed the relationship between the increase in serum 25(OH)D after supplementation and body fat. We studied a group of 42 homebound elderly subjects over 65 years old (31 women) in order to assess whether there is a need for adjustment of the doses of cholecalciferol administered to this group according to their adipose mass. Baseline measurements of 25(OH)D, intact parathyroid hormone and bone remodeling markers (osteocalcin and carboxy-terminal fraction of type 1 collagen) were performed. Percent body fat was measured by dual-energy X-ray absorptiometry. The patients were divided into three groups according to their percent body fat index and were treated with cholecalciferol, 7,000 IU a week, for 12 weeks. The increases in serum levels of 25(OH)D were similar for all groups, averaging 7.46 ng/mL (P < 0.05). It is noteworthy that this increase only shifted these patients from the insufficiency category to hypovitaminosis. Peak levels of 25(OH)D were attained after only 6 weeks of treatment. This study demonstrated that adipose tissue mass does not influence the elevation of 25(OH)D levels following vitamin D supplementation, suggesting that there is no need to adjust vitamin D dose according to body fat in elderly homebound individuals.

Absorptiometry, Photon↗

PubMed1990

The rate of bone mineral loss in normal men and the effects of calcium and cholecalciferol supplementation.

OBJECTIVE: To determine the rate of bone loss in normal men, and to examine the effects of dietary calcium and cholecalciferol supplementation on bone loss in men. DESIGN: Double-blinded, placebo-controlled 3-year trial of supplementation with calcium (1000 mg/d) and cholecalciferol (25 micrograms/d). SETTING: Clinical research center at a university medical facility. SUBJECTS: Normal men 30 to 87 years old, recruited from the Portland community. MEASUREMENTS AND MAIN RESULTS: Radial bone mineral content (assessed by single-photon absorptiometry) fell by 1.0%/y (95% CI, -1.3% to 0.7%) at a proximal radial site and 1.0%/y (95% CI, -1.4% to -0.6%) at a distal radial site. Vertebral bone mineral content (assessed by dual-energy quantitative computed tomography) declined by 2.3%/y (95% CI, -2.8% to -1.8%). In these healthy men with a high basal dietary calcium intake (1159 mg/d), calcium and cholecalciferol supplementation did not affect bone loss at any site. CONCLUSIONS: Normal men experience a substantial bone loss at both axial and appendicular sites that is not prevented by calcium and vitamin D supplementation in a well-nourished population.

Adult↗

PubMed2003

[Cholecalciferol Reference Standard (Control 031) of National Institute of Health Sciences].

The raw material of cholecalciferol was examined for the preparation of the "Cholecalsiferol Reference Standard (Control 031)", The analytical data obtained were: melting point, 86.3 degrees C; UV spectrum, lambda max of 264.6 nm and specific absorbance in ethanol at 265 nm = 483.6; IR spectrum, same as that of the cholecalciferol Reference Standard (Control 003); optical rotation [alpha]20(D) = 105.1 degrees; thin-layer chromatography, one impurity was detected at 50 micrograms; high-performance liquid chromatography, total amount of impurities estimated to be less than 0.04%. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Cholecalciferol Reference Standard (Control 031) of the National Institute of Health Sciences.

Chemical Phenomena↗

PubMed2006

Cholecalciferol (vitamin D3) and the retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) are synergistic for chemoprevention of prostate cancer.

Prostate cancer, the most commonly diagnosed cancer among American men, develops slowly over many years. The long latent period of 20 to 30 years, involved in the multistep process of carcinogenesis, provides an important opportunity to block or reverse progression to a malignant state. Vitamin A (retinoids) and vitamin D not only have the ability to block steps in the process of carcinogenesis but they can also modulate or reverse some malignant characteristics of cancer cells. However, at high levels, vitamins A and D have undesirable side effects, thus, limiting effective dose levels and efficacy. Therefore, combination treatment at low doses, to increase efficacy and avoid toxicity, is of special interest. This study examines the effects of the synthetic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) in combination with cholecalciferol (vitamin D3) on growth, and on the expression of vimentin, matrix metalloproteinase-2 (MMP-2), and retinoid and vitamin D receptor expression, using the non-tumorigenic, human prostate epithelial cell line RWPE-1. Treatment with 4-HPR and cholecalciferol resulted in synergistic growth inhibition when compared to that caused by each agent alone. A decrease in vimentin expression and MMP-2 activity, and up-regulation of vitamin D receptor (VDR) and some of the retinoid-X (RXRs) and retinoic acid receptor (RARs) subtypes, was observed. These results suggest that combined treatment with 4-HPR and cholecalciferol, at doses lower than what might be effective with single agents, increases their efficacy and suggest that this may serve as an effective strategy for chemoprevention and treatment of prostate cancer.

Anticarcinogenic Agents↗

PubMed1984

Phosphate intestinal secretion and absorption by isolated ileal loop: effects of cholecalciferol and diet phosphate.

The effect of diet phosphate content and cholecalciferol on intestinal phosphate secretion and absorption was investigated in rachitic chicks. Phosphate absorption was determined by the in situ ligated loop technique. Phosphate secretion was estimated by a method proposed by the authors. Hydroxyapatite, placed in the lumen of a ligated loop, acts as trapping agent of 32P leaving the intestinal tissue. The fraction of rapid exchangeability of tissue phosphate was taken as the precursor pool of secreted phosphate. Control chicks fed diets containing 0.3% P (group 1) or 1.0% (group 2) showed similar Pi absorption; the secretion was larger for group 2. After cholecalciferol treatment for 2 or 4 consecutive days an increment of Pi absorption with simultaneous reduction of Pi secretion was evident for both groups of animals. Chicks treated for 7 days gave values similar to those of controls. It is concluded that the regulation of intestinal phosphate absorption and secretion could be one important mean of homeostatic control. Intestinal phosphate movement is adapted to dietary phosphate and is partially independent of cholecalciferol.

Animals↗

PubMed1993

[Cholecalciferol Reference Standard (Control 921) of National Institute of Health Sciences].

The raw material for cholecalciferol was tested for preparation of the "Cholecalciferol Reference Standard (Control 921)". Analytical data obtained were as follows: melting point, 89.9 degrees C; UV and infrared spectra, the same as those for JP Cholecalciferol Reference Standard (Control 901), respectively; specific absorbance at 265 nm E1%1 cm = 472.2; optical rotation, [alpha]20D = 107.1 degrees; thin-layer chromatography and high-performance liquid chromatography (HPLC), no impurities were detected; assay, 99.97% by HPLC. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Reference Standard (Control 921).

Cholecalciferol↗

PubMed1994

Effects of type of dietary fat and cholecalciferol on magnesium absorption in rats with intestinal resection.

We studied the effect of type of dietary fat and supplementation with cholecalciferol on magnesium absorption in the duodenum, jejunum and proximal colon in rats with resection of 50% of the distal small intestine. Magnesium transport against the concentration gradient was found to occur in all three intestinal segments, although transport increased significantly only in the proximal colon of intestinally resected rats fed a diet supplemented with cholecalciferol at a rate of 0.425 mg/kg diet and mixture of equal parts of medium chain triglycerides, sunflower oil and olive oil as the source of dietary fat (diet B), in comparison with magnesium absorption in control rats subjected to intestinal transection and fed diet B, and in resected rats fed a diet without cholecalciferol supplementation and in which olive oil was the sole source of dietary fat (diet A). Magnesium absorption due to active and passive transport together, was greater in resected than in transected rats in all three intestinal segments, although the difference was significant only in the jejunum (the segment closest to the anastomosis), because of the greater increase in mucosal mass in resected animals. When the three intestinal segments were compared, magnesium absorption in favour of and against the concentration gradient in the proximal colon was significantly greater than in the duodenum or the jejunum, in resected and transected animals fed diet A or diet B. These findings show that the colon is the segment that most efficiently absorbs magnesium in rats with intestinal resection, especially when diet B is given.

Animals↗

PubMed1995

[Cholecalciferol reference standard (Control 941) of the National Institute of Health Sciences].

The raw material for cholecalciferol was tested for preparation of the "Cholecalciferol Reference Standard (Control 941)". Analytical data obtained were as follows: melting point, 88.5 degrees C; UV and infrared spectra, the same as those for JP Cholecalciferol Reference Standard (Control 923), respectively; specific absorbance at 265 nm E1%1cm = 471; optical rotation, [alpha]20D = +107.3 degrees; thin-layer chromatography and high-performance liquid chromatography (HPLC), no impurities were detected, respectively; assay, 101.3% by HPLC. Based on the above results, the candidate raw material was authorized as the Japanese Pharmacopoeia Reference Standard (Control 941).

Chemical Phenomena↗

PubMed2001

Serum 25-hydroxy cholecalciferol in infants and preschool children in the Western region of Saudi Arabia. Etiological factors.

OBJECTIVE: Low vitamin D status has been frequently reported among Saudi subjects of all ages. No attempt has been made to relate this status to dietary intake or to diseases leading to malabsorption, for example diarrhea. This study was performed to investigate the various factors leading to low vitamin D status, and their relative importance in infants and preschool children. METHODS: Nine hundred and thirty-five healthy subjects aged 4-72 months were selected randomly form the Jeddah area of the Kingdom of Saudi Arabia. Medical history, time and frequency of exposure to sunlight and dietary intake were recorded. Blood samples were obtained form 739 subjects for the determination of 25-hydroxy cholecalciferol. The Subjects were divided into 5 age groups. The mean +/- standard deviation and other statistical parameters for serum 25-hydroxy cholecalciferol were calculated. Mean +/- standard deviations of exposure time and vitamin D intake were calculated, and subjects divided according to the adequacy of their intake. RESULTS: Age had no effect on the mean serum 25-hydroxy cholecalciferol (p=0.63). Mean dietary intake of the vitamin increased initially (p<0.05), decreased in the next group (p<0.005), then remained constant. There was significant correlation between serum level and dietary intake of the vitamin. No exposure to sunlight was noted in the youngest group. Low serum levels were associated mainly with repeated diarrheal attacks. This was the same in the next group. The mean exposure time in the 3rd group increased significantly (p<0.001). Low serum levels were found in subjects with low exposure time plus either or both of low dietary intake and repeated attacks of diarrhea. Increased mean exposure time (p<0.0005), and decreased incidence of repeated diarrheal attacks were found in the next age group with low serum levels noted in subjects with low exposure time and low dietary intake. In the oldest age group, mean exposure time increased further (p<0.0005), and low levels were found in subjects with low exposure time (mainly girls). CONCLUSION: Diet was the major source of the vitamin in subjects <12 months of age, and hence low levels were associated with frequent diarrheal attacks. A decrease in dietary intake, and more dependence on endogenous vitamin synthesis was apparent in older children, leading to low vitamin status in ones with low dietary intake and inadequate exposure to sunlight

Age Factors↗

PubMed1980

Stability of solid drugs: degradation of ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) at high humidities and elevated temperatures.

Ergocalciferol and cholecalciferol powders were studied at 25 and 40 degrees and at different humidities. Ergocalciferol decomposed rapidly at 25 and 40 degrees when stored in dry air. Decomposition of ergocalciferol led to the formation of products of higher polarity. Cholecalciferol was not as labile under dry conditions, but decomposed rapidly at high temperature.

Cholecalciferol↗

PubMed1983

The effect of cholecalciferol in vivo on proteins and lipids of skeletal muscle from rachitic chicks.

The protein and lipid constituents of skeletal muscle subcellular fractions isolated from chicks fed a vitamin D-deficient diet for 3 weeks and chicks replated with cholecalciferol (vitamin D3) were analyzed. Administration of the sterol markedly altered the protein composition of mitochondria. The changes were localized in the inner membranes and consisted of a modification of the relative amounts of proteins of approximate mol wt of 83,000, 58,000, 42,000, and 34,000. In addition, treatment with vitamin D3 modified the distribution pattern of components of the actomyosin contractile complex. An increase in actin and troponin C was particularly noticeable. No differences between rachitic and treated animals were detected in the protein composition of sarcoplasmic reticulum membranes and postmicrosomal soluble fraction. A significant increase in the phospholipid content of sarcoplasmic reticulum (P less than 0.05), and to a lesser extent of mitochondria, was observed in repleted chicks. The relative proportions of individual phospholipids, however, were not changed. Injection of an acute dose of cholecalciferol to chicks less severely depleted in vitamin D significantly stimulated the incorporation of 32PO4 in vivo to muscle homogenates, mitochondria, and sarcoplasmic reticulum (P less than 0.05). As the increases in specific activities of sarcoplasmic inorganic P and membrane lipid P were similar whereas that of serum remained unchanged, the results are compatible with the idea that vitamin D3 stimulates phosphate fluxes across muscle membranes. The sterol produced minor modifications in the fatty acid composition of sarcoplasmic reticulum (P less than 0.05).

Animals↗

PubMed1987

The cholecalciferol sulphate system in mammals.

7-Dehydrocholesterol sulphate has been identified in human and rat skin. The compound was isolated by anion exchange chromatography and following hydrolysis it was characterized by high-performance liquid chromatography and gas chromatography-mass spectrometry. Experiments with rats showed that 7-dehydrocholesterol sulphate can serve as a precursor of cholecalciferol sulphate and 25-hydroxy-cholecalciferol 3-sulphate, the latter compound being present in significant amounts in human blood. The sulphated sterols identified represent a previously unknown secosteroid system in mammals.

Animals↗

PubMed1982

Cholecalciferol sulfate identification in human milk by HPLC.

Synthetic vitamin D3 sulfate was prepared by reacting cholecalciferol with sulfamic acid in pyridine. Vitamin D3 sulfate ammonium salt was purified by crystallisation and transformed in sulfate sodium salt. Homogeneity was controlled by reverse phase high pressure liquid chromatography (HPLC). Purified synthetic vitamin D3 sulfate sodium salt was used as a reference. Milk whey was obtained after protein precipitation by adding ethanol. Vitamin D3 sulfoconjugate was identified in supernatant (lyophylized) after purification by Sephadex LH 20 and HPLC. Milk whey purified fraction obtained exhibited the same ultra-violet absorption (UV) as synthetic vitamin D3 sulfate; after solvolysis, cholecalciferol was liberated from natural and synthetic sulfoconjugate. The results confirmed that vitamin D3 sulfate was present in human milk.

Cholecalciferol↗