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PubMed1994

Vitamin D prophylaxis during infancy: comparison of the long-term effects of three intermittent doses (15, 5, or 2.5 mg) on 25-hydroxyvitamin D concentrations.

Serum 25-hydroxyvitamin D [25(OH)D], calcium, phosphorus, and alkaline phosphatase activities were measured from birth to 6-9 mo of age in 60 healthy neonates to assess the effectiveness and potential toxicity of three intermittent oral doses of cholecalciferol. Two weeks after a first dose of 15, 5, or 2.5 mg, 25(OH)D concentrations reached 307 +/- 160, 150 +/- 55, and 92 +/- 42 nmol/L, respectively. Prolonged vitamin D overload, up to 6 mo, was found in 50% of the children given 15 mg, but not in the other infants. Serum calcium transiently increased 2 wk after 15 mg but not after the lower doses. Oral doses of 2.5 mg given every 3 mo appear to provide the best protection against vitamin D deficiency and vitamin D overload in high-risk infant populations that are unsuitable for daily vitamin D supplementation.

25-Hydroxyvitamin D 2↗
PubMed1996

Increased efficiency of calcium absorption during short periods of inadequate calcium intake in girls.

Adequate calcium intake is essential for skeletal integrity, particularly during the period of peak bone mass acquisition from 9 to 17 y of age. Currently, the calcium intake of many adolescent girls is below the recommended dietary allowance. The purpose of this study was to evaluate the ability of girls to respond to acute periods of inadequate dietary calcium intake. Calcium absorption was evaluated in 11 girls aged 11.6 +/- 2.4 y after 10 d on both a low-calcium (7.05 +/- 2.03 mmol/d) and a high-calcium (35.30 +/- 2.28 mmol/d) diet. Fractional calcium absorption was determined by using oral (46Ca) and intravenous (42Ca) stable isotopes of calcium. During a low calcium intake, fractional calcium absorption was significantly greater (0.582 +/- 0.087 compared with 0.260 +/- 0.068, P < 0.0001) and urinary calcium excretion was significantly lower (1.30 +/- 0.83 compared with 3.08 +/- 1.98 mmol/d, P < 0.004) than values obtained during a high calcium intake. Concentrations of 1,25-dihydroxyvitamin D (combination of cholecalciferol and ergocalciferol) were greater during the low calcium intake, although the difference was not significant (108.7 +/- 30.6 compared with 90.0 +/- 25.1 pmol/L, P < 0.1; n = 9). Excretion of N-telopeptide was significantly greater during the low calcium intake (761 +/- 508 compared with 413 +/- 341 nmol bone collagen equivalent (BCM)/mmol creatinine, P < 0.02; n = 9), indicating that bone resorption was increased. These results suggest that during short periods of inadequate calcium intake, girls are able to significantly increase the efficiency of calcium absorption and decrease urinary calcium losses to conserve calcium required for bone mineral acquisition.

Absorption↗
PubMed2000

Decreased bioavailability of vitamin D in obesity.

BACKGROUND: Obesity is associated with vitamin D insufficiency and secondary hyperparathyroidism. OBJECTIVE: This study assessed whether obesity alters the cutaneous production of vitamin D(3) (cholecalciferol) or the intestinal absorption of vitamin D(2) (ergocalciferol). DESIGN: Healthy, white, obese [body mass index (BMI; in kg/m(2)) > or = 30] and matched lean control subjects (BMI </= 25) received either whole-body ultraviolet radiation or a pharmacologic dose of vitamin D(2) orally. RESULTS: Obese subjects had significantly lower basal 25-hydroxyvitamin D concentrations and higher parathyroid hormone concentrations than did age-matched control subjects. Evaluation of blood vitamin D(3) concentrations 24 h after whole-body irradiation showed that the incremental increase in vitamin D(3) was 57% lower in obese than in nonobese subjects. The content of the vitamin D(3) precursor 7-dehydrocholesterol in the skin of obese and nonobese subjects did not differ significantly between groups nor did its conversion to previtamin D(3) after irradiation in vitro. The obese and nonobese subjects received an oral dose of 50000 IU (1.25 mg) vitamin D(2). BMI was inversely correlated with serum vitamin D(3) concentrations after irradiation (r = -0.55, P: = 0.003) and with peak serum vitamin D(2) concentrations after vitamin D(2) intake (r = -0.56, P: = 0.007). CONCLUSIONS: Obesity-associated vitamin D insufficiency is likely due to the decreased bioavailability of vitamin D(3) from cutaneous and dietary sources because of its deposition in body fat compartments.

Adult↗
PubMed2006

The case against ergocalciferol (vitamin D2) as a vitamin supplement.

Supplemental vitamin D is available in 2 distinct forms: ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). Pharmacopoeias have officially regarded these 2 forms as equivalent and interchangeable, yet this presumption of equivalence is based on studies of rickets prevention in infants conducted 70 y ago. The emergence of 25-hydroxyvitamin D as a measure of vitamin D status provides an objective, quantitative measure of the biological response to vitamin D administration. As a result, vitamin D3 has proven to be the more potent form of vitamin D in all primate species, including humans. Despite an emerging body of evidence suggesting several plausible explanations for the greater bioefficacy of vitamin D3, the form of vitamin D used in major preparations of prescriptions in North America is vitamin D2. The case that vitamin D2 should no longer be considered equivalent to vitamin D3 is based on differences in their efficacy at raising serum 25-hydroxyvitamin D, diminished binding of vitamin D2 metabolites to vitamin D binding protein in plasma, and a nonphysiologic metabolism and shorter shelf life of vitamin D2. Vitamin D2, or ergocalciferol, should not be regarded as a nutrient suitable for supplementation or fortification.

Biomarkers↗
PubMed2001

Overview of hypercalcemia of malignancy.

The etiology, pathophysiology, and diagnosis of hypercalcemia associated with malignant diseases are discussed. In humans, calcium is controlled by three mechanisms: parathyroid hormone, which regulates bone resorption and renal reabsorption of calcium; calcitonin, an antagonist of parathyroid hormone; and cholecalciferol, which regulates calcium absorption from the gastrointestinal tract. Hypercalcemia of malignancy (HCM) results primarily from increased bone resorption by osteoclasts and, to a lesser extent, from increased renal tubular reabsorption. In most tumors, parathyroid hormone-related protein (PTHrP) is the primary mediator of calcium. PTHrP stimulates increased bone resorption by osteoclasts. This stimulation also activates transforming growth factor-beta (TGF-beta), which stimulates tumor cells, thus perpetuating the cycle. Hypercalcemia is usually defined as a serum calcium concentration greater than 12 mg/dL, corrected for the serum albumin concentration. In diagnosing HCM, it is important to rule out other causes of hypercalcemia, such as primary hyperparathyroidism.

Bone Resorption↗
PubMed1998

Separation from related compounds and assay of calcipotriol by high-performance liquid chromatography.

In this paper, two methods are presented. One involves the separation of calcipotriol, a new synthetic analogue, from two related compounds, specifically cholecalciferol (Vitamin D3) and calcitriol (1,25-dihydroxyvitamin D3). The other involves the isolation and assay of calcipotriol from a topical ointment. The study was performed with reversed-phase high-performance liquid chromatography using an RP18 column and ultraviolet detection. Applying the method of Snyder, a mobile phase mixture containing methanol-acetonitrile-water (67:23:10, v/v) was found which achieved a total separation within 18 min. A mobile phase of methanol-water (80:20, v/v) attained a slower elution of calcipotriol. For isolation and assay of calcipotriol from an ointment (Daivonex), dissolution in chloroform gave the highest recovery (> 98%). The isolation and assay process can be performed within 2 h.

Acetonitriles↗
PubMed1978

Differential response of calcium transport systems in laying hens to exogenous and endogenous changes in vitamin D status.

Changes in intestinal calcium absorption, calcium deposition into egg shell, and intestinal, renal and uterine calcium-binding protein (CaBP) in laying hens were related to changes in 25 hydroxycholecalciferol-1-hydroxylase activity (1-hydroxylase), or to the supplementation of 1alpha-hydroxycholecalciferol (1alpha-OH-CC). The onset of egg production resulted in an increased kidney 1-hydroxylase activity and intestinal and uterine CaBP. Renal concentrations of CaBP remained unchanged. Intestinal calcium and phosphorus absorption, during the period of egg shell formation, and duodenal calcium-binding protein (CaBP), were higher in 1alpha-OH-CC-fed than in cholecalciferol-fed hens. Renal or uterine CaBP and calcium deposition into the egg shell did not fluctuate with the vitamin D source or concentration. 1alpha-OH-CC injection into non-laying Nicarbazinfed hens resulted in an increase in intestinal but not renal or uterine CaBP concentrations. It is suggested that (a) CaBP in various organs responded independently to the same stimuli; and (b) calcium deposition into egg shell and uterine CaBP level are not related to kidney 1-hydroxylase activity or concentration of 1,25 dihydroxycholecalciferol.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1981

Effect of lead ingestion on functions of vitamin D and its metabolites.

A study of the effect of ingestion of lead on the metabolism and function of vitamin D was carried out in rats fed diets varying in calcium and phosphorus content. The ingestion of 0.82% lead as lead acetate suppressed plasma levels of 1,25-dihydroxycholecalciferol in rats fed either a low phosphorus or a low calcium diet while it had no effect on this parameter in rats fet either a high calcium diet or a normal phosphorus diet. Most important, the ingestion of lead totally blocked the intestinal calcium transport response to cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. On the other hand, the ingestion of lead acetate had no influence on the mobilization of calcium from bone, the elevation of serum inorganic phosphorus and in the mineralization of rachitic bone in the same animals. Thus by the feeding of 0.82% lead on the intestinal responses to vitamin D and its metabolites was greatest in animals fed a low calcium or a low phosphorus diet, it was present with all diets tested.

Animals↗
PubMed1982

Vitamin D compounds in cows' milk.

The milk from cows fed normal levels of vitamin D has been found to contain approximately 40 IU per liter of vitamin D activity. A 14-fold increase in dietary vitamin D intake causes only a doubling of the amount of vitamin D in milk. This was determined by measuring stimulation of intestinal calcium transport in the vitamin D-deficient rat. Four vitamin D compounds were then isolated from cow's milk using a combination of conventional chromatography on Sephadex LH-20 and Lipidex 5000 followed by high-performance liquid chromatography. 24,25-Dihydroxycholecalciferol and 1,25-dihydroxycholecalciferol were measured using binding protein assays. One liter of milk contained 27 ng and 4.9 ng, respectively, of these two metabolites. Together these account for about 15% of the vitamin D activity. Cholecalciferol was found to be present at a concentration of 281 ng/liter or 11 IU/liter of biological activity. The milk contained 145 ng/liter 25-hydroxycholecalciferol or 29 IU/liter of activity. Therefore the known vitamin D compounds fully account for the biological activity observed in milk. It is therefore clear that no evidence could be found for the existence of a highly active water-soluble form of vitamin D in milk.

24,25-Dihydroxyvitamin D 3↗
PubMed1988

Vitamin D metabolism in the hooded seal (Cystophora cristata).

Fish-eating mammals, such as seals, appear to ingest levels of vitamin D that are toxic to most mammals. To determine how seals cope with high vitamin D intakes, the metabolism of tritiated cholecalciferol ([3H]D3) was investigated in hooded seal (Cystophora cristata) pups during their postweaning fast and pups and adults consuming herring alone or supplemented with 400,000 iu D3 daily. [3H]D3 was metabolized to 25-[3H]OHD3 and 24,25-[3H](OH)2D3. 1,25-[3H](OH)2D3 was not detected, but plasma levels of 1,25-(OH)2D were similar to those in other mammals and were not affected by vitamin D intake. Plasma vitamin D, 25-OHD and 24,25-(OH)2D increased with vitamin D intake, but 25-OHD did not increase to the extent seen in other mammals. The supplemented seals showed no evidence of toxicity. Levels of 24,25-(OH)2D were higher in the unsupplemented seals (4 to 33 ng/mL) than reported in other mammals with similar 25-OHD levels and did not decrease with 25-OHD. High levels of 24,25-(OH)2D relative to 25-OHD have also been found in hooded seals in the wild. The half-lives of vitamin D, 25-OHD and 24,25-(OH)2D were shorter than those reported for most other mammals. Increased conversion of 25-OHD to 24,25-(OH)2D and a high capacity for vitamin D storage in their large blubber mass appeared to be factors in the resistance of seals to vitamin D toxicity.

Animals↗
PubMed1988

Evidence that discrimination against ergocalciferol by the chick is the result of enhanced metabolic clearance rates for its mono- and dihydroxylated metabolites.

Studies on the discrimination between ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) by chickens have led to conflicting conclusions. To investigate this problem in more detail, radiolabeled vitamin D and vitamin D metabolites were administered intravenously, which allowed determination of their relative plasma clearance rates. The study involved three groups of adult male chickens (five per group). Birds in group 1 were co-dosed with [3H]vitamin D2 and [3H]vitamin D3. Birds in group 2 were co-dosed with [3H]25-dihydroxyvitamin D2 and [3H]25-dihydroxyvitamin D3 and birds in group 3 were co-dosed with [3H]1,25-dihydroxyvitamin D3 and [3H]1,25-dihydroxyvitamin D2. The results indicated that the plasma turnover rate of [3H]vitamin D2 is 1.5 times faster than that of [3H]vitamin D3. Plasma turnover of the 25-hydroxylated metabolites differed, with [3H]25-dihydroxyvitamin D2 clearing faster (11 times) than [3H]25-dihydroxyvitamin D3. The largest difference appeared in the 1,25-dihydroxyvitamin D2 turnover rates with 1,25-dihydroxyvitamin D2 clearing approximately 33 times faster then [3H]1,25-dihydroxyvitamin D3. These data, therefore, indicate that discrimination against vitamin D2 sterols in the chick occurs primarily between steps in the metabolism of vitamin D and not at the point of metabolism or excretion of the parent vitamin.

25-Hydroxyvitamin D 2↗
PubMed1991

Some observations on the dietary vitamin D requirement of weanling pups.

A study was conducted to test the hypothesis that growing dogs do not require supplementation with cholecalciferol (vitamin D-3) in a nonpurified extruded diet. Twenty-eight weanling pups from four litters of English pointers and two litters of German Shepherd dogs were allotted equally to two groups by gender and weight. Dogs were raised in indoor-outdoor kennel runs for the 102-wk evaluation. One group was fed a diet that contained no added vitamin D while the other group was fed the same diet to which had been added 60.5 micrograms cholecalciferol/kg diet. Both diets contained approximately 14% calcium and 1.0% phosphorus. Growth as measured by body weight and length, serum calcium, phosphorus and alkaline phosphatase and urine hydroxyproline were not significantly different (P greater than 0.05) between the two treatment groups. There was no relationship between dietary treatment and nutritional secondary hyperparathyroidism (NSH), rickets or other skeletal abnormalities. The data support the concept that addition of vitamin D to typical commercial dog foods for purposes of prevention or amelioration of rickets, NSH or other skeletal diseases is unnecessary.

Alkaline Phosphatase↗
PubMed1996

Dietary butter protects against ultraviolet radiation-induced suppression of contact hypersensitivity in Skh:HR-1 hairless mice.

Dietary fats modulate a wide variety of T cell functions in mice and humans. This study examined the effects of four different dietary fats, predominantly polyunsaturated sunflower oil, margarine, and predominantly saturated butter, clarified butter, on the T cell-mediated, systemic suppression of contact hypersensitivity by ultraviolet radiation in the Skh:HR-1 hairless mouse. Diets containing either 200 g/kg or 50 g/kg butter or clarified butter as the sole fat source protected against systemic photoimmunosuppression, whether the radiation source was unfiltered ultraviolet B (280-320 nm) or filtered solar simulated ultraviolet radiation (290-400 nm), in comparison with diets containing either 200 or 50 g/kg margarine or sunflower oil. There was a linear relationship (r > 0.9) between protection against photoimmunosuppression and the proportion of clarified butter in mice fed a series of 200 g/kg mixed fat diets that provided varying proportions of clarified butter and sunflower oil. The dietary fats did not modulate the contact hypersensitivity reaction in unirradiated animals. The observed phenomena were not primary due to the carotene, tocopherol, cholecalciferol, retinol, lipid hydroperoxide or the nonfat solid content of the dietary fats used and appeared to be a result of the different fatty acid composition of the fats.

Animals↗
PubMed1999

Growing kittens require less dietary calcium than current allowances.

We previously demonstrated that a purified diet containing 3.125 microg of cholecalciferol/kg was adequate to maintain plasma concentrations of 25-hydroxyvitamin D in growing kittens. With the use of this concentration of cholecalciferol, the response of growing kittens to varying levels of calcium in purified diets was measured. Five groups (treatments 1-5), each comprised of seven weaned kittens, were given diets containing 3.8, 5.0, 6.0, 7.2 or 8. 1 g calcium/kg diet (Ca:P ratio of 1:1.25) from 9 to 18 wk of age. Two further groups of kittens (treatments 6 and 7) received similar diets containing 6.0 g Ca/kg diet, with Ca:P ratios of 1:1.55 and 1:2.61, respectively. No clinical signs of calcium deficiency were observed, i.e., growth rate, energy intake and plasma total calcium were not affected by the treatments. However, ionized calcium was significantly lower in kittens in treatment 7. Plasma phosphorus was lower in kittens in treatment 7 than in kittens in treatments 1, 2, 3 and 4, and there was a negative relationship between dietary and plasma phosphorus concentrations. Kittens in treatment 7 had a significantly higher alkaline phosphatase concentration in plasma than kittens in treatments 1, 2, 3 and 5. Kittens in treatment 1 had a lower percentage of bone minerals measured by dual-energy X-ray absorptiometry than kittens in treatments 2-6. These results indicate that the calcium requirement of growing kittens is not >6.0 g/kg diet, (calculated metabolizable energy approximately 20 kJ/g) and that kittens are not very sensitive to inverse Ca:P ratios up to 1:1.55.

Animals↗
PubMed2003

Bone resorption activity of all-trans retinoic acid is independent of vitamin D in rats.

The mechanism by which all-trans retinoic acid (ATRA) induces bone resorption is unknown. However, an interaction between vitamin A and vitamin D has been established. In fact, although the mechanism is still unclear, vitamin A has been shown to be a weak antagonist of the actions of vitamin D. Taking into account this interaction and the influence of vitamin D on other calcitropic hormones, such as parathyroid hormone, the effect of vitamin D on ATRA-induced bone resorption was investigated. Vitamin D-deficient rats were fed diets containing 0 or 150 micro g of ATRA/g of diet. The rats then were orally administered 0 or 625 ng of cholecalciferol (vitamin D(3)) daily. Various bone parameters were measured after 3-8 wk. Regardless of the presence or absence of vitamin D(3), ATRA was able to cause bone resorption. In addition to examining the effect of vitamin D on ATRA-induced bone resorption under normal conditions, this effect also was studied under conditions that inhibit bone mineralization or growth by altering dietary calcium (Ca) and phosphorus (P) levels. Changes in dietary levels of Ca and P did not affect the ability of ATRA to cause bone resorption. Interestingly, despite its ability to stimulate bone resorption, ATRA did not affect serum calcium or phosphorus levels. Overall, the ability of ATRA to cause bone resorption is not dependent on vitamin D(3), dietary Ca or dietary P.

Animals↗
PubMed2005

The vitamin D epidemic and its health consequences.

Vitamin D deficiency is now recognized as an epidemic in the United States. The major source of vitamin D for both children and adults is from sensible sun exposure. In the absence of sun exposure 1000 IU of cholecalciferol is required daily for both children and adults. Vitamin D deficiency causes poor mineralization of the collagen matrix in young children's bones leading to growth retardation and bone deformities known as rickets. In adults, vitamin D deficiency induces secondary hyperparathyroidism, which causes a loss of matrix and minerals, thus increasing the risk of osteoporosis and fractures. In addition, the poor mineralization of newly laid down bone matrix in adult bone results in the painful bone disease of osteomalacia. Vitamin D deficiency causes muscle weakness, increasing the risk of falling and fractures. Vitamin D deficiency also has other serious consequences on overall health and well-being. There is mounting scientific evidence that implicates vitamin D deficiency with an increased risk of type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common deadly cancers. Vigilance of one's vitamin D status by the yearly measurement of 25-hydroxyvitamin D should be part of an annual physical examination.

Animals↗
PubMed1998

Vitamin D deficiency alters the immune responses of broiler chicks.

Three experiments were conducted to test the hypothesis that a vitamin D deficiency alters the immune responses of female broiler chicks. The control diet contained 800 IU of cholecalciferol (vitamin D3)/kg and the deficient diet was the same except without supplemental vitamin D3. The vitamin D deficiency status was established on the basis of a significantly lower blood ionized calcium or total serum calcium (75 to 85% of the control). Vitamin D-deficient chicks also had lower growth rate and bone ash. In Experiment 1 at 8 d of age, and Experiment 2 at 23 d of age, the cutaneous basophil hypersensitivity response as determined by the increase in interdigital skin thickness 20 h after a single injection of 100 microg phytohemagglutinin-P was significantly depressed in vitamin D-deficient chicks (62 to 64% of the control). Thymus weight, adjusted for body weight, was significantly lower in the vitamin D-deficient chicks at 24 d of age (61% of the control). Primary and secondary antibody responses against SRBC in vitamin D-deficient chicks were not different from the control. In Experiment 3, in 17-d-old chicks, vitamin D deficiency decreased the number of abdominal macrophages phagocytizing SRBC in vitro within 45 min from 14.7 to 10.1%. These results indicate that vitamin D deficiency depresses the cellular immune responses in young broiler chicks.

Animal Feed↗
PubMed2000

Nutrition and skeletal problems in poultry.

Several excellent reviews regarding nutrition and skeletal disorders have appeared in the last 20 yr. This review will cover several areas of vitamin D research, the area of feed deprivation, and bone abnormalities, because there has been considerable interest in these areas during the past 10 yr. Studies indicate that the quantitative requirement for cholecalciferol (D3) for broiler chickens is much greater than previously thought. Ascorbic acid may play a role in stimulating 1-hydroxylation of 25-hydroxycholecalciferol [25-(OH)D3], but the evidence is not clear under exactly what conditions this relationship is important in practical prevention of tibial dyschondroplasia. Studies indicate that dietary supplementation with 1,25-dihydroxycholecalciferol [1,25(OH)2D3] will reduce the incidence of tibial dyschondroplasia in three different strains of broilers bred to develop a high incidence of the disease. But it did not prevent the disease totally in the strains, unless high enough levels of 1,25-(OH)2D3 were fed to reduce growth rate. These studies indicate that these high tibial dyschondroplasia strains have a defect(s) in vitamin D metabolism. Studies continue to elucidate the role of ultraviolet light in preventing leg abnormalities. Only a few studies have been conducted on the efficacy of various vitamin D3 derivatives to prevent tibial dyschondroplasia. Feed deprivation continues to be an intriguing method of preventing tibial dyschondroplasia, and examination of exactly how this prevents the bone abnormality could open avenues for explaining the disease.

Animal Nutritional Physiological Phenomena↗