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Query: UMLS:C0205700 (ash)
15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of dietary phosphorus deficiency on the performance and on various parameters of calcium, phosphorus, and vitamin D metabolism was studied in laying hens. Phosphorus deficiency resulted in a decline in rate of production and egg weight, probably through appetite depression. The latter, or any secondary calcium deficiency, does not appear to cause the observed reduction in shell quality due to the deficiency. Similar to the response in the chick, phosphorus deficiency resulted in an increase in calcium-binding protein in intestine and kidney, there was no change in the activity of kidney 25-hydroxy-vitamin D3-1-hydroxylase. Percentages of calcium and phosphorus absorption were also higher during phosphorus deficiency. Medullary bone ash, decreased during phosphorus deficiency, was probably due to a reduction in the rate of bone formation.
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PMID:Egg shell quality, medullary bone ash, intestinal calcium and phosphorus absorption, and calcium-binding protein in phosphorus-deficient hens. 654 88

To evaluate the importance of 1- and 24-hydroxylation of 25-hydroxyvitamin D3 on skeletal mineralization, male and female rats from vitamin D-deficient mothers were administered from weaning either 100 pmol/day of 25-hydroxyvitamin D3, 50 pmol/day of 1,25-dihydroxyvitamin D3, or 100 pmol/day of 24,24-difluoro-25-hydroxyvitamin D3 as their sole source of vitamin D. A separate group of rats did not receive any vitamin D. 1,25-Dihydroxyvitamin D3 was given by constant infusion at a dose that normalized plasma calcium concentrations and produced normal body weight gains. Skeletal mineralization was studied by determining femur organic and ash weights. Femurs were obtained from male rats 6 wk after weaning, from female rats at conception, at the end of lactation, and 6 wk after lactation, and from weanling pups born to the female rats. No striking differences in femur organic and ash weights were found between 25-hydroxyvitamin D3 groups and either the 1,25-dihydroxyvitamin D3 group or the 24,24-difluoro-25-hydroxyvitamin D3 group, whereas the vitamin D-deficient rats had poorly mineralized femurs. These results indicate that 1,25-dihydroxyvitamin D3 at a lower dose is as fully active as 25-hydroxyvitamin D3 in promoting skeletal mineralization in the rat and that preventing the 24-hydroxylation of 25-hydroxyvitamin D3 by administering 24,24-difluoro-25-hydroxyvitamin D3 does not elicit any obvious skeletal abnormality, especially on mineralization.
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PMID:1- but not 24-hydroxylation of vitamin D is required for skeletal mineralization in rats. 668 12

The biological activity of subcutaneously injected 24,24-difluoro-25-hydroxycholecalciferol was compared with that of 25-hydroxycholecalciferol in the vitamin D-deficient growing chick. 24,24-Difluoro-25-hydroxycholecalciferol is equal to 25-hydroxycholecalciferol in the stimulation of: 1) growth, 2) intestinal calcium absorption, 3) elevation of serum calcium and serum phosphorus, 4) healing of rachitic cartilage (radiography), and 5) mineralization of rachitic bone (bone ash). The response appears to be linear in the range of 13.0 to 325 pmol daily. Since 24,24-difluorocholecaliferol cannot be 24-hydroxylated to produce either 24,25-dihydroxycholecalciferol or 1,24,25-trihydroxycholecalciferol, while it can be 1 alpha-hydroxylated to produce 24,24-difluoro-1,25-dihydroxycholecalciferol, these results demonstrate that 24-hydroxylation is not required for the known functions of cholecalciferol in the chick.
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PMID:Biological activity of 24,24-difluoro-25-hydroxycholecalciferol in chicks. 668 69

During lactation in the rat, vitamin D is required for maintenance of a normal serum calcium level and maximal enhancement of active calcium transport in the duodenum. Vitamin D does not appear to be required for part of the adaptive increase in intestinal calcium transport or for calcium transport into the milk. The functions of vitamin D appear to be mediated by 1,25-(OH)2D3, the circulating level of which increases during lactation. Two days after sudden weaning, the serum level of 1,25-(OH)2D3 falls to levels below the pre-pregnant control level in parallel with a sharp increase in serum calcium; normal levels of calcium and 1,25-(OH)2D3 are observed one week after weaning. The initial stimulus for the increase in circulating 1,25-(OH)2D3 during lactation appears to be a small decrease in serum calcium which stimulates parathyroid hormone secretion, which in turn enhances synthesis of 1,25-(OH)2D3. Vitamin D is also required by the lactating rat to insure normal development of the suckling pup, since vitamin D deprivation during pregnancy and lactation causes significant decreases in body weight gain, in serum levels of 25-OHD3, calcium and phosphorus, in bone ash content and clear evidence of histological rickets by 20 days of age.
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PMID:Circulating levels and function of 1,25-(OH)2D3 in lactation. 668 49

To determine whether vitamin D has a direct action on bone growth and mineralization, severely vitamin D-deficient rats were infused continuously for 10 days with calcium and phosphorus solutions intrajugularly to maintain plasma calcium and phosphorus levels equal to those in rats on the same diet given vitamin D. Rats from the same litters identically treated were given 75 IU of vitamin D3 every 3 days and infused with saline for the 10-day period for comparison. Infusion of calcium and phosphorus to the vitamin D-deficient rats induces bone growth and mineralization equal to that of the rats given vitamin D as revealed by femur length, femur weight, total femur ash, percent femur ash, and epiphyseal plate width. The mineral deposited had a calcium-to-phosphorus ratio of 1.6 identical to the mineral deposited in the rats given vitamin D and unlike controls maintained in the vitamin D-deficient state without infusions. The vitamin D-deficient rats infused with calcium and phosphorus had greater amounts of mineral and matrix in their femurs than did those treated with vitamin D. This result demonstrates that some form of vitamin D does have a direct effect on bone. The most likely possibility is that bone resorption in relation to modeling or calcium mobilization for calcium homeostasis or both are compromised in extreme vitamin D deficiency. The above results strongly support the concept that vitamin D is not necessary for and does not stimulate directly bone growth and mineralization. Vitamin D therefore supports bone growth and mineralization indirectly by elevating plasma calcium and phosphorus levels.
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PMID:Vitamin D is not directly necessary for bone growth and mineralization. 674 12

The therapeutic effects of vitamin D analogs, 1,24(R)-dihydroxycholecalciferol [1,24(R)-(OH)2D3], 1,24(S)-dihydroxycholecalciferol [1,24-(S)(OH)2D3], and 1,25-dihydroxycholecalciferol [1,25(OH)2D3] on immobilization osteoporosis were studied in rats. The right hind limb was immobilized through application of a plaster cast following the section of the sciatic nerve. The left hind limb was intact. Vitamin D analogs were orally administered for 6 weeks at dose levels of 0.02 and 0.10 micrograms/kg/day, respectively. The mean lengths of the immobilized femurs were not significantly different from those of the intact femurs in all the experimental groups. In the immobilized femur of animals treated with 1,24(R)(OH)2D3, 0.10 micrograms/kg, dry and ash weights were heavier and calcium and phosphorus contents greater than those in the nontreated group. Furthermore, the amount of calcified bone mass and the cortical thickness of the femurs of the immobilized limb in 1,24(OH)2D3-treated animals were greater than those in the nontreated animals. Treatment with 1,25(OH)2D3 at 0.10 micrograms/kg caused an increase of the bone mass in both immobilized and intact femurs when compared with those of the control group. It was concluded that the administration of 1,24(R)(OH)2D3 diminished the effect of immobilization in the development of osteoporosis without any side effects.
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PMID:Immobilization osteoporosis and active vitamin D: effect of active vitamin D analogs on the development of immobilization osteoporosis in rats. 679 74

The effects of maternal vitamin D deprivation on rat pups were examined in terms of serum levels of Ca, phosphorus (P), and 25-hydroxyvitamin D (250HD), ash content, and histological appearance of long bones. In each of 10 experiments, litters of 8--10 young were examined at 2 or 3 different ages within the range of 5--57 days. Pregnant mothers were fed a diet containing 0.4% Ca, and 0.4% P and either no vitamin D(--D) or 5 IU D3/g diet (+D). Mothers fed the --D diet developed marked hypocalcemia (4--5 mg/dl) during lactation, but no change in milk Ca or P. The earliest changes in pups suckled by mothers on --D diets compared to pups suckled by mothers on +D diets were significant reductions at 8 days in serum P (6--12% in 3 of 5 experiments) and in serum 250HD3. By the 15th day, serum 250HD3 was undetectable, body weight was reduced by 26%, serum Ca was reduced by 9%, and serum P was reduced by 15%. During the following 10 days, when gradual weaning took place, serum Ca decreased progressively, serum P returned to normal, serum Mg became elevated, bone ash (as percent of dry weight of tibia) was decreased, and decalcified sections of the proximal end of the tibia revealed irregularity and widening (1.5- to 3-fold) of the hypertrophic cartilage layer and the metaphyseal trabeculae. All of these changes were also prominent in 8-week-old --D rats. The results indicate that rat pups suckling vitamin D-deprived mothers can develop biochemical evidence (including hypophosphatemia) as well as histological evidence of vitamin D deficiency similar to that of human vitamin D deficiency rickets. This is in contrast to rats deprived of vitamin D after weaning, who do not develop hypophosphatemia or characteristic histological evidence of rickets unless deprived of P as well as vitamin D.
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PMID:Hypocalcemic, hypophosphatemic rickets in rat pups suckling vitamin D-deprived mothers. 697 64

Three replicates (pens of 10 birds each) of a 2 X 2 factorial design experiment (25 and 10,000 IU vitamin E/kg diet on 25 and 500 IU vitamin D/kg diet) were utilized in order to assess effects of excessive intakes of vitamin E on calcium metabolism in the growing chick. A one-week equilibration period was followed by a two-week experimental period. Excessive vitamin E supplementation resulted in reduced calcium and phosphorus in blood plasma, in dry fat-free bone, and in bone ash, calcium, and phosphorus. Inadequate vitamin D supplementation reduced total feed consumption, terminal body weight, plasma calcium, dry fat-free-bone, bone ash, bone calcium, and bone phosphorus. Significant vitamin E X vitamin D interactions were noted for plasma calcium, dry bone, and bone ash, excessive vitamin E apparently interfering with vitamin D utilization.
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PMID:An apparent rachitogenic effect of excessive vitamin E intakes in the chick. 732 83

The effects of three dietary levels of vitamin D (500, 1500 and 3000 IU/kg diet) on magnesium metabolism and on some bone parameters related to bone mineralization were studied in vitamin D-repleted pigs fed normal magnesium intakes (0.2 per cent) for two months. Apparent absorption and retention was measured in 10-day balance studies (prior to slaughter) in three groups of four 10-week old pigs. Except for vitamin D, the pigs received the same diet which met the recommended dietary allowances for growing pigs. The highest vitamin D level used was only three times the recommended level in French pig husbandry. At slaughter, the fibula and two main metatarsals (right hind leg) were collected to determine bone breaking strength, apparent density and bone mineral (ash, calcium, magnesium) contents. Blood was collected to determine plasma concentrations of calcium, magnesium and vitamin D metabolites. Magnesium absorption increased linearly from 28-39 per cent intake with increasing dietary vitamin D. Urinary magnesium was not affected, thus magnesium retention also increased linearly as a function of vitamin D intake. Plasma calcium and magnesium were not altered by vitamin D. Plasma 25-hydroxycholecalciferol concentrations reflected vitamin D intakes, while plasma 1,25 dihydroxycholecalciferol was unchanged. Density, breaking strength and mineral contents of the bones were lower in the pigs fed 1500 or 3000 than in those fed 500 IU vitamin D/kg diet. This suggests that bone resorption was stimulated by the higher dietary vitamin D. Thus, vitamin D at physiological doses may enhance magnesium absorption in non previously vitamin D-depleted pigs fed diets with abundant magnesium. This nutritional situation may help explain the predominant bone-resorbing effect of vitamin D supplementation.
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PMID:Effects of dietary vitamin D on magnesium absorption and bone mineral contents in pigs on normal magnesium intakes. 766 4

Sex steroid hormones are known to have gender-dependent effects on bone and cartilage in vivo and in vitro. To investigate whether this is a general property of steroids, or is specific to the sex steroid hormones, we examined whether the effects on bone of 1,25-(OH)2D3 and 24,25(OH)2D3, the two active metabolites of vitamin D, are also gender-dependent. One-month-old male and female rats were treated for 1 month with various doses of 1,25-(OH)2D3, 24,25-(OH)2D3, or a combination of both metabolites. The direct effects of both metabolites on the skeleton of the treated animals were similar in male and female rats. 24,25-(OH)2D3 alone or in combination with 1,25-(OH)2D3 increased bone calcium and phosphorus, while 1,25-(OH)2D3 slightly decreased bone mineral content. 24,25-(OH)2D3 also enhanced the differentiation of cartilage in the growth plate, increasing the size of the hypertrophic zone. In addition, an increased metaphyseal bone volume was observed following 24,25-(OH)2D3 treatment in rats of both sexes, but not with 1,25-(OH)2D3. Vitamin D metabolites affected the weight gain of the experimental animals in a gender-dependent manner; 1,25-(OH)2D3 increased weight gain of male rats and 24,25-(OH)2D3 decreased weight gain of female rats. In addition, 1,25-(OH)2D3 increased bone weight and ash weight in male animals. These gender-dependent effects of vitamin D metabolites may occur indirectly via effects of sex steroid hormones, the latter being a sex-related effect.
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PMID:Gender-related effects of vitamin D metabolites on cartilage and bone. 769 89


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