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

The effects of pregnancy and lactation on endosteal bone formation and resorption were evaluated in vitamin D-depleted (-D) and vitamin D-repleted (+D) rats. Pregnancy induced a marked stimulation of osteoclastic bone resorption and of static and dynamic parameters of bone formation and mineralization. Bone resorption increased independently of vitamin D status and did not correlate with plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D] levels, but it was associated with increased plasma immunoreactive parathyroid hormone (iPTH) concentrations. Stimulation of the endosteal bone formation rate was mainly impaired in D-depleted rats, resulting in trabecular bone loss, which, in -D mother rats, was associated with decreased bone ash and total bone calcium. Lactation further stimulated bone resorption and reduced the trabecular bone volume; ash weight and bone calcium content were also decreased independently of the vitamin D status and changes in plasma iPTH levels. In presence of vitamin D, the bone formation rate increased fourfold during lactation but was unchanged in -D lactating rats. During lactation, vitamin D-depleted rats lost twofold more calcified bone than +D rats because of impaired mineralization. Thus, the present study shows that both the endosteal bone resorption and formation are stimulated by pregnancy and lactation and that vitamin D is required for normal bone mineralization during the reproductive period.
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PMID:Bone changes due to pregnancy and lactation: influence of vitamin D status. 376 25

Effects of supplemental dietary calcium and vitamin D on lipid distribution and aortic mineralization were examined in young goats. Twenty-four goats, 2-4 wk of age, were allotted one of four dietary treatments for a 20-wk period and fed a basal milk diet (Basal), a calcium-supplemented diet (Basal + Ca), a cholecalciferol-enriched diet (Basal + D3) or a diet with both calcium and cholecalciferol (Basal + Ca + D3). Goats in the Basal + Ca group had plasma cholesterol concentrations that were 16.6% of those of the Basal group. Percentage absorption and fecal excretion of total lipids were unaffected by dietary treatment. Generally, total lipid and cholesterol concentrations were unaltered in liver, other viscera and carcass tissues. Dietary cholecalciferol increased concentrations of cholesterol and total lipid in aortas, whereas dietary calcium decreased total lipids in aortas. Concentrations of calcium, magnesium and total ash were increased in aortas by dietary treatment, with a marked increase observed in the Basal + Ca + D3 group. Sudan IV and gross calcium staining in aortas revealed both lipid and mineral deposition that confirmed composition data. A high intake of vitamin D accompanied by excessive intake of calcium seems to accelerate the development of atherosclerosis. Supplemental calcium with normal amounts of vitamin D, however, is hypocholesterolemic and seems protective against the atherogenic process.
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PMID:Dietary calcium and vitamin D: risk factors in the development of atherosclerosis in young goats. 396 86

The effects of varying dietary calcium and phosphorus content, vitamin D deficiency, oophorectomy, adrenalectomy, and simultaneous pregnancy on bone mineral loss during lactation were examined in rats. Unless otherwise stated, the diet contained 0.47% calcium and 0.3% phosphorus and the rats were given 26 nmol of vitamin D3. Femur ash weights were determined after 21 days of lactation and on age-matched nonlactating rats. Decreasing dietary calcium to 0.02% caused an increased loss of bone mineral, whereas increasing dietary calcium to 1.4% increased plasma calcium levels to 12 mg/100 ml but did not diminish the bone mineral loss observed during lactation. Varying dietary phosphorus did not have a major effect on bone mineral loss during lactation. In vitamin D-deficient rats, bone mineral loss during lactation was independent of dietary calcium levels and slightly greater than the loss observed in vitamin D-replete rats fed the normal calcium diet. Oophorectomy and adrenalectomy did not produce changes in femur ash weights of nonlactating rats or reduce bone mineral loss during lactation. Rats mated during their postpartum estrus and thus simultaneously pregnant and lactating, lost the same amount of bone mineral as caused by lactation alone.
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PMID:Regulation of bone mineral loss during lactation. 397 Jan 93

The effect of mild, non-insulin-dependent diabetes (NIDDM) on bone calcification and calcium (Ca) homeostasis was studied in growing rats (males and females). The diabetic state was characterized by mild insulin deficiency, plasma levels being 73% of controls, and mild hyperglycemia, with nonfasting plasma glucose levels of 1.5 times normal. There was no difference in plasma levels of Ca, phosphate (Pi), magnesium (Mg), alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), calcitonin, 25-(OH)vitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]2D), and 24,25-dihydroxyvitamin D (24,25[OH]2D) between the NIDDM rats and their controls of either sex. Metabolic Ca and Pi balance studies revealed that the experimental animals of both sexes were in positive Ca and Pi balance similar to that of their controls. Histologic studies of the kidney and intestinal slices from the experimental group were normal. Ca and Pi bone content calculated per gram bone ash of the femur, mandible, and second and fourth caudal vertebrae, and the organic content in the bones of the NIDDM animals showed no difference from their controls. Femur bone density and tibial epiphyseal growth plate width and morphology were similar histologically in the experimental and control rats. No decreased osteoid content in the tibial bone was found in the diabetic rats compared with controls. Physiologic sex differences, consisting of lower plasma Pi, higher plasma calcitonin levels, increased ratio of femur dry bone weight to total body weight, and increased percentage of mineralized and total bone volume at the tibial metaphysis seen in female compared with male control rats were also seen in the diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone calcification and calcium homeostasis in rats with non-insulin-dependent diabetes induced by streptozocin. 397 85

The bones of vitamin D-deficient, phosphate-deficient rats have a lipid composition that is significantly different from that of normal bones. Specifically, these bones have elevated cholesterol and reduced lysophosphatide and free fatty acid contents. Treatment of these animals with a single dose of vitamin D and phosphate produces healing within 72 h and causes rapid corrections of alterations in growth plate and cancellous bone lipid composition. Healing of the rachitic/osteomalacic state in these animals was demonstrated radiographically and histologically. Histomorphometric measurements showed that the relative osteoid volume of the cancellous bone rapidly approached the 7% value of normal controls, decreasing from 29% in the rachitic animals to 16% by 12 h and 8.5% by 72 h. Significant changes in ash weight, Ca:P ratio, and crystal-lite size and perfection were detectable at 12 h, with these parameters approaching values found in normal animals within 72 h. Calcium-acidic phospholipid-phosphate complexes, which are known to promote hydroxyapatite formation, peaked in concentration at 12 h in epiphysis, cancellous, and cortical bone, returning rapidly to normal values after that time. In untreated animals the complexed acidic phospholipid content of the nonmineralized epiphysis was comparable to that in normal mineralizing epiphysis, whereas the content of the complexes was reduced in the cancellous bones of the untreated animals.
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PMID:Lipid changes in the bones of the healing vitamin D-deficient phosphate-deficient rat. 402 95

Mineral, hormonal and skeletal changes were determined in vitamin D-deficient (-D) and vitamin D-replete (+D) mother rats and in their litters on day 20 of lactation. These results were compared with those obtained in -D mothers and pups, after giving the mothers an oral supplement (10 i.u. vitamin D3/day) during the period of lactation (20 days). Compared to +D animals, both -D lactating mothers and their pups exhibited extremely low plasma levels of 25-hydroxyvitamin D3 (25-OH-D3), diminished 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and increased levels of immunoreactive parathyroid hormone (iPTH). Vitamin D-deficient mothers also had higher levels of calcitonin and lower levels of prolactin than +D mothers. All -D animals (mothers and pups) showed increased osteoclastic bone resorption and severe osteomalacia as shown by decreased bone ash, decreased calcification rate and increased endosteal osteoid surface, volume and thickness. In mothers treated with vitamin D3 during lactation, nearly all the plasma variables measured, as well as bone histomorphometric features, were normal. In contrast, their pups still showed rickets and osteomalacia, despite normal levels of 25-OH-D3 and calcium in the plasma. These pups had raised plasma levels of 1,25(OH)2D3 and iPTH associated with persistent stimulation of bone resorption. This study showed that (1) severe vitamin D deficiency in lactating rats produced marked osteomalacia and secondary hyperparathyroidism in both mothers and pups, and (2) vitamin D treatment of -D mother rats during lactation (10 i.u. vitamin D3/day) reversed the mineral, hormonal and skeletal abnormalities in mothers but not in pups.
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PMID:Influence of vitamin D on mineral metabolism, hormonal status and bone histology in lactating rats and their pups. 403 44

1. Female rats fed on a vitamin D deplete (D-) diet for 90 days prior to mating gave birth to litters having significantly fewer young than females fed a diet containing vitamin D (2.2 IU/g, D + diet). 2. Neither age nor body weight of females had a significant influence on litter size. 3. Serum calcium and phosphorus levels in D+ and D- dams were not significantly different, nor were serum calcium and phosphorus levels and bone ash of D+ and D- weanlings. 4. The level of 25-hydroxyvitamin D3 [25(OH)D3], the main circulating form of vitamin D, was low in D- dams and was not detected in D- weanlings. 5. These data suggest that vitamin D is required for reproduction in the rat.
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PMID:Reduced fecundity of vitamin D deficient rats. 613 40

Day-old turkeys fed vitamin D-deficient diets became rachitic within 17-24 days. The symptoms included reductions in body weight, plasma calcium and inorganic phosphorus, plasma and intestinal calcium-binding protein (CaBP), plasma 25-hydroxycholecalciferol [25(OH)D3], bone ash, and kidney 25(OH)D3-24-hydroxylase and a rise in kidney 25(OH)D3-1-hydroxylase activity. Supplementation of the diet with 12.5 micrograms cholecalciferol per kilogram was sufficient to promote maximal body weight and normal plasma calcium, Plasma calcium, plasma phosphorus and bone ash. Feeding diets containing 250 or 1250 micrograms cholecalciferol per kilogram resulted in a reduced body weight. An increased in the concentration of plasma 25(OH)D3 with increasing dietary cholecalciferol concentration was observed. Feeding vitamin D-deficient rachitic birds for 4 days a diet containing 50 micrograms cholecalciferol per kilogram restored plasma calcium and phosphorus and bone ash. Body weight remained lower than that of the control for an additional 6-day period. Additional cholecalciferol, 25(OH)D3 or 1 alpha-hydroxycholecalciferol in the diet, intramuscular injection of the vitamin D derivatives, or a high-calcium, high-phosphorus diet did not accelerate the recovery from the rachitic state.
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PMID:Cholecalciferol requirements of young turkeys under normal conditions and during recovery from rickets. 628 10

A growth assay was conducted for six consecutive 28-day periods by using triplicate groups of 110 rainbow trout with an average initial body weight of 3.0 g. Ergocalciferol (vitamin D2 or D2) and cholecalciferol (vitamin D3 or D3) were included to provide levels of 200, 400 and 800 iu/kg in a semipurified casein, gelatin diet. Further treatments with 0 vitamin D and 1600 IU/kg of D3 were also included. The resulting growth curves were significant for parallelism. Statistical analysis showed that D3 was 3.27 times as potent as D2 (limits 2.33 to 4.58). The dietary requirement for D3 was found to be in excess of 800 iu/kg of diet. Vitamin D-deficient fish showed no change in bone ash but exhibited clinical manifestations of tetany with no hypocalcemia. A complete absence of tetany was seen only in the groups fed 800 and 1600 IU of D3 per kilogram. None of the levels of D2 used were sufficient to completely alleviate symptoms of this disorder. These studies of rainbow trout provide evidence that vitamin D is required for the normal functioning of white muscle without altering the calcium content of the plasma or epaxial musculature.
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PMID:Relative biopotency of dietary ergocalciferol and cholecalciferol and the role of and requirement for vitamin D in rainbow trout (Salmo gairdneri). 629 Jun 24

Weanling vitamin D-deficient rats fed a high calcium, low phosphate diet were injected daily with 1 alpha-hydroxyergocalciferol or 1 alpha-hydroxycholecalciferol at doses of 2.5, 25 or 250 ng. Intestinal calcium and phosphate transport, serum phosphorus level, epiphyseal plate calcification, and percent femur ash increased as a function of the dose. Both compounds were equally effective in eliciting these responses demonstrating their equivalency as antirachitic compounds.
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PMID:Antirachitic activity of 1 alpha-hydroxyergocalciferol and 1 alpha-hydroxycholecalciferol in rats. 633 1


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