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

The ionized plasma calcium concentration in foetal lambs during the last third of gestation is greater than that in the ewe. Since foetal plasma immunoreactive parathyroid hormone is less than that in the ewe the role of the foetal parathyroid glands is not clear. The effects of foetal parathyroidectomy (PTX) on the foetal:maternal gradient and on skeletal development are examined. The histomorphometry and ash content of six PTX lambs was compared with that of 11 intact animals. A reversal of the plasma ionized calcium gradient took place within 3 days without significant change in the foetal plasma inorganic phosphate or 1,25-dihydroxycholecalciferol content. Skeletal changes consistent with rickets were observed and increased in severity with the time after PTX. It is concluded that the foetal parathyroid glands play an important role in placental calcium transfer and skeletal calcification. However, the agent may be a hypercalcaemic substance other than parathyroid hormone.
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PMID:The parathyroid glands in the skeletal development of the ovine foetus. 276 12

The synthetic metabolite of vitamin D3 [1 alpha(OH)D3] caused a significant plasma calcium elevation in rats only when dietary calcium was low. Animals given the low calcium diet (0.005%) had lower plasma parathyroid hormone (PTH) levels when the diet contained 1 alpha(OH)D3 and significantly higher levels than animals on a high calcium (0.95%) diet, with or without the vitamin. The nutritional stress of a low calcium diet without 1 alpha(OH)D3 resulted in a prolonged severe hypocalcemia and elevated serum PTH levels. A higher ash, phosphate, and calcium content was found in the bones of animals fed the high calcium diet, with no vitamin D3 that were given etidronate (EHDP). When animals received the same calcium diet with 1 alpha(OH)D3 supplementation, EHDP administration increased the percentage of bone ash but had no effect on ash weight. 1 alpha(OH)D3 or EHDP did not affect ash weight, dry fat free weight, and percentage of ash of bone of animals receiving a low calcium diet. The percentage of calcium and phosphorus in bone ash was similar among all groups, although the amounts per humerus were characteristically related to the calcium intake. There was approximately 20-25% less bone mineral and calcium and phosphorus in the humeri of low calcium intake animals than in animals provided an adequate dietary calcium.
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PMID:An investigation of calcium intake, 1-alpha(OH)D3, and etidronate on bone. 303 92

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

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

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

Diabetes mellitus was induced in Lewis rats by streptozotocin, and these animals and control rats fed ad lib were studied after 7 weeks. At the time of sacrifice, nondecalcified histological sections of bone were prepared and subsequently quantitated by micromorphometric techniques. In addition, tibial alkaline phosphatase and mineral ash content were determined. The bones obtained from the diabetic animals are characterized by significant decrements in the quantities of osteoid and osteoclasts and by failure to acquire a tetracycline label. These histological features are attended by reduced quantities of urinary hydroxyproline and tibial alkaline phosphatase. As compared with control animals fed ad lib, diabetic rats are hyperphosphatemic and markedly hypercalciuric. Circulating alkaline phosphatase is also elevated and associated with a parallel increase in intestinal content of this enzyme. Although serum corticosterone levels are increased, diabetes is associated with decrements in both circulating immunoreactive parathyroid hormone and 1,25(OH)2D. We conclude that prolonged streptozotocin-induced diabetes mellitus in the rat results in reduced bone turnover. The relative roles that functional caloric deprivation, low circulating levels of 1,25(OH)2D, hypercalciuria, hypercortisolemia, and decreased blood parathyroid hormone levels play in the genesis of these skeletal abnormalities remain to be determined.
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PMID:The effect of streptozotocin-induced chronic diabetes mellitus on bone and mineral homeostasis in the rat. 645 Feb 54

1. The effect of long-term administration of parathyroid hormone (PTH) on whole-body calcium and ash weight of individual bones has been studied in normal and osteoporotic adult female rats in order to examine whether such a treatment could induce a positive calcium balance. 2. Osteoporosis was induced by calcium restriction during pregnancy and lactation. Sequential measurements of whole-body calcium were made by neutron activation. 3. In non-osteoporotic intact and thyroparathyroidectomized rats a daily dose of 75 units of human PTH 1-34 given subcutaneously for 3 weeks increased whole-body calcium. 4. In osteoporotic animals 25-50 units of either bovine PTH 1-84 or human PTH 1-34 given subcutaneously twice daily for 6 weeks increased both whole-body calcium and ash weight of individual bones. Microradiographic examination of the tibiae indicates, however, that PTH administration does not result in the restoration of individual trabeculae lost during the development of osteoporosis. 5. The results show that PTH can enhance skeletal mass in both normal and osteoporotic rats. In osteoporotic animals the restoration of whole-body calcium and ash weight of individual bones is not accompanied by a return of the morphological structure of the tibia to normal.
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PMID:Increase of whole-body calcium and skeletal mass in normal and osteoporotic adult rats treated with parathyroid hormone. 646 66

For study of the effects of an iron overload on bone remodeling, 5 control pigs were compared with 5 pigs given a total dose of 10.8 g of parenteral iron in 36 days. Treated pigs developed an iron tissue overload demonstrated by a marked increase in bone and liver iron. Except for a modest increase in SGOT, there was no biochemical or histologic sign of liver damage. Serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were unchanged in the treated pigs. There was no accumulation of iron in the parathyroid glands and the serum immunoreactive parathyroid hormone level was unchanged in the treated animals. Bone histomorphometry after double tetracycline labeling showed that in the treated pigs osteoblast cell surfaces, double and total labeled surfaces, appositional rate, and formation at tissue level were significantly decreased, and reversal surfaces were increased. Mineralization was not impaired because the osteoid thickness was unchanged. From the morphometric measurements it was concluded that osteoblast recruitment and the collagen synthesis rate were decreased. Mean wall thickness, which indicates the amount of bone synthesized, was also lowered. In contrast, the osteoclastic resorption surfaces and the depth of lacunae resulting from osteoclast resorption were unchanged by treatment. Despite this imbalance between formation and resorption, trabecular bone mass estimated on trabecular bone volume and bone ash was unchanged after 36 days' treatment. Perls' stain revealed that iron deposits were present in osteoblast and osteoclast cells and also inside the bone matrix, because there was a linear deposit along the trabecular surfaces, cement line, and osteoid-mineralized bone interface. Therefore, because treatment induced no modification of the major humoral regulators of bone metabolism, it is suggested that iron, which was present in bone cells and matrix, could play a role in bone remodeling.
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PMID:Effects of iron overload on bone remodeling in pigs. 647 75

Previous studies have shown that chronic dietary deficiency of calcium can result in more rapid orthodontic tooth movement. The purposes of this study were to confirm that finding in a calcium-deficient, lactating rat model and to quantify the degree to which the area of root surface resorption is affected by these conditions. Thirty-five adult female Sprague-Dawley rats were divided into two groups: (1) nonlactating animals on a control diet and (2) lactating animals on a calcium-deficient diet. A 60-gm orthodontic force designed to tip maxillary molars mesially was applied for varying times. At sacrifice, tooth movement was quantified by measuring the space created between maxillary molars; percent bone ash was measured for each humerus, and root surface resorption was estimated by means of a morphometric technique to measure the area of cratering on the mesial roots of first molars. Both groups showed a typical two-phased tooth movement cycle lasting for 10 days, although the magnitude of movement was significantly greater (p less than 0.001) in the test animals. The "humerus" test from animals exhibited a significantly decreased (p less than 0.001) fat-free dry weight, ash, and percent ash weight. The test group also displayed a significantly reduced percent area of root surface resorption (p less than 0.05) by 7 and 10 days following appliance activation. These findings confirm earlier observations that lactation, coupled with calcium deficiency, will produce decreased bone density which is consistent with increased parathyroid hormone secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Root resorption and tooth movement in orthodontically treated, calcium-deficient, and lactating rats. 658 81

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


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