Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0205700 (ash)
 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dichloromethylene diphosphonate (Cl2MDP) was given at doses of 4 mg/kg and 10 mg/kg daily for 7 days to adult thyroparathyroidectomized rats fed a low calcium diet. Primary metaphyseal trabeculae in Cl2MDP-treated rats were more numerous and longer than in controls. The light and electron microscopic appearance of osteoblasts, osteocytes and osteoclasts were unaltered by Cl2MDP. Bone alkaline phosphatase was significantly elevated in rats given Cl2MDP but adenosine triphosphatase activity was unchanged. Bone fat-free weight, fat-free minus ash weight, and bone calcium and phosphorus concentration were reduced significantly in rats given 10 mg/kg Cl2MDP compared to controls. Bone magnesium concentration was significantly elevated in rats given 10 mg/kg Cl2MDP. Serum calcium and phosphorus concentration were lower in Cl2MDP-treated rats. These results suggest that Cl2MDP is capable of altering bone remodeling, enzyme activity and mineral content, without significantly altering bone cell morphology, independent of the effects of parathyroid hormone, calcitonin, and dietary calcium.
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PMID:Effect of dichloromethylene diphosphonate on morphology, enzyme activity, and ash content of bones of thyroparathyroidectomized rats. 14 84

There is much experimental evidence which indicates that calcitonin in hibits bone mineral resorption, but there are few data available in support of the proposal that calcitonin may also promote mineralization. Ethane-1-hydroxy-1,1-diphosphonate (EHDP) administered to immature rats inhibited mineralization as evidenced by widened tibial epiphyseal plates and decreased bone ash to dry weight ratios. Concurrent dosing with salmon calcitonin (SCT) prevented or reversed the EHDP-blocked mineralization in a dose dependent manner. Administration of SCT during the period after EHDP treatment significantly improved mineralization of tibial epiphyseal plates as shown by plate width narrowing and increased uptake of radioactive calcium. These results suggest that SCT increased mineralization in EHDP-treated rats, and provide supportive evidence for the proposal that calcitonin may also promote mineralization, in addition to its well known ability to inhibit bone mineral resorption.
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PMID:Inhibition of diphosphonate-blocked bone mineralization. Evidence that calcitonin promotes mineralization. 46 51

In antrectomized (B-I) and control rats, bone mineralization, the fractional intestinal absorption of calcium, magnesium and phosphorus, the balances of these minerals, their serum concentration and renal excretion, together with serum gastrin, calciotropic hormones (parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D), and osteocalcin were assessed four months after surgery. B-I evoked hypogastrinemia, but no changes in the serum concentrations of minerals and calciotropic hormones, or urinary cyclic AMP. The major significant changes brought about by B-I were: (1) a decrease in bone dry weight, specific density, bone ash calcium and magnesium content; (2) a decrease in the fractional absorption and urinary excretion of calcium and magnesium; (3) an increase in urinary hydroxyproline and serum osteocalcin in the presence of normal serum bone isoenzyme of alkaline phosphatase. It is concluded that in the rat (1) B-I over the long term decreases both bone mineral content and calcium and magnesium absorption, in the absence of any counterregulation; (2) B-I rats may have attained a new equilibrium which is characterized by decreased absorption and urinary excretion of calcium and magnesium, but maintenance of normocalcemia at the expense of bone; (3) the concomitant changes of serum bone markers are contradictory, which makes their interpretation and use in the present context difficult.
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PMID:Disturbances of mineral and bone metabolism following gastric antrectomy in the rat. 133 20

The effects of both isograft transplantation and immobilization by sciatic and femoral neurotomy on bone changes in the tibia were studied in adult rats. The effects of the administration of (Asu1,7)-eel calcitonin on bone changes in the tibia induced by the same procedures were also examined. Bone volume, dry weight, ash weight, calcium weight, and strength were measured. Bone density of the tibia in the isograft transplantation group was less than that of the immobilization group, indicating that the osteoporosis induced by sciatic and femoral neurotomy and isograft transplantation differed. (Asu1,7)-eel calcitonin increased tibia bone density, ash per volume, calcium per volume, and phosphorus per volume, when subjected to isograft transplantation but not in sciatic neurotomy. Bone atrophy induced by immobilization through sciatic and femoral neurotomy and that induced by isograft transplantation were thus shown to differ.
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PMID:The effect of calcitonin on osteoporosis of the rat hind limb induced by denervation and isograft transplantation. 158 15

We studied changes in bone mass induced by immobilization and the ability of salmon calcitonin to inhibit immobilization osteoporosis in rat. The bone mass of the immobilized hind leg of rat was compared with the contralateral non-treated leg. Neurectomy and cast immobilization reduced the bone mineral mass to an equal extent. However, the dose-response of calcitonin was different with these immobilization techniques. Calcitonin 15 IU kg-1 administered once daily reduced bone ash weight difference significantly after 2 weeks' neurectomy (P less than 0.001). This had no significant effect on the bone loss induced by cast immobilization, but the dose had to be delivered as two injections given every 12 h. Two weeks' immobilization decreased the incorporation of 45Ca into bones. Calcitonin could not prevent this. However, calcitonin tended to inhibit the overall incorporation of 45Ca into bones in immobilized rats but yet had no effect on 45Ca incorporation in non-immobilized rats. Immobilization decreased serum alkaline phosphatase activity in cast-immobilized animals. Neurectomy did not change serum alkaline phosphatase activity from a sham operation level. The tartrate-resistant acid phosphatase to total acid phosphatase ratio in the serum increased significantly in neurectomized rats and in cast-immobilized calcitonin-treated rats.
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PMID:Calcitonin treatment of immobilization osteoporosis in rats. 205 38

Total body bone mineral (TBBM) content in rats was measured by dual photon absorptiometry (DPA). TBBM showed significant increases over 4 weeks in control groups with significant bone loss over the same time in prednisolone-injected rats on low calcium feed. Daily injections of calcitonin significantly reduced loss of bone mass. Both prednisolone- and prednisolone-calcitonin-injected groups showed significantly elevated serum alkaline phosphatase with the prednisolone-calcitonin group also exhibiting elevated serum calcium and phosphate levels, confirming the impact of the experimental protocol. TBBM measured by DPA in all groups correlated well (r = 0.928, P less than 0.001 n = 20) with the total ash weight suggesting that the method reflects total skeletal mineral content in the small animal. TBBM measurement by DPA proves well-suited to monitoring bone mineral in a small animal experimental setting.
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PMID:Effect of calcitonin on total body bone mineral contents of experimental osteoporotic rats determined by dual photon absorptiometry. 229 81

Experimental osteoporosis was induced in the rat by a combination of ovariectomy and immobilization by hemicordotomy. (Asu1,7)-eel calcitonin (CT) was administered at doses of 0.1, 0.5, 1.0, 2.5, and 5.0 MRC unit/kg, and its preventive effect on bone loss was examined. Significant bone loss was observed in the untreated control group by photo-densitometry and measurement of bone mass. CT at doses of above 1.0 MRC unit/kg significantly increased femur scores and at doses of above 2.5 MRC unit/kg resulted in significantly higher photodensity. Dry weight and ash weight were significantly higher in the 2.5 and 5.0 MRC unit/kg CT-treated groups. Administration of CT had a nearly dose-dependent effect on bone mass. Histomorphometry revealed significantly lower fractional formation surface and fractional resorption surface in the 5.0 MRC unit/kg CT-treated group. Bone mineralization was studied by the quantitative analysis of tetracycline incorporation. Tetracycline uptake was significantly lower in the groups treated with CT at doses above 1.0 MRC unit/kg. The kinetic bone formation activity studied by 45Ca and 14C-proline tracer examination, in the 5.0 MRC unit/kg CT-treated group was significantly lower than that in the control group, but not lower than that in the sham-operated group.
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PMID:Effect of (Asu1,7)-eel calcitonin on the prevention of osteoporosis induced by combination of immobilization and ovariectomy in the rat. 273 52

Ipriflavone administered for 10 days to orchiectomized rats did not show androgenic or androgen-augmenting activities. The wet weight of the accessory sexual organs, and dry weight, ash content and calcium content of the femur were decreased by orchiectomy and were restored by androgen administration, but were not influenced by ipriflavone administered alone or in combination with androgen for 21 days. In intact rats, ipriflavone increased these variables slightly or definitely. Basal and calcium-stimulated calcitonin levels in orchiectomized rats were not influenced by pretreatment with estrone (0.25, 0.5 and 1 microgram/kg body weight/day) or ipriflavone (100 mg/kg body weight/day) for 42 days but were increased significantly by simultaneous pretreatment with these compounds. Therefore, it might be concluded that the increase in bone variables in intact rats that received ipriflavone resulted, at least in part, from the augmentation by ipriflavone of estrogen, which exists in the peripheral blood of male rats, in addition to intrinsic androgen, which maintains bone mineral content.
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PMID:Effect of ipriflavone on accessory sexual organs and bone metabolism in male rats. 350 62

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


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