Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two metabolically distinct types of bone cell populations were isolated from mouse calvaria by a repetitive digestive procedure with a mixture of collagenase and trypsin. Cells released early in the digestion showed approximately two-fold increases in cAMP when treated with either parathormone or calcitonin. These populations were denoted CT type. Later eluting cells showed larger parathormone-induced increases in cAMP but did not respond to calcitonin. These populations were denoted PT type. Six metabolic and enzymatic activites were measured in the two types of populations: acid and alkaline phosphatases, hyaluronate synthesis, citrate decarboxylation, prolyl hydroxylase, and general protein synthesis. Although each of these activites was present in both cell types, the basal levels of acid phosphatase and hyaluronate synthesis were higher in the CT cells, whereas alkaline phosphatase, citrate decarboxylation, and prolyl hydroxylase were higher in te PT cells. Parathormone stimulated acid phosphatase and hyaluronate synthesis by 100-200% only in the CT cells; in inhibited alkaline phosphatase, citrate decarboxylation, and prolyl hydroxylase by 75-90% only in the PT cells. Calcitonin alone had no effect on any of these activities other than cAMP production, but in inhibited the action of parathormone in the CT cells. The sensitivities, time courses of development,and magnitudes of these hormonal effects were similar to those observed previously in intact calvaria, indicating that the isolated cell system is a reliable model for the study of bone metabolism. Based on the metabolic responses of the cells, we postulate that the CT type of populations is enriched in osteoclasts and, possibly, osteocytes, and the PT type of population is enriched in osteoblasts.
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PMID:Biochemical characterization with parathormone and calcitonin of isolated bone cells: provisional identification of osteoclasts and osteoblasts. 18 58

The actions of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] and parathormone, both effective bone-resorptive agents in vivo and in vitro, were tested on CT (osteoclast-like) and PT (osteoblast-like) bone cells maintained in culture. Both agents stimulated acid phosphatase activity and hyaluronate synthesis in the CT cells and decreased alkaline phosphatase, citrate decarboxylation, and collagen synthesis in the PT cells. Calcitonin inhibited the changes induced in the CT but not in the PT cells. The activity of 1,25-(OH)2D3 differed from that of parathormone in one key respect: it did not increase cellular cyclic adenosine monophosphate, whereas parathormone did. Prior incubation of the bone cells with 1,25-(OH)2D3 for 6 to 24 hours made the cells refractory to the effect of parathormone on cyclic adenosine monophosphate formation. These data suggest that 1,25-(OH)2D3 and parathormone induce bone resorption by affecting the same cell types (osteoblasts and osteoclasts) although at different cellular sites.
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PMID:1,25-dihydroxycholecalciferol and parathormone: effects on isolated osteoclast-like and osteoblast-like cells. 19 43

Calcitonin has been used in the treatment of Paget's Disease of bone because of its ability to inhibit osteoclastic bone resorption. This results in a return of bone turnover towards normal, as reflected by urinary hydroxyproline and serum alkaline phosphatase. A plateau is reached with these parameters, at about 50% of the pre-treatment level. The cause of this plateau is unknown, but does not indicate resistance to treatment, since it occurs with all forms of calcitonin. Most treated patients experience pain relief, and there is radiological and histological evidence of arrested progression of Paget's Disease in patients treated with calcitonin. Both primary and secondary resistance to calcitonin occur with all calcitonins, including homologous hormone. Antibodies develop commonly in patients treated with pig or salmon calcitonin, but antibody-based clinical resistance has been demonstrated only in a few patients. Methods of selection of patients for treatment and of assessment of response are discussed, and treatment schedules summarized.
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PMID:Treatment of Paget's disease with the calcitonins. 28 41

Twenty-eight patients with symptomatic Paget's disease of bone were treated with synthetic salmon calcitonin for periods of 9 to 42 months (average, 23 months). Serum alkaline phosphatase concentration and urinary hydroxyproline excretion, which had been elevated before treatment, were decreased by calcitonin treatment in all patients, and some decrease was sustained in 23 in association with variable decreases in pain, heat and stiffness of major joints. Improvement was sustained further in approximately half of these patients; the other half had partial return of symptoms. Calcium absorption was increased in 9 of 10 patients studied; the increase did not correlate with plasma concentrations of parathyroid hormone. The mean endogenous fecal calcium excretion was decreased significantly but there was no significant change in mean urinary calcium excretion. Mean accretion rate of calcium to bone, studied in 10 patients, was decreased by 35% after 6 months of treatment and by a further 23% 1 year later. There was no consistent effect of calcitonin treatment on bone mineral mass. No serious adverse effects of treatment such as allergic reactions were observed. Calcitonin appears to be effective initially in most patients with Paget's disease of bone, but with long-term treatment resistance may be acquired.
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PMID:Long-term treatment of Paget's disease of bone with salmon calcitonin. 56 31

Algodystrophy (AD) attacks all tissues in the affected region and results in the rapid demineralization of bones. Osteocalcin (OC) and alkaline phosphatase (AP) are markers of bone turnover. Calcitonin is the treatment of choice of AD. Two groups of patients were studied: Group I (n = 8)--acute stage of AD (before and during the calcitonin treatment), Group II (n = 5)--late chronic stage of AD. In the acute stage of AD both OC level and AP activity were increased. They were normal in the chronic stage of AD. During the calcitonin treatment OC level normalized after 14 days and then increased again. During the treatment, AP activity temporarily increased and then returned to the initial level. We confirm that an increased bone turnover is observed in the acute stage of AD. Discrepancy between OC level and AP activity reflects the local metabolic disturbances. Salmon calcitonin inhibits the algodystrophic process and probably contributes to the activation of the skeletal restoration.
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PMID:Influence of calcitonin treatment on the osteocalcin concentration in the algodystrophy of bone. 128 Oct 61

Serum calcium, sodium, potassium, chloride, magnesium, phosphorus, osmolarity, total protein, albumin, parathyroid hormone, and calcitonin values were systematically surveyed in 135 patients who underwent thyroidectomy and in 104 control surgical patients. A transient and moderate hypocalcemia developed after operation in thyroidectomized and control patients. Concentrations of other electrolytes, osmolarity, proteins, and albumin followed the same pattern of evolution. After thyroidectomy, the degree and duration of hypocalcemia increased with the extent of thyroid resection. A profound hypocalcemia (less than 2.0 mmol/L) and a marked reduction of the parathyroid hormone concentration (below normal) were present in 12% and 8% of cases after subtotal thyroidectomy and in 22% after total thyroidectomy. Calcitonin values did not increase after thyroidectomy. A slight correlation was observed between the preoperative serum alkaline phosphatase level and the minimal postoperative serum calcium level. It is concluded that post-thyroidectomy hypocalcemia is a multifactorial phenomenon. It is due, at least in part, to hemodilution. A temporary parathyroid insufficiency after subtotal and total thyroidectomy, and an avidity of the skeleton for calcium in hyperthyroid patients, may aggravate the hypocalcemia.
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PMID:Hypocalcemia after thyroidectomy. 152 86

Eleven premenopausal women with uterine myoma who received 300 micrograms of intranasal Gn-RH agonist (buserelin) three times daily for 6 months participated in this study. Serum estradiol, some parameters related to calcium metabolism and bone mineral density of the lumbar vertebrae assessed by quantitative computerized tomography were evaluated prior to, at the end of and 3 months after the treatment. Hypo-estrogenism was sustained during the treatment period. Calcitonin levels decreased rapidly after the first 2 weeks of the treatment and the fasting urinary hydroxyproline to creatinine excretion value increased in 1 month. Both serum alkaline phosphatase and osteocalcin increased slightly during the treatment. The serum m-parathyroid hormone levels showed no significant changes. There was no significant reduction in the mean lumbar vertebral bone mineral content (BMC) at the end of the treatment, but 4 out of 11 cases showed a decrease in BMC, which returned to the pretreatment level in 3 months after the cessation of treatment. From these findings, this therapy appears to have some effects on calcium metabolism during medication, but no adverse ones in the 3 months after treatment.
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PMID:Calcium metabolism in premenopausal women treated by a Gn-RH agonist for uterine myoma. 196 83

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

Calcitonin had direct and dose-dependent actions on human osteoblast-line cells (in serum-free monolayer culture) to increase cell proliferation and alkaline phosphatase activity/mg cell protein. Salmon calcitonin increased (human osteosarcoma) SaOS-2 cell proliferation, as evidenced by dose-dependent increases in 3[H]-thymidine incorporation into DNA (e.g., 153% of control after 20 h exposure at 0.1 nM, P less than 0.01), and MTT (thyzolyl blue) reduction/deposition (e.g., 161% of control after 72 h exposure at 0.03 nM). Continuous exposure was not required to elicit these proliferative responses. These effects were not unique to salmon calcitonin or to SaOS-2 cells. Similar effects were seen with human calcitonin (but not heat-inactivated human calcitonin) and with (human osteosarcoma) TE-85 cells and human osteoblast-line cells prepared from femoral heads. In addition to effects on cell proliferation, calcitonin also increased alkaline phosphatase-specific activity in SaOS-2 cells (e.g., 180% of control after 72 h of exposure to 0.1 nM salmon calcitonin, P less than .005).
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PMID:Calcitonin has direct effects on 3[H]-thymidine incorporation and alkaline phosphatase activity in human osteoblast-line cells. 205 13

Different therapeutic regimens have been proposed by Authors in the treatment of involutional (and particularly postmenopausal) osteoporosis. Following the up to date concepts on bone remodelling, an ADFR (Activate, Depress, Free, Repeat) trial was performed in 20 females affected by involutional osteoporosis. They were treated with Calcitriol 2 mcg/d for 7 days, followed by a 21 days period of 100 U/d Salmon Calcitonin + 1 g/d Calcitonin, followed by a 2-month period of Calcium alone. The cycles were repeated for 1 year and the results of densitometric examinations (radial mineral content evaluated by single photon absorptiometer, and vertebral mineral content evaluated by dual photon absorptiometer) and of biochemical markers (Ca++, P, osteocalcin, alkaline phosphatase, hydroxyproline) controlled every 3 months, were compared with those obtained in a group of patients treated only with Salmon Calcitonin and in a group treated with Calcium for 1 year. After two therapeutical cycles radial bone mineral density significantly increased; vertebral bone density also increased but not significantly. The effects were more evident in comparison to calcitonin alone treatment. A significant reduction in serum osteocalcin was documented. At the end of the therapy no further improvement was registered. This suggests that some variations and adaptation of therapeutic strategy are needed to achieve a more important and substantial improvement of bone conditions.
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PMID:[Sequential calcitriol-calcitonin in the therapy of osteoporosis]. 265 53


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