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)

We studied the effect of 17 beta-estradiol (E) on the proliferation and alkaline phosphatase activity of cultured UMR106 cells, a clonal osteoblastic cell line. Growth rates were reduced and alkaline phosphatase activity was increased in cells incubated for 2 days in medium containing E (10(-8) M). In contrast, E had no effect on the growth rates or alkaline phosphatase of a human fibroblastic cell line, S90E. The effect of E was not observed with low cell density or at confluence. 1,25-Dihydroxyvitamin D3 antagonized the response to E. Preincubation of the cells with dexamethasone, a potent inducer of differentiation, reversed the effect of E or 1,25-dihydroxyvitamin D3. These results indicate that cellular and/or extracellular factors such as cell density, the phase of the cell cycle, the state of differentiation, and the presence or absence of other steroids influenced the response of UMR106 cells to E. Serum was removed from the culture medium to minimize the effect of the steroids, growth factors, and nutrients present in serum. A striking stimulation of alkaline phosphatase by E occurred with serum-free conditions. This stimulation was biphasic over an E concentration from 10(-12) to 10(-8) M, with the peak response at 10(-10) M. The action of E on UMR106 cells was metabolite-specific, since the isomer 17 alpha-estradiol produced no effect on proliferation rates or alkaline phosphatase activity. The cyclic AMP response to parathyroid hormone (residues 1-34) was not altered by E treatment of these cells. In contrast, dexamethasone exposure did increase the cyclic AMP response to parathyroid hormone. These results demonstrate a direct effect of E on an osteoblastic cell line. They also raise the possibility that similar or identical actions of E occur in cultured normal osteoblasts.
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PMID:17 beta-estradiol acts directly on the clonal osteoblastic cell line UMR106. 281 69

The effect of small calcium and vitamin D supplements on mineral metabolism in normal persons is unclear. To investigate the biochemical response to these medications, we administered 1000 mg Ca and 25 micrograms cholecalciferol per day or a placebo to 92 normal men for 1 y. The Ca and cholecalciferol were tolerated well. 25-Hydroxycholecalciferol [25-(OH)D] and 24,25-dihydroxycholecalciferol [24,25-(OH)2D] levels rose in treated subjects; there was no definite change in 1,25-(OH)2D concentrations. The average difference in 25-(OH)D levels between treated and untreated subjects was 30 nmol/L at 1 y. Fasting serum Ca, alkaline phosphatase, creatinine, and parathyroid hormone levels and the fasting urinary excretion of Ca, phosphorus and cAMP, were not affected. However, 24-h urinary Ca excretion was higher in the supplemented group (3.5 +/- 1.9 vs 4.7 +/- 1.7 mmol/d, p = 0.006). Serum P concentrations were slightly higher in the supplemented group at 1 y. In normal men small calcium and cholecalciferol supplements are safe, provide adequate vitamin D nutrition and apparently increase net gastrointestinal Ca absorption.
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PMID:Calcium and cholecalciferol: effects of small supplements in normal men. 283 25

Hepatic vitamin D-25-hydroxylase activity is greater in vitamin D-depleted than replete animals. We investigated whether vitamin D itself or a metabolite of vitamin D was responsible for modulating the activity of vitamin D-25-hydroxylase. Accordingly, we repleted vitamin D-depleted rats with subcutaneous injections of 2600, 520, and 130 pmoles of cholecalciferol (D3), 25-hydroxycholecalciferol (25(OH)D3), and 1,25-dihydroxycholecalciferol (1,25(OH)2D3), respectively, for up to 3 weeks. Repletion resulted in accelerated weight gain and in increased activity of gut mucosal alkaline phosphatase. Using an improved assay to measure vitamin D-25-hydroxylase activity in liver homogenates, we found 78% reduction (P less than 0.001) in the D3-repleted group, maximal by 1 week, in contrast to no change in those groups treated with D3 metabolites. D3, 25(OH)D3, and D3-esters remaining in livers at the time of assay were estimated in a parallel experiment using [3H]D3-repleted rats. Residual D3 accounted for only a 9% dilution of substrate in the assay. 25(OH)D3 was present in the liver at concentrations two orders of magnitude lower than the amount required to inhibit vitamin D-25-hydroxylase activity in vitro. D3 esters had no inhibitory effect in vitro at 250-fold excess of that found in the repleted rat liver. Vitamin D appears to modulate its D-25-hydroxylase activity in biological systems by a mechanism other than feedback inhibition by 25(OH)D3, 1,25(OH)2D3, or D3-esters.
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PMID:Suppression of rat hepatic vitamin D-25-hydroxylase by cholecalciferol, but not by 25-hydroxy- or 1,25-dihydroxymetabolites. 284 Jan 81

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] was examined for a possible stimulative effect on osteoblastic MC3T3-E1 cells. During the early period of culture, 1,25-(OH)2D3 had a stimulative effect. During the growth phase, however, the steroid had little effect on either the protein or DNA content of the cultures. 1,25-(OH)2D3 increased bone-liver-kidney-type alkaline phosphatase activity in a dose-related manner up to a concentration of 5 pg/ml; the increase was 2.2-fold over the control value. Studies on the effect of actinomycin D or cycloheximide treatment indicated that the vitamin may enhance de novo synthesis of ALP. The steroid also stimulated type I collagen production dose dependently via an increase in collagen synthesis rather than by inhibition of collagen degradation. MC3T3-E1 cells have a specific receptor for 1,25-(OH)2D3 which has a dissociation constant of 4.17 X 10(-11) M and a sedimentation coefficient of 3.67S. The receptor concentration varied with the period of culture, being higher during the growth phase and lower at confluence, but its affinity did not change. The results indicate that 1,25-(OH)2D3 has a direct specific anabolic effect on osteoblastic cells in vitro during the growth phase and that this effect is related to receptor concentration.
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PMID:Effects of 1,25-dihydroxyvitamin D3 on osteoblastic MC3T3-E1 cells. 300 1

In the human system calcium is the major constituent of bone and the regulator of important bioelectric and biochemical effects. Calcium homeostasis is underlying exact control mechanisms in which vitamin D is a predominant factor. Cholecalciferol (VD3) is metabolized and the active form 1 alpha, 25-dihydroxycholecalciferol (1,25(OH)2D3) is formed by the kidney. 1,25(OH)2D3 acts on the cell nuclei and on the luminal membrane of the intestinal mucosal cell. It enhances intestinal Ca absorption and the Ca transport to the blood system. VD3 metabolism and mechanisms of action are reported in the introduction. Early reports have described the important influence of bile for the intestinal Ca absorption. Up to now conclusive investigations are missing and became major topics as new regulator mechanisms were described recently. One of the main questions arising is, whether VD3 and other vitamin D metabolites can be absorbed in the absence of the biliary system and which effect on the enterocyte can be observed. Intestinal Ca absorption and transport was estimated in piglets using triple lumen tube system and duodenal perfusion. 4 untreated animals and 3 experimental animals with bile deprivation for a period of 5 (7) days were studied. Ductus choledochus ligation and concommittant cholecysto-colic anastomosis was applied for this purpose. The effect of vitamin D metabolites was estimated on 3 experimental animals applying a daily dosage of 600.000 I.E. VD3 orally, measuring Ca absorption 5 days afterwards; 3 animals in addition were administered a daily dosage of 2 micrograms 1,25(OH)2D3, measuring the Ca absorption 5 (7) days afterwards. Electrolytes, bilirubin, transaminases, total protein, albumin, triglycerides, Ca, phosphate, alkaline phosphatase, parathormone (PTH), 25 hydroxycholecalciferol (25OHD3) and 1,25(OH)2D3 were measured in all the animals before and after the experimental procedure. Data were calculated statistically. VD3 absorption was measured in 3 untreated control animals and 3 animals with bile deprivation, absorption of 1,25(OH)2D3 in 2 animals with bile deprivation. The basis for the evaluation of the experimental model was given by the laboratory values after bile deprivation. Changes in electrolyte and intermediary metabolism were observed postoperatively only and are assigned to the surgical treatment, thus ruling out severe metabolic disorders, which means that the experimental model should be appropriate for our purpose to look for Ca homeostasis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Effect of bile on intestinal calcium and vitamin D absorption. Animal experiment studies in swine]. 300 48

Since it has been suggested that long-term treatment with indomethacin and other non-steroidal anti-inflammatory drugs (NSAIDs) may result in destructive changes in the hip joint, we have examined the effect of indomethacin and aspirin on the secretory and mitotic activity of human osteoblasts in culture. Both indomethacin and aspirin inhibited the secretion of alkaline phosphatase and the uptake of [3H]thymidine by osteoblasts in a dose-dependent fashion at therapeutic concentrations. Both drugs also inhibited insulin- and 1,25-dihydroxycholecalciferol-stimulated alkaline phosphatase production and [3H]thymidine uptake by human osteoblasts. It is concluded that indomethacin and aspirin, and possibly other NSAIDs, may have an inhibitory effect on osteoblast function.
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PMID:The effect of indomethacin and aspirin on alkaline phosphatase secretion and [3H]thymidine incorporation by human osteoblasts. 304 73

A double-blind, placebo-controlled study on 21 postmenopausal osteoporotic women was performed in order to assess the effects of 1 year estrogen therapy (Premarin, 1.25 mg/day) on bone mass, intestinal calcium absorption, and mineral metabolism. Bone mineral content (BMC), measured by dual photon absorptiometry on the vertebral bodies and the femoral shaft, increased in both areas, but the changes were more evident at the former site, which is predominantly trabecular (+8.3%, P less than 0.05), than at the latter, which is mainly cortical (+2.6%, P less than 0.05). An improvement of intestinal calcium absorption was also detected at the end of the study (P less than 0.05) in the estrogen-treated group. Parameters of bone metabolism showed a decrease in hydroxyproline/creatinine ratio and osteocalcin, an increase in calcitonin, and no significant changes in parathyroid hormone (PTH) and alkaline phosphatase. Serum 1,25-dihydroxycholecalciferol (1,25(OH)2D3) levels increased after estrogen therapy, whereas 25-hydroxycholecalciferol (25OHD3) remained stable during the study period. Renal 25-hydroxyvitamin D 1 alpha-hydroxylase reserve, assessed by the PTH-stimulation test, showed a more rapid response in producing a 1,25(OH)2D3 peak in the estrogen-treated patients compared with the control subjects. However, estrogens did not induce an absolute improvement in the secretory reserve. This study demonstrates that 1 year treatment with estrogens improves both intestinal calcium absorption and BMC in postmenopausal osteoporotic women. The latter effect appears to be induced by an inhibition of bone resorption, associated to an increased secretion of calcitonin, whereas vitamin D metabolites do not seem to contribute substantially to the mediation of estrogen action on bone.
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PMID:Effects of one-year treatment with estrogens on bone mass, intestinal calcium absorption, and 25-hydroxyvitamin D-1 alpha-hydroxylase reserve in postmenopausal osteoporosis. 312 28

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] and 24,25-(OH)2D3 differentially affect the specific activity of alkaline phosphatase (ALPase) and phospholipase-A2 (PLA2) of plasma membranes and extracellular matrix vesicles produced by costochondral reserve zone and growth zone cartilage chondrocytes in culture. In the present study, growth zone and cartilage and reserve zone matrix vesicles and plasma membranes were isolated from confluent chondrocyte cultures and incubated with hormone for 3 and 24 h in vitro. Addition of 1,25-(OH)2D3 to GC matrix vesicles and plasma membranes resulted in dose-dependent increases in ALPase and PLA2 specific activities in both membrane fractions. Addition of 24,25-(OH)2D3 to RC membrane fractions stimulated matrix vesicle ALPase at 10(-7) and 10(-8) M and plasma membrane ALPase at 10(-8) M only. However, 24,25-(OH)2D3 inhibited matrix vesicle and plasma membrane PLA2 activity. The effects of the vitamin D metabolites were noticed after both 3 and 24 h. Neither hormone metabolite had any effect on these enzymes in membrane fractions from cultures of neonatal rat muscle mesenchymal cells, which do not calcify their matrix in vivo. These data suggest that 1,25-(OH)2D3 and 24,25-(OH)2D3 can directly affect chondrocyte membrane enzymes without genomic influence or protein synthesis and that membrane response depends on the stage of chondrocyte differentiation. Changes in PLA2 activity may change membrane fluidity and may be a mechanism by which the hormones affect cell membranes.
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PMID:Direct effects of 1,25-dihydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 on growth zone and resting zone chondrocyte membrane alkaline phosphatase and phospholipase-A2 specific activities. 326 40

A short-term in vivo system was developed to examine simultaneously bone formation and resorption, and the effects of dietary calcium and vitamin D on these processes. In experiment 1, 25 male Long-Evans rats were each implanted with two gelatin capsules containing mineralized bone (MB) powder subcutaneously in the thorax region. At 4, 6, 8, 10 and 12 d after implantation the acid phosphatase activity (resorption) increased significantly (P less than 0.01), whereas alkaline phosphatase activity (formation) did not change. In experiment 2, both MB and demineralized bone (DB) powder were implanted on contralateral dorsal sites of the thorax in 40 male Long-Evans rats and harvested after 7, 9, 11 and 13 d. Enzyme, mineral and histological assessment indicated bone formation in DB implants with bone resorption in MB implants. In experiment 3, the effects of dietary calcium (0.2 or 1.0%) and vitamin D (cholecalciferol at 300 ng/d or 1,25-dihydroxycholecalciferol [1,25(OH)2D3] at 75 ng/d) were examined using 40 male Long-Evans rats. These rats were implanted with both DB and MB powders and the implants were harvested on d 12. Both low (0.2%) dietary calcium and 1,25(OH)2D3 stimulated resorption of MB implants. Therefore, the physiological processes of bone formation and resorption were mimicked in this system of bone powder implants. Further, dietary calcium and 1,25(OH)2D3 were shown to modulate these processes.
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PMID:Calcium and vitamin D in bone metabolism: analyses of their effects with a short-term in vivo bone model in rats. 333 45

The activity and localization of alkaline phosphatase activity (AP) in aorta and heart, and the incidence of calcifications in aorta, heart and kidney as well as cardial fibrosis were studied in uraemic rats treated with 1,25-dihydroxycholecalciferol (1,25-DCHH) and Nifedipine. 1,25-DHCC treatment elevated the serum Ca x P product and aggravated the development of renal and aortic calcifications and cardial fibrosis. Nifedipine did not protect against calcifications, but decreased the incidence of cardial fibrosis. The activity of AP was increased in the thoracic aorta in uraemia independent of 1,25-DHCC or Nifedipine treatment or presence of calcification. No changes of the AP activity were found in the heart.
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PMID:Tissue calcification and alkaline phosphatase activity in uraemic rats. 338 11


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