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

A child with hypophosphatemic vitamin D-resistant rickets was treated for three years with the conventional vitamin D-inorganic phosphate supplementation followed by a new therapeutic regimen consisting of 1,25 dihydroxyvitamin D3 (1,25 (OH)2D3) and half of the previous phosphate supplementation. The effectiveness of the two treatment regimens was compared by calcium, phosphate, and magnesium balance techniques and by serial radiological examinations as well as careful height measurements. In addition, the lowering of the urinary pH with ascorbic acid supplementation seems to be associated with improvement in the renal tubular reabsorption of phosphate, but its distinct effect, separate from the rest of the treatment modalities, was not tested in this study. The conventional treatment did not correct the hypophosphatemia and alkaline phosphatase elevation, whereas the 1,25 (OH)2 D3-inorganic phosphate regimen is well tolerated and effective in achieving a sustained normalization of these variables. In addition, the improved growth and healing of rickets further attest to the efficacy of the new treatment.
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PMID:Hypophosphatemic vitamin D-resistant rickets: metabolic balance studies in a child receiving 1,25 dihydroxyvitamin D3, phosphate, and ascorbic acid. 2 11

Plasma 25-hydroxycholecalciferol (25-H.C.C.) has been measured in 67 consective cases of fracture of the proximal femur. The values found in these patients were not different from values found in these patients were not different from those in control groups at the same time of the year. Plasma 25-H.C.C. was not correlated to plasma calcium or phosphorus, the Ca times P product, or the alkaline phosphatase. X-rays showed Looser zones in only 1 patient, in whom the lowest plasma 25-H.C.C. was found. Osteomalacia is not uncommon among elderly people in Denmark, but it is more likely to depend on a decline in the renal efficiency to convert 25-H.C.C. to 1,25-dihydroxycholecalciferol than a low dietary intake of vitamin D.
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PMID:25-Hydroxycholecaliferol and fractures of the proximal. 5 May 9

A survey has been carried out on 206 healthy Pakistani women attending with their sick children at the paediatric outpatients department and 252 pregnant Pakistani women near term attending the antenatal clinic of the Karachi Prosgraduate Medical Centre. 12-6% of helathy women and 33% of pregnant women had biochemical abnormalities in serum calcium, phosphorus, and alkaline phosphatase which were corrected with subsequent administration of vitamin D. The absence of clinical disease has been ascribed to the supplementation received through the ultraviolet irradiation of the skin.
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PMID:Occult osteomalacia amongst healthy and pregnant women in Pakistan. 6 39

Vitamin D and mineral metabolism status was examined in five children maintained chronically on combined ketogenic diet-anticonvulsant drug therapy (KG), and the results compared to those obtained in 18 patients treated with anticonvulsant drugs alone (AD) and 15 normal controls. KG patients exhibited biochemical findings of vitamin D deficiency osteomalacia: decreased serum 25-hydroxyvitamin D (25OHD) and calcium concentrations, elevated serum alkaline phosphatase and parathyroid hormone concentrations, decreased urinary calcium and increased urinary hydroxyproline excretion, and decreased bone mass. Although the KG and AD groups demonstrated similar reductions in serum 25OHD concentration, the KG patients exhibited a significantly greater reduction in bone mass. In response to vitamin D supplementation (5000 IU/day), mean bone mass in the KG group increased by 8.1 +/- 0.9% (P less than 0.001) over a 12-month period. These results suggest that ketogenic diet and anticonvulsant drug therapy have additive deleterious effects on bone mass and that these effects are partially reversible by vitamin D treatment.
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PMID:Disordered mineral metabolism produced by ketogenic diet therapy. 11 48

Effects of chronic ethanol ingestion on duodenal calcium transport were investigated in rats ingesting 20 per cent ethanol. Calcium transport was inhibited by ethanol ingestion and the defect could not be reversed by vitamin D or 25-hydroxycholecalciferol administrationmethanol ingestion by vitamin D-deficient rats did not further suppress transport activity nor interfere with an increase in transport induced by vitamim D. Levels of intestinal calcium-binding activity were not suppressed. Brush-border alkaline phosphatase activity was suppressed by chronic ethanol ingestion as compared to ad libitum-fed control animals and administration of vitamin D to animals ingesting ethanol restored alkaline phosphatase activitymthe results suggest that ethanol interferes with calcium transport by a mechanism at least in part independent of the vitamin D pathway and that changes in alkaline phosphatase and calcium transport, although both affected by vitamin D, may represent independent metabolic consequences.
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PMID:Effect of ethanol ingestion on duodenal calcium transport. 12 48

The effects of diphenylhydantoin (DPH) and ouabain were studied in vitro on Mg-ATPase, Ca-ATPase and alkaline phosphatase (AlPase) in isolated brush borders from rat jejunum, and in vivo on intestinal calcium absorption. Vitamin D-deficient, -repleted and normal rats were used in this study. Repletion of deficient animals with vitamin D restored Ca-ATPase activity and AlPase activity partly. Ca-absorption was normalized by repletion with the vitamin. DPH greatly stimulated Ca-ATPase activity in vitro and Ca-absorption in vivo, but it inhibited AlPase activity. Mg-ATPase was not affected by vitamin D, nor by DPH. Ouabain had no consistent effect on any of the parameters studied. It was concluded that Ca-ATPase, and not AlPase, is involved in the transport of calcium through the jejunal microvillous membrane, and that DPH enhances Ca-absorption by activation of Ca-ATPase.
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PMID:Stimulation of vitamin D-dependent Ca-ATPase and of intestinal caldium absorption by diphenylhydantoin. 12 71

Dichloromethylene diphosphonate (Cl2MDP) antagonized the action of vitamin D on bone in thyroparathyroidectomized rats by reducing the metabolic activity of osteoblasts and osteocytes and decreasing the number of osteoclasts. Ultrastructurally, osteoblasts in Cl2MDP-treated rats were interpreted to be less active in bone matrix synthesis. Osteocytes in Cl2MDP-treated rats were interpreted ultrastructurally to be inactive; there was no evidence of bone resorption when compared to osteocytes in rats given vitamin D alone. Abnormal osmiophilic densities in the pericellular bone matrix of rats given vitamin D alone were not present in rats given vitamin D and Cl2MDP. The ultrastructure of osteoclasts was unaltered by Cl2MDT. These cellular changes were associated with a decrease in serum calcium and increase in bone ash and magnesium concentration in rats given high levels (10 mg/kg) of Cl2MDP. Bone adenosine triphosphatase and alkaline phosphatase activities were not affected by Cl2MDP. These results suggest that Cl2MDP may limit the hypercalcemia of hypervitaminosis D by directly inhibiting bone cells in addition to its physicochemical action.
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PMID:Interaction of dichloromethylene diphosphonate and vitamin D on bone of thyroparathyroidectomized rats. 14 91

Rats were fed a low calcium diet deficient in vitamin D for 14 days. Changes in alkaline phosphatase activities in odontoblasts dissected out from incisor teeth were studied biochemically. A strong increase in pNPP-ase, PPi-ase, total ATP-degradation and Ca2+- ATPase was observed in the deficient animals compared with animals fed a control diet.
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PMID:Odontoblast metabolism in rats deficient in vitamin D and calcium. II. Changes in activities of alkaline phosphatases. 14 75

The pattern of response of the intestinal enzymes Ca2+-activated adenosine triphosphatase and alkaline phosphatase in the chick to 1,25-dihydroxycholecalciferol is consistent with a role for the former but not the latter enzyme in the vitamin D-dependent absorption of calcium.
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PMID:Differentiation of the changes in alkaline phosphatase from calcium ion-activated adenosine triphosphatase activities associated with increased calcium absorption in chick intestine. 15 34

Briefly reviewed herein are some of the contemporary findings on the metabolism of vitamin D, and the biochemical and physiological effects of this steroid in the animal. Certainly the most accepted major action of vitamin D is to enhance the intestinal absorption of calcium. Historically, there is also considerable evidence that the vitamin D is required for the resorption of calcium from bone, thereby aiding in maintaining normal serum calcium levels. Increasing evidence is becoming available that vitamin D does have a direct effect at the kidney level, and that the absorption and metabolism of the phosphate ion is also significantly affected by this steroid. As a consequence of vitamin D administration to the rachitic animal, some molecular changes in the intestine have been identified and these include the induction of the vitamin D dependent calcium binding protein, an increase in intestinal levels of alkaline phosphatase and calcium ATPase, and a stimulation of the adenylate cyclase system. A hallmark of recent efforts is a further understanding of the metabolism of vitamin D and the formation of its most active form, 1,25-dihydroxycholecalciferol. All of this knowledge will prove valuable in the rational treatment of certain abnormalities of calcium and bone metabolism for which examples are already available.
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PMID:Metabolism, function and clinical aspects of vitamin D. 16 68


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