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)

The effect of combined oestrogen/progestogen and calcium therapy on vitamin D metabolites was studied in a double-blind, controlled clinical study over a period of 12 mth. Seventeen healthy post-menopausal women were randomly allocated for treatment with either oestrogen/progestogen or placebo. All the participants received a daily calcium supplement of 0.5 g throughout the study. The oestrogen-treated group showed the well-known changes in calcium metabolic variables, i.e. decreases in serum phosphate (P less than 0.001), serum alkaline phosphatase (P less than 0.001) and 24-h urinary calcium excretion rate (P less than 0.01). However, the serum calcium and serum 1,25-dihydroxycholecalciferol concentrations were unchanged. In the placebo group all the measured values remained virtually unchanged throughout the study. The findings indicate that calcium seems to potentiate the bone-preserving effect of oestrogen treatment in early post-menopausal women by keeping the serum calcium level unchanged and thus maintaining an unchanged vitamin D metabolism.
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PMID:Does calcium potentiate the bone-preserving effect of oestrogen treatment in early post-menopausal women by a change in vitamin D metabolism? 638 68

The possible relationship between red blood cell (RBC) deformability and secondary hyperparathyroidism (HPT) in 23 patients on maintenance hemodialysis was examined. Secondary HPT was evaluated by means of serum biochemistry (parathyroid hormone, calcium, phosphorus, and alkaline phosphatase) and radiographic examinations. This study showed that RBC deformability is markedly reduced in hemodialyzed patients when compared with normal controls. No significant correlation between RBC deformability and the hematochemical changes associated with secondary HPT was found. No difference in RBC deformability was observed as far as the activity (alkaline phosphatase) and the severity (radiographic findings) of secondary HPT are concerned. Effective treatment of secondary HPT by either pharmacological means (1 alpha, 25-dihydroxycholecalciferol therapy) or surgical removal was not associated with consequent improvement in RBC deformability. It is concluded that secondary HPT is probably not a major factor influencing RBC deformability in uremic patients on maintenance hemodialysis.
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PMID:Red blood cell deformability and secondary hyperparathyroidism in uremic patients on maintenance hemodialysis. 654 27

Bone metabolism was estimated by serum alkaline phosphatase (index of bone formation) and fasting urinary excretions of calcium and hydroxyproline (indices of bone resorption) in a group of early postmenopausal women and a group of 70-year-old women, during 12 months' treatment with 1,25-dihydroxycholecalciferol (1,25(OH)2D3), and compared to oestrogen/gestagen treatment or placebo treatment. The groups treated with 1,25(OH)2D3 did not show any change in bone metabolism, neither in bone resorption nor in bone formation, during the treatment period when compared to the placebo group, whereas treatment with female hormones decreased both bone resorption and bone formation.
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PMID:Effect of 1,25-dihydroxyvitamin D3 on biochemical indices of bone turnover in postmenopausal women. 654 63

1,25 Dihydroxyvitamin D3 suppressed colony formation in soft agar and increased alkaline phosphatase activity in clonal rat osteosarcoma cells. Sodium butyrate enhanced these effects of the hormone partly through a mechanism involving an alteration of nuclear binding of the hormone. It is suggested that 1,25 dihydroxyvitamin D3 in conjunction with sodium butyrate might be able to regulate differentiation and proliferation of neoplastic cells.
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PMID:Sodium butyrate (SB) augments the effects of 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) on neoplastic and osteoblastic phenotype in clonal rat osteosarcoma cells. 658 71

Serum levels of the circulating form of vitamin D3, 25-hydroxycholecalciferol [25-(OH)D3], were determined in 59 university students, 26 males and 33 females, aged 18 to 26 yr and in 24 elderly subjects, 13 males and 11 females, with a mean age of 62 +/- 13 yr. The level of 25-(OH)D3 was significantly lower in the elderly persons (p less than 0.001) than in young students of both sexes, and was significantly higher in females than in males. Serum levels of 1, 25- and 24, 25-dihydroxycholecalciferol were measured in adult males and found to be within the normal range. A group of elderly patients were exposed to natural uv light, and the circulating levels of 25-(OH)D3, serum phosphorus, and alkaline phosphatase were determined both before and 1 day after the last exposure. The exposure to natural uv light resulted in a 2 1/2-fold increase in the level of 25-(OH)D3 and a significant decrease in the activity of alkaline phosphatase, but no significant change in serum phosphorus concentrations was observed. It is concluded that the low vitamin D3 status in Saudis is mainly due to avoidance of sunlight exposure and other factors discussed below.
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PMID:Sunlight and vitamin D status in normal Saudi subjects. 660 40

The effect of vitamin D status on the topography of intestinal cell membranes was studied in isolated brush borders, as well as their purified membranes, by limited proteolysis. Addition of papain to brush borders isolated from vitamin D3-treated and deficient chicks resulted in a differential solubilization of leucine aminopeptidase, maltase, and sucrase activities (114, 195, and 79%, respectively, of appropriate control levels) but not alkaline phosphatase activity. In comparison, proteolysis of purified membranes exhibited vitamin D3- and 1,25-dihydroxycholecalciferol [1,25(OH)2D3]-dependent differences in release of all four marker hydrolases monitored. Calcium uptake studies revealed that preincubation with papain yielded vesicles with a calcium content that was 125% of corresponding native vesicles, in preparations from vitamin D3-treated, as well as deficient birds. Membrane vesicles prepared from 1,25(OH)2D3-treated chicks initially accumulated calcium to a greater extent than those from rachitic birds, but thereafter exhibited a decline in calcium content to basal levels. Preincubation with papain, however, abolished this loss of calcium. The combined results indicate that vitamin D mediates alterations in brush border protein topography and raise the possibility that this action of the seco-steroid might be involved in calcium absorption. However, if vitamin D-stimulated calcium transport across the brush border is dependent on a protein carrier, the molecular entity is not sensitive to inactivation by papain.
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PMID:Vitamin D-mediated alterations in the topography of intestinal brush border proteins: effect of papain on hydrolase release and calcium uptake. 684 6

Nine patients with renal osteodystrophy were tested for 6.5 to 35 months with 1,25-dihydroxycholecalciferol (1,25-DHCC). A close biochemical follow-up was performed during the first 6 months of treatment, including biweekly determinations of serum calcium, phosphorus, magnesium, alkaline phosphatase and creatinine levels. A bone biopsy, radiologic investigations and determinations of plasma levels of immunoreactive parathyroid hormone (IPTH) and intestinal absorption of calcium 47 were performed before and after the 6 months. Although the five patients with osteitis fibrosa showed a significant improvement, the four with predominantly osteomalacic lesions showed no response to treatment. These four had a normal initial plasma iPTH level, higher serum calcium levels than the other five patients, extreme sensitivity to 1,25-DHCC, with frequent episodes of hypercalcemia, and only a slightly increased serum alkaline phosphatase level, which remained unchanged during treatment. All but one of the patients, irrespective of the histologic abnormality, showed a decrease in the uptake of radionuclide by bone after treatment. The renal function of one patient, a man with long-standing stable renal failure who had not undergone dialysis, deteriorated during treatment.
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PMID:Treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol. 689 3

We describe a sporadic, vitamin-D-resistant osteomalacic syndrome in 19 patients undergoing hemodialysis. The syndrome was found in less than 1.5% of patients from referring dialysis centers. All 19 patients had multiple fractures, severe myopathy, and many developed spontaneous hypercalcemia. Severe osteomalacia without evidence of secondary hyperparathyroidism distinguished this syndrome from other forms of renal osteodystrophy. Bone aluminum, measured in six patients, was greatly elevated. Therapy with calcitriol (1 alpha, 25-dihydroxycholecalciferol) lad to clinical improvement in seven patients with reduced pain and myopathy, decreased serum alkaline phosphatase, or both, but no improvement in bone histology. Patients who did not respond clinically to calcitriol developed marked hypercalcemia. The cause of this severe osteomalacia, which occurs despite normal or slightly elevated levels of serum calcium and phosphorus and fails to mineralize with calcitriol, is unclear.
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PMID:Vitamin-D-resistant osteomalacia in hemodialysis patients lacking secondary hyperparathyroidism. 689 20

Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.
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PMID:Long-term therapy of uremic osteodystrophy in adults with calcitriol. 689 93

1,25-Dihydroxycholecalciferol increases the incorporation of leucine into a protein component (Mr = 84000) of the chick intestinal brush-border membrane. Evidence has now been obtained showing this protein to be sub-unit of alkaline phosphatase. Pure chick intestinal alkaline phosphatase was prepared and antibodies raised against it in rabbits. This enzyme and the brush-border protein behaved identically on gel electrophoresis, and in terms of their phosphorylating activity and enzyme activity whether as the enzymically active dimeric form or when reduced to the sub-unit form. The anti-(alkaline phosphatase) reacted with the protein into which the incorporation of leucine was stimulated by 1,25-dihydroxycholecalciferol.
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PMID:Incorporation of labelled leucine into alkaline phosphatase in response to 1,25-dihydroxycholecalciferol in chick intestinal brush borders. 689 55


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