Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Because defective bone mineralization occurs in hypophosphatasia (HP) and the source of bone alkaline phosphatase is the osteoblast, we investigated another marker of osteoblast activity, namely the production of osteocalcin in an HP family and controls. The mean basal osteocalcin levels in the two affected young adults and their parents (the apparent heterozygotes) were 3.4 ng/ml (range 2.5-4.6) and were not different from the levels in age- and sex-matched controls (3.6 ng/ml; range 2.5-4.6). Furthermore, the ratio of carboxylated to total osteocalcin was normal. The rise in osteocalcin after 1,25-dihydroxycholecalciferol stimulation (2 micrograms daily for one week) was slightly greater in the controls than in the HP family. These results support the concept that there is no global defect in osteoblast function in this family with HP.
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PMID:Serum osteocalcin levels before and after 1,25 dihydroxy-vitamin D stimulation in a family with hypophosphatasia. 179 76

Bone mineral content, estimated by single-photon absorptiometry of the forearm, serum values of intact parathyroid hormone (PTH(1-84], osteocalcin, alkaline phosphatase, 1,25-dihydroxycholecalciferol (1,25(OH)2D3), and aluminium were determined during treatment with calcium carbonate (CaCO3) or aluminium hydroxide (Al(OH)3) in 11 dialysis patients participating in a randomised cross-over study. Each treatment period lasted 6 months. Serum phosphorus was maintained in the range 1.5-2.0 mmol/l. During Al(OH)3 treatment bone mineral content (BMC) decreased by 11% per half-year (mean), but only by 3% per half-year during CaCO3 treatment (P less than 0.05). Comparing the CaCO3 and Al(OH)3 periods the following differences were found: serum calcium increased during CaCO3 treatment, PTH(1-84) decreased (79% of initial values during CaCO3 versus 196% during Al(OH)3, mean area under curve, P less than 0.05), osteocalcin decreased (89% versus 117%, P less than 0.01), alkaline phosphatase decreased (92% versus 116%, P less than 0.05), and aluminium decreased (56% versus 189%, P less than 0.05). 1,25(OH)2D3 remained unchanged in both periods. No increase in soft-tissue calcification was demonstrated on X-ray of the shoulders in any of the periods. Thus, CaCO3 treatment seems to slow down loss of bone mineral content, and using CaCO3 as phosphate binder may have a more beneficial effect on the progression of uraemic bone disease than Al(OH)3 due to the reduction of hyperparathyroidism and bone turnover.
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PMID:Comparison of calcium carbonate and aluminium hydroxide as phosphate binders on biochemical bone markers, PTH(1-84), and bone mineral content in dialysis patients. 185 34

Micromolar concentrations of aluminum sulfate consistently stimulated [3H]thymidine incorporation into DNA and increased cellular alkaline phosphatase activity (an osteoblastic differentiation marker) in osteoblast-line cells of chicken and human. The stimulations were highly reproducible, and were biphasic and dose-dependent with the maximal stimulatory dose varied from experiment to experiment. The mitogenic doses of aluminum ion also stimulated collagen synthesis in cultured human osteosarcoma TE-85 cells, suggesting that aluminum ion might stimulate bone formation in vitro. The effects of mitogenic doses of aluminum ion on basal osteocalcin secretion by normal human osteoblasts could not be determined since there was little, if any, basal secretion of osteocalcin by these cells. 1,25 Dihydroxyvitamin D3 significantly stimulated the secretion of osteocalcin and the specific activity of cellular alkaline phosphatase in the human osteoblasts. Although mitogenic concentrations of aluminum ion potentiated the 1,25 dihydroxyvitamin D3-dependent stimulation of osteocalcin secretion, they significantly inhibited the hormone-mediated activation of cellular alkaline phosphatase activity. Mitogenic concentrations of aluminum ion did not stimulate cAMP production in human osteosarcoma TE 85 cells, indicating that the mechanism of aluminum ion does not involve cAMP. The mitogenic activity of aluminum ion is different from that of fluoride because (a) unlike fluoride, its mitogenic activity was unaffected by culture medium changes; (b) unlike fluoride, its mitogenic activity was nonspecific for bone cells; and (c) aluminum ion interacted with fluoride on the stimulation of the proliferation of osteoblastic-line cells, and did not share the same rate-limiting step(s) as that of fluoride. PTH interacted with and potentiated the bone cell mitogenic activity of aluminum ion, and thereby is consistent with the possibility that the in vivo osteogenic actions of aluminum ion might depend on PTH. In summary, low concentrations of aluminum ion could act directly on osteoblasts to stimulate their proliferation and differentiation by a mechanism that is different from fluoride.
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PMID:Aluminum stimulates the proliferation and differentiation of osteoblasts in vitro by a mechanism that is different from fluoride. 192 12

Intestinal Ca2+ malabsorption has been described in spontaneously hypertensive rats (SHRs), but the molecular basis for this defect is unknown. In this study, we measured intestinal alkaline phosphatase and vitamin D-dependent Ca(2+)-binding protein (calbindin-D9k), two proteins implicated in the active pathway of intestinal Ca2+ absorption. Both proteins were measured in the small intestines of SHRs and their normotensive controls, Wistar-Kyoto rats, before, during, and after development of hypertension (4, 9, 14, 18, and 28 wk of age). At all ages, alkaline phosphatase activity in duodenum (0-6 cm) was decreased by 30-57% (P less than 0.001) and by 47-75% in the 2nd intestinal segment (6-12 cm) (P less than 0.001-0.05). Calbindin-D9k was decreased similarly. The decreases of calbindin were statistically significant (P less than 0.001-0.05) in the duodena at 4, 14, 18, and 28 wk (9-30% decreases) and in the 2nd segment at 4, 14, and 18 wk (38-69% decreases; P less than 0.001-0.005). Decreased calbindin in SHRs was documented in animals from two suppliers. The deficiencies of calbindin-D9k and alkaline phosphatase could not be attributed to malnutrition or to a generalized brush-border defect as indicated by body weights and the intestinal marker enzyme sucrase. Although calbindin-D9k was decreased in young SHRs, the serum 1,25-dihydroxycholecalciferol [1,25(OH)2D3] was increased by 59 and 129% in 4- and 9-wk-old SHRs (P less than 0.001), respectively; by contrast, serum 1,25(OH)2D3 was unchanged or decreased in older SHRs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal vitamin D-dependent calbindin-D9k and alkaline phosphatase in spontaneously hypertensive rats. 203 38

The aim of the present work was to reveal the relationship between vitamin A serum levels and some indicators of metabolic calcium and phosphorus disorders in patients in a long-term dialyzation programme. Thirty-six patients in a long-term dialyzation programme were divided into three groups. Group A comprised 11 patients who were treated for 3-9 months but without specific treatment, group B was formed by 10 patients treated for 2-5 years who were given calcium carbonate, 3 g/24 h, by the oral route for a period of six months and group C which comprised 15 patients treated for 3-10 years who were given 1 alpha, 25-dihydroxycholecalciferol (Rocaltrol), 0.25 micrograms/24 h for a period of six months. At the end of the investigation a significant rise of total calcium and serum Ca2+ occurred in all three groups of patients an a significant decrease of increased value of phosphorus, C-PTH and vitamin A in serum in groups B and C. In group A which was without treatment there was a significant increase of serum C-PTH and vitamin A after six months. The concentration of retinyl esters in serum was within the reference range of there were undetectable values throughout the investigation in all patients. A direct relationship was found between total calcium and vitamin A, alkaline phosphatase and C-PTH in serum in all 36 patients at the onset of the dialyzation programme. Moreover there was a direct relationship between C-PTH and vitamin A in groups, A, B and C at the onset of the investigation and in groups and vitamin C at the end of the investigation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vitamin A and metabolic disorders of calcium and phosphorus in patients on a long-term dialysis program]. 205 9

Mineral metabolism was studied in 31 patients with chronic renal failure on continuous ambulatory peritoneal dialysis (CAPD) for a year. After baseline observations, 1-year calcifediol treatment was started in all the patients (100 micrograms/day). After therapy, progressive normalization of calcium levels was found in all the patients, while plasma phosphate did not change. After therapy, plasma alkaline phosphatase and parathyroid hormone decreased significantly. 1,25-Dihydroxyvitamin D showed a slight increase, and 25-hydroxyvitamin D (extremely low at the start of the study) rose, reaching normal levels, after 1 year of treatment. Bone mineral density and bone biopsy indexes showed general improvement after calcifediol. In conclusion, calcifediol seems to act positively on the disorders of mineral metabolism in CAPD.
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PMID:Effects of calcifediol treatment on the progression of renal osteodystrophy during continuous ambulatory peritoneal dialysis. 207 92

We treated nineteen haemodialysis patients with secondary hyperparathyroidism with increasing oral doses of 1,25 dihydroxycholecalciferol (calcitriol) over a 12-week period and used low calcium dialysate (1.0 mmol/l) to prevent hypercalcaemia. Nine patients received daily calcitriol and ten received calcitriol thrice weekly, and at the end of the study the mean doses were 2.0 micrograms daily and 2.6 micrograms thrice weekly respectively. The regimen was well tolerated with nine episodes of mild hypercalcaemia, none of which were symptomatic. Mean PTH and alkaline phosphatase concentrations decreased from 62.0 pmol/l (15-125) to 22.0 pmol/l(1-70) (P less than 0.01), and 144 IU/l (48-461) to 123 IU/l (61-346) (P less than 0.05) respectively. Mean serum calcium increased from 2.33 mmol/l (2.05-2.55) to 2.52 mmol/l (2.26-2.67) (P less than 0.01). There were no significant changes in serum phosphate, magnesium, or aluminium concentrations and there were no significant differences in outcome between patients receiving daily therapy compared to those receiving it thrice weekly. A combination of high-dose oral calcitriol and low calcium dialysate can reverse secondary hyperparathyroidism without causing hypercalcaemia and these results suggest a benefit over conventional low-dose calcitriol.
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PMID:Low calcium dialysate and high-dose oral calcitriol in the treatment of secondary hyperparathyroidism in haemodialysis patients. 212 83

The purpose of the present study was to explore the effect of local application with Vitamin D metabolite, 1,25 dihydroxycholecalciferol (1,25 (OH)2D3), on experimental tooth movement in rats. 1. According to Waldo's method, a piece of orthodontic elastic band was inserted between the upper first and second molars of Wistar male rats weighing 200 g. The amount of 20 microliters of 1,25 (OH)2D3(10(-12)-10(-7) M) was injected locally in the submucosal palatal area of the root bifurcation of the right first molar. The left side was injected with vehicle. The number of osteoclasts was counted in a 700 x 1050 micron 2 area of the inter-radicular septum. The number of osteoclasts was dose-dependently increased 2-fold at 10(-10) M 1,25 (OH)2D3 compared to that in the vehicle-injected side. The maximal increase of osteoclast number was observed 3 days after local injection of 10(-10) M 1,25 (OH)2D3 on experimental tooth movement. 2. The upper first molar of Wistar male rats was moved in a buccal direction by a helical spring. The amount of 20 microliters of the local administration of 10(-10) M 1,25 (OH)2D3 was repeated every 3 days until sacrifice at day 20. The tooth movement in the 1,25 (OH)2D3-treated rats was accelerated about 2-fold compared to that in the control rats. 3. The effect of bone formation in the rats receiving experimental tooth movement was examined by fluorescent labeling and quantitative histology. Thus, the local application of 10(-10) M 1,25 (OH)2D3 tended to prevent the decrease of the mineral apposition rate of the alveolar bone following orthodontic tooth movement. 4. Serum samples of these 1,25 (OH)2D3-treated rats was obtained from abdominal aorta 3 hours after the final injection. Serious effects were not found in the values for parameters such as calcium, phosphorus and alkaline phosphatase. These findings suggested that the local use of 1,25 (OH)2D3 on experimental tooth movement in the rats caused increase in osteoclasts number and accelerated tooth movement. However, no obvious side effects were noted. 1,25 (OH)2D3 was expected to stimulate mineral apposition rate of alveolar bone on the tension side.
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PMID:[Effects of local application of 1,25 (OH)2D3 on experimental tooth movement in rats]. 213 2

1. Calcitriol (1,25-dihydroxyvitamin D3) concentrations in plasma of humans and pigs with pseudo-vitamin D deficiency rickets type I (PVDRI) have been reported to be significantly lower than in normal subjects and animals. Sometimes, however, calcitriol concentrations are relatively high in these subjects and animals (50-80 pmol/l) and nevertheless clinical symptoms of rickets develop. We have studied whether or not the development of rachitic lesions in piglets with PVDRI is due to altered binding properties of the intestinal calcitriol receptor in addition to the defective renal production of calcitriol. PVDRI piglets with clinical and biochemical symptoms of rickets (hypocalcaemia, increased activity of alkaline phosphatase) and with calcitriol concentrations in plasma of 83.7 +/- 4.2 pmol/l (n = 7) were used. They were compared with unaffected piglets with normal calcitriol concentrations (178.0 +/- 17.7 pmol/l, n = 9). 2. The equilibrium dissociation constant (Kd) of the receptor in the PVDRI piglets (0.31 +/- 0.05 nmol/l) and in control piglets (0.33 +/- 0.05 nmol/l) and the maximum binding capacity (Bmax.) (674 +/- 103 and 719 +/- 122 fmol/mg of protein, respectively) were not different (n = 9). 3. The association rate constant (kass) at 4 degrees C [0.15 x 10(7) and 0.24 x 10(7) (mol/l)-1 min-1] and the dissociation rate constant (kdiss) (0.40 x 10(-3) and 0.48 x 10(-3) min-1; half-life of dissociation = 24.1 and 28.9 h, respectively) were also not different between diseased and control piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of the porcine intestinal calcitriol receptor in pseudo-vitamin D deficiency rickets type I. 217 64

Treatment with 1,25-(OH)2D3 (calcitriol) was compared with placebo in a double-blind, randomized, parallel clinical trial of 24 months' duration. Subjects were white women with postmenopausal osteoporosis. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. Positive slopes were observed in the active treatment group for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. In contrast, negative slopes were observed for the bone mineral measurements in the placebo group. Measurement of urinary hydroxyproline and of serum alkaline phosphatase and osteocalcin suggested that the mechanism of action of 1,25-(OH)2D3 involved reduction of bone resorption. Hypercalciuria occurred regularly and preceded hypercalcemia by about 2 weeks. A decline in creatinine clearance was observed in two patients, one of whom had nephrolithiasis on sonography. Calcitriol is effective in preventing bone loss, but must be used with caution.
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PMID:Role of calcitriol in the treatment of postmenopausal osteoporosis. 218 76


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