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)

We investigated bone mineral content and factors related to decreased bone mineral content in maintenance hemodialysis patients. Bone mineral contents, epsilon GS/D, radius-bone mineral content (R-BMC) and L3-bone mineral density (L3-BMD), were measured with a micro densitometer, a bone mineral analyzer and a dual energy quantative CT scanner, and relative bone mineral contents (% epsilon GS/D, %R-BMC and %L3-BMD) were calculated respectively. The desferrioaxmine infusion test was carried out for diagnosis of aluminium associated bone disease, and an elevated level of aluminium (delta aluminium) was observed. There was reverse correlation between epsilon GS/D and age in female hemodialysis patients. Serum bone gla protein, alkaline phosphatase and PTH-C levels were high in cases with increased epsilon GS/D and who were receiving little medication with activated Vitamin D in maintenance hemodialysis patients. A correlation was observed between delta aluminium and total medication of aluminium hydroxide-gel. Hemodialysis patients with bone pain had long term hemodialysis, high total medication of aluminium and high aluminium. Relative bone mineral contents (% epsilon GS/D, %R-BMD) were useful for estimating bone mineral content in hemodialysis patients. Hemodialysis patients were divided in four groups by PTH-C and delta aluminium levels as follow, 1) normal, 2) aluminium associated bone disease, 3) secondary hyperparathyroidism with aluminium associated bone disease, 4) secondary hyperparathyroidism. These results indicate that secondary hyperparathyroidism, and medication with aluminium may play a role in decreased bone mineral content in hemodialysis patients, and menopause may also be an important factor in female hemodialysis patients.
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PMID:[Clinical study of concerning factors of decreased bone mineral content in hemodialysis patients]. 192 Sep 39

The effects of prolonged administration of anticonvulsants were analyzed on different biochemical parameters related to phosphocalcium metabolism in 98 children aged 1 to 14, not affected by other chronic pathology, and to whom no Vitamin D nor other vitamin-mineral complexes had been administered. We take as reference a group of normal children studied during the same period. Determinations were accomplished with the usual chemical controls in our laboratory (autoanalysis of continuous flow, radioimmunoassay and colorimetric measurements) and the following mean levels were obtained for treated children: Calcium: 9.2 +/- 0.4 mg/dl, phosphorous: 3.5 +/- 1.9 mg/dl, alkaline phosphatase: 252 +/- 72 U/L, 25-Hydroxycholecalciferol: 35.6 +/- 18 ng/ml, Osteocalcine: 5.4 +/- 3.6 ng/ml, and parathyroid hormone: 0.4 +/- 0.1 ng/ml. These values differed significantly from those found in the control group for phosphorous, lower in children under treatment (p = 0.000), and the 25-Hydroxycholecalciferol was likewise lower (p = 0.000). In other way the mean levels of alkaline phosphatase were higher in treated children (p = 0.000). No significant differences were obtained for mean levels of calcium, parathyroid hormone and osteocalcine. These differences are maintained when distributing patients among different age groups. Solar radiation received by treated children during the months preceding the extraction, did not produce significant differences on 25-Hydroxycholecalciferol, with mean values that were similar at the end of summer (34 +/- 9 ng/ml) and the end of winter (36.6 +/- 18 ng/ml).
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PMID:[Phosphorus-calcium metabolism in children under long-term anticonvulsant therapy]. 195 57

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

A cohort of 101 patients were treated with enteric-coated sodium fluoride tablets and calcium supplements. Vitamin D was also given in supra-physiologic doses in 70% of the cases. Lumbar bone mineral density (BMD), as measured by dual-photon absorptiometry, increased in a linear fashion up to four years, irrespective of the value of initial BMD and of the underlying condition, be it involutional osteoporosis (the vast majority), glucocorticoid osteoporosis, or even osteogenesis imperfecta. Estrogen replacement therapy (ERT) seemed to promote the fluoride-induced increase in lumbar BMD, as did the vitamin D supplements. Of these patients, 17% proved "resistant" to the therapy. There was no way of predicting who would be in this category. Compared with an age- and sex-matched control group, women showed significantly different behavior of their bone mass. In the control group, the losses were highly significant at the lumbar spine and at all three scanning sites of the forearm, as measured by single-photon absorptiometry. In contrast, the fluoride group had a significant gain of BMD at the lumbar spine and changes of BMC at the forearm were not significant. Fluoride thus preserved bone mass at the appendicular skeleton, while increasing it at the axial skeleton. When comparing the patients who received vitamin D supplements and those who did not, there was a significant difference in the appendicular skeleton. The distal forearm in the vitamin D-supplemented group tended to gain, whereas the midforearm lost significant bone mass. The trend was reversed in the group without vitamin D-supplementation, a more favorable pattern. Therefore, vitamin D supplements should not, as a rule, be provided to such patients. The biochemical hallmark of the fluoride-induced changes is a slight rise of the alkaline phosphatase within the normal range. Alkaline phosphatase levels that exceed the upper limit of normal signal a warning that too much fluoride and/or too little calcium supplements are being administered, or that a fluoride-related complication is impending or has occurred (e.g., a stress fracture). Osteosclerosis was achieved in 69% of the cases who had a radiological followup of at least four years (average period of appearance: 1.8 years). Stress fractures in the lower limbs occurred in 17 patients, almost exclusively in females, and appeared on average 2.2 years after initiation of therapy. In this group of stress fractures there was significant cortical bone loss at midforearm.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment of the vertebral crush fracture syndrome with enteric-coated sodium fluoride tablets and calcium supplements. 218 27

Preterm infants (birth weight, 1,089 +/- 91 g; gestational age, 28.9 +/- 0.7 weeks; mean +/- SEM) with mixed medical and surgical indications for parenteral nutrition (PN) were observed to determine the adequacy of infusates with fixed, low-dose vitamin D (25 IU/dl) and two combinations of calcium and phosphorus. The duration of low-dose vitamin D PN ranged from 5 to 52 days, with a median of 27 days. Twelve infants were randomly assigned to low (standard) Ca and P doses (5 mM each; 20 mg/dl of Ca and 15.5 mg/dl of P) and 13 high Ca and P doses (15 mM each; 60 mg/dl of Ca and 46.5 mg/dl of P). The maximum daily vitamin D intake was similar for both groups (31 +/- 1.3 versus 33 +/- 1.2 IU/kg). Vitamin D status in either group, as indicated by serum 25-hydroxyvitamin D (25-OHD) concentrations, was normal. There was no significant difference in observed changes of serial measurements of serum calcium, magnesium, phosphorus, alkaline phosphatase, creatinine (Cr), 25-OHD, and vitamin D-binding protein concentrations or urinary Ca:Cr and Mg:Cr ratios. In the low-dose Ca and P group, the serum P level was consistently less than 4 mg/dl in five infants, serum 1,25-dihydroxyvitamin D concentrations were higher, and tubular reabsorption of phosphorus was consistently greater than 95% and significantly higher than in the high-dose Ca and P groups. Severe bone demineralization apparent on X-ray occurred in two infants, with a fractured distal left ulna in one of the two infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Minimal vitamin D and high calcium and phosphorus needs of preterm infants receiving parenteral nutrition. 249 13

The intestinal absorption of calcium is certainly a complex process, dependent on several factors of which vitamin D, via 1,25(OH)2D3, is the major controlling hormone. The efficiency of calcium absorption is a function of calcium status and calcium need. As the body's demand for calcium increases, the process commonly termed, adaptation, is activated in which the synthesis of 1,25(OH)2D3 from precursor is increased, resulting in the stimulation of the rate of calcium absorption. The increased demand for calcium might result from the ingestion of a diet deficient in calcium, from growth, pregnancy, lactation and egg shell formation in the laying hen. Accomapanying the change in calcium absorptive efficiency are molecular modifications of the transporting enterocytes, some mentioned herein and elsewhere (Wasserman & Chandler, 1985; Wasserman, 1980; Wasserman et al., 1984). Highly correlated with the rate of calcium absorption under a wide variety of conditions is the concentration of the vitamin D-induced calcium-binding protein, calbindin-D28K (avian type) and calbindin-D9K (mammalian intestinal type). The role of calbindin-D in this transport process is not precisely known but is considered to act at the present time as a cytosolic facilitator of Ca2+ diffusion from the brush border membrane to the basolateral membrane. In addition to the induction of calbindin-D synthesis, 1,25(OH)2D3 exerts other effects on the intestinal epithelium that can have consequences on the calcium absorptive process. Some of these effects are summarized in Figure 14. Vitamin D-dependent reactions might be either direct effects of 1,25(OH)2D3 or indirect effects due to elevated intracellular Ca2+ concentrations. These include changes in the fluidity of the brush border membrane, an increase in microvillar alkaline phosphatase-low affinity Ca-activated ATPase activity, an association of calmodulin with the 105 kD brush border cytoskeletal protein and, following calbindin D synthesis, the binding of calbindin D to a 60 kD brush border protein and to microtubules. The latter has been suggested to be related to the proposed transfer of Ca2+ by an endocytotic-exocytotic mechanism. In addition, a vitamin D-dependent intestinal membrane calcium-binding protein has been identified (Kowarski & Schachter, 1980). Playing into this multi-component system is a stimulation of cyclic nucleotide synthesis by 1,25(OH)2D3 which, through activation of cyclic nucleotide-dependent protein kinases, might modify membrane Ca2+ "channels" by phosphorylation reactions.4+ Intracellular organelles, i.e., the endoplasmic reticulum, mitochondria, the Golgi apparatus, are potent sequesters of Ca2+ and could contribute to the protection of the cell from excessively high Ca2+ concentrations by transiently storing absorbed Ca2+.
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PMID:On the molecular mechanism of intestinal calcium transport. 254 94

Matrix vesicles are membrane organelles found in the extracellular matrix of calcifying cells. Vitamin D-responsive alkaline phosphatase specific activity has been localized to matrix vesicles in chondrocyte and osteoblast cultures. The effect of hormone is both metabolite and cell specific. Alkaline phosphatase in matrix vesicles produced by resting zone chondrocytes is stimulated by 24,25(OH)2D3 whereas alkaline phosphatase in matrix vesicles produced by growth zone chondrocytes is responsive to 1,25(OH)2D3. However, mesenchymal cell cultures, which exhibit a chondrogenic phenotype when exposed to bone inductive proteins in vitro, produce vesicles with alkaline phosphatase activity that is unaffected by either 1,25(OH)2D3 or 24,25(OH)2D3. Incorporation and release of arachidonic acid into phosphatidylethanolamine is also differentially regulated by 1,25(OH)2D3 and 24,25(OH)2D3 in chondrocytes. These data suggest that vitamin D metabolites may regulate endochondral ossification by altering matrix vesicle enzyme activities, perhaps through changes in membrane phospholipid metabolism.
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PMID:Regulation of matrix vesicle metabolism by vitamin D metabolites. 268 84

The present study evaluated 12 infants with birth weights less than 2000 g who received human milk plus a multivitamin supplement and 20 similar infants who received standard cow's milk formula for 16 weeks from the time of initial hospital discharge. Examination at birth, at hospital discharge (study entry), at 4 and 16 weeks after hospitalization, and at 52 weeks of age revealed no intergroup differences in body weight, length, and head circumference. Hypophosphatemia (plasma phosphorus concentration less than or equal to 1.45 mmol/L) developed in 6 infants fed human milk (5 infants at 4 weeks and 1 infant at 16 weeks of study). Mean vitamin D intakes, but not calcium and phosphorus intakes, were significantly lower during hospitalization in human milk-fed infants with hypophosphatemia (44 [25, SD] IU/d) compared with those without hypophosphatemia (322 [180] IU/d). These data indicate that human milk-fed, low-birth-weight infants are at risk for hypophosphatemia following initial hospital discharge. Plasma calcium, phosphorus, and alkaline phosphatase concentrations at hospital discharge may not predict the infants at risk. Vitamin D supplementation early in the infants' hospital course may prevent hypophosphatemia.
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PMID:Hypophosphatemia in breast-fed low-birth-weight infants following initial hospital discharge. 280 61

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

The present study was undertaken to investigate the effect of the Hyp mutation and diet-induced hyperparathyroidism on renal responsiveness to PTH and forskolin and to determine whether the renal brush border membrane phosphate transport defect is expressed in the vitamin D- and calcium-deficient Hyp mouse. Our results indicate that PTH is a potent activator of cAMP synthesis in renal slices obtained from vitamin D-replete normal mice and Hyp littermates. However, in the mutants, the amount of cAMP produced in response to similar concentrations of PTH (0.005-5 U/ml) is 55% of normal (P = 0.0076). PTH-dependent cAMP synthesis is significantly reduced in both normal and Hyp mice fed the vitamin D-deficient low calcium diet, and under these conditions, genotype differences are no longer apparent. In contrast, forskolin-stimulated cAMP production is identical in vitamin D-replete normal and mutant mice. Furthermore, cAMP accumulation in response to forskolin is not decreased by diet-induced hyperparathyroidism in either genotype. Vitamin D and calcium deprivation results in a significant decrease in renal brush border membrane Na+-dependent phosphate transport in both genotypes, and under these conditions, the phosphate transport defect persists in Hyp mice. Finally, vitamin D and calcium deprivation has no effect on renal brush border membrane alkaline phosphatase activity. The present results suggest that the catalytic subunit of adenylate cyclase is intact in the mutant strain and that the blunted renal response to PTH in vitamin D-replete Hyp mice as well as in vitamin D- and calcium-deficient mice may be due to uncoupling of the PTH-receptor-adenylate cyclase system. The data also suggest that the expression of the renal phosphate transport defect in Hyp mice is independent of PTH status and alkaline phosphatase activity.
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PMID:Effect of the Hyp mutation and diet-induced hyperparathyroidism on renal parathyroid hormone- and forskolin-stimulated adenosine 3',5'-monophosphate production and brush border membrane phosphate transport. 300 90


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