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)

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

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

Records of the dietary intake of 52 preschool vegetarian children seen from 1974 to 1976 revealed that macrobiotic vegetarian diets provided amounts of vitamin D, calcium, and phosphorus that were marginal as well as less than the amounts provided by other vegetarian diets. Vitamin D supplements were rarely given. Two subjects had roentgenographic evidence of rickets. The medical histories of 32 children on macrobiotic diets who were examined in 1977 more frequently included prior physical and roentgenographic findings indicative of rickets, whereas those of 17 other vegetarian children did not. Children in the former group were more likely to have elevated levels of serum alkaline phosphatase. Two additional cases of rickets in children consuming a macrobiotic diet confirmed by roentgenograms were brought to our attention during the study.
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PMID:Risk of nutritional rickets among vegetarian children. 42 Jan 81

In an 18-year-old boy with Bartter's syndrome, hypophosphatemia was discovered (2.4 mg/100 ml) with normal serum calcium concentration (9.7 mg/100 ml) and elevated alkaline phosphatase level: 528 mU/ml (normal less than or equal to 150). Skeleton X-rays showed osteomalacia on the pelvic bones and metaphyseal rickets on the wrists. Plasma 25-hydroxycholecalciferol (25-OHCC) concentration was 7.2 ng/ml (normal = 13 +/- 4.4), and serum immunoreactive parathyroid hormone (iPTH) concentration 160 micron1Eq/ml (normal less than or equal to 150). Ca infusion (1500 mg/m2/12 h) induced an increase in serum P level to 3.2 mg/100 ml, in tubular phosphate reabsorption from 72 to 90%, while serum iPTH decreased to 33 micron1Eq/ml. Vitamin D2 administration (45 mg) resulted in increased 25-OHCC concentration to 28 ng/ml and in healing of pelvic osteomalacia. However, there was little change of the radiological aspect of the wrist and of serum phosphorus and iPTH concentrations. In a control 6-year-old hypokalemic girl, administration of parathyroid hormone (8 USP/kg) produced a marked phosphaturic response and an increase in urinary cyclic AMP excretion. These data suggest that hypophosphatemia can be attributed to secondary hyperparathyroidism in the patient with Bartter's syndrome. Hypokalemia does not impair the renal activity of parathyroid hormone.
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PMID:Hypophosphatemia and hyperparathyroidism in a case of Bartter's syndrome. 71 93

The findings in 20 cases of nutritional rickets treated on an out-patient basis with oral calciferol and calcium gluconate are reported. Attention was paid to their clinical, biochemical and radiological responses. If was noted that presentation at the hospital out-patient department was always delayed until there were obvious and sometimes severe deformities in the children. Biochemical changes noted during the early phase of treatment showed an initial fall in the level of serum calcium and plasma phosohorus and a rise in the serum alkaline phosphatase. About three months after initiating treatment, calcium and phosphorus reverted to normal levels but serum alkaline phosphatase still remained high. Twelve of our cases (60 per cent) suffered from protein calorie malnutrition of the marasmic type and showed an apparent resistance to vitamin D therapy in what may be regarded as normal dosages. Response was however, achieved with substantial increase in the amount of vitamin given. There was a striking sex difference in the ratio of 15 males to five females indicating that males are more likely to develop nutritional rickets than females when subjected to predisposing environmental conditions. Vitamin D resistant type of rickets was not encountered in this study.
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PMID:Rickets in Nigerian children--response to vitamin D. 108 35

The serum levels of the active Vitamin D metabolites 25-hydroxyvitamin D[25(OH)D], 1,25-dihydroxyvitamin D[1,25(OH)2D] and 24,25 dihydroxyvitamin D [24,25(OH)2D], were studied in 21 children with Down's syndrome (DS) in Cantabria, a northern region of Spain, located at 44 degrees N latitude. Serum calcium, magnesium, phosphate, alkaline phosphatase, parathormone and osteocalcine were also determined. In the DS group, the average values of the three Vitamin D metabolites were comparable to those of an age-matched group both in winter and summer times. No child with DS showed values below the normal range, either in Vitamin D metabolites, or in the other parameters of calcium metabolism. The normal increment of 25(OH)D and 24,25(OH)2 values from March to October was not observed in five children. This anomaly was corrected in three, after adequate rules of sun exposure during summer time were followed. In the other two, the 25(OH)D levels were high throughout the study. This investigation shows that children with DS do not require Vitamin D prescription when appropriate periods of sunlight exposure are provided.
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PMID:Vitamin D status in children with Down's syndrome. 153 19

Experiments were performed to investigate the effects of lindane and linuron on calcium metabolism, femur morphometry and nephrotoxicity. Long-Evans hooded rats were dosed daily for 10 weeks with 0, 10 or 20 mg lindane or 10, 20 or 40 mg linuron/kg body weight beginning at weaning. Lindane significantly decreased urinary calcium concentration, serum alkaline phosphatase concentration and the cross-sectional medullary area of the bone. Lindane was nephrotoxic at both dose levels as demonstrated by elevated kidney weights, kidney-to-body-weight ratios, urinary LDH, tubule regeneration and hyaline droplet degeneration. Linuron significantly reduced medullary cross-sectional area at the 2 higher dose levels and decreased the total femur cross-sectional area at the highest dose level in the absence of effects on calcium excretion. Femur density and strength were also significantly reduced at the highest dose level of linuron. Neither compound affected the serum concentrations of parathyroid hormone or 1,25-dihydroxy Vitamin D-3. Both linuron and lindane exposure significantly increased serum cholesterol concentrations and reduced serum triglyceride concentrations. Both compounds affected calcium metabolism and/or bone morphometry but possibly by different mechanisms since the effects were not the same.
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PMID:The effects of lindane and linuron on calcium metabolism, bone morphometry and the kidney in rats. 169 Apr 64

Progesterone, which is normally produced in the endoplasmic reticulum, was found to be rapidly degraded in the cytosolic fraction of the guinea pig adrenal cortex in vitro. Assuming this finding reflects what happens in vivo raises a question as to the source of progesterone for interacting with a nuclear progesterone-binding protein (P4-BP) that exists in this model system. It was subsequently found that pregnenolone, which in contrast to progesterone is relatively stable in the cytosol, was converted to progesterone by endogenous nuclear 3 beta-ol dehydrogenase. It was also determined that the nuclear-derived progesterone specifically bound to the nuclear P4-BP which is distinct from the classical progesterone receptor. The guinea pig adrenocortical cytosol contains a specific pregnenolone-binding protein (P5-BP) that could be virtue of its pregnenolone binding activity regulate the conversion of pregnenolone to progesterone in the nuclear compartment and thereby reduce the binding of progesterone to the nuclear P4-BP. A partially purified P5-BP preparation markedly inhibited the nuclear conversion of pregnenolone to progesterone and reduced the binding of progesterone to the nuclear P4-BP (P5-BP did not directly inhibit binding of progesterone to the nuclear P4-BP). The ability of P5-BP to inhibit the conversion of pregnenolone to progesterone was destroyed by heat and alkaline phosphatase treatment. The binding of pregnenolone to the P5-BP, as previously reported, is regulated by phosphorylation/dephosphorylation, and alkaline phosphatase-treated P5-BP loses the ability to bind pregnenolone; this process can be reversed by a cytosolic kinase. This provides a mechanism for controlled release of bound steroid. These results suggest that P5-BP regulates the nuclear conversion of pregnenolone to progesterone and thus the binding of progesterone to the nuclear P4-BP.
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PMID:The nuclear conversion of pregnenolone to progesterone and subsequent binding to the nuclear progesterone-binding protein in the guinea pig adrenal cortex: a possible regulatory role for the pregnenolone-binding protein. 169 80

The research described in this article has focused on the complex autocrine, paracrine, and endocrine regulation of endochondral ossification using vitamin D metabolites and TGF-beta as models. By comparing results from a number of laboratories utilizing a diverse array of in vivo and in vitro systems, a coherent picture is beginning to emerge. Vitamin D metabolites influence cell differentiation and maturation and have direct effects on cell function. Differentiation of the mesenchymal cells into chondroblasts is regulated by both 1,25-(OH)2D3 and 24,25-(OH)2D3, as well as by TGF-beta. The resting zone chondrocytes respond primarily to 24,25-(OH)2D3 in terms of matrix synthesis and matrix vesicle biochemistry. They synthesize both metabolites and other factors that stabilize matrix vesicle enzymes like AHSG. In addition to the paracrine role these factors may play in regulating the matrix, it is possible that they may influence the cells in the growth plate itself. Growth zone chondrocytes also synthesize both metabolites, but respond primarily to 1,25-(OH)2D3 for the parameters measured in the studies described. These cells also synthesize TGF-beta which further increases alkaline phosphatase activity, perhaps via an autocrine stimulation of the cell. While cells from the calcified zone have not yet been studied directly in culture, it is likely that they respond to paracrine signals from the avascular cartilage as well as to serum-derived factors. How the signals are transferred among the cells is unknown. Certainly one can postulate information flow in both upward and downward directions. The signal transduction mechanisms for the factors at the cellular level are complex. While it is known that 1,25-(OH)2D3 stimulates gene transcription and stabilization of mRNA for proteins like alkaline phosphatase, its nongenomic effects are only beginning to emerge. Membrane effects of this metabolite have been shown in intestine and kidney in conjunction with studies on Ca flux. It is becoming increasingly evident that other steroid hormones may operate in similar ways. Studies with the rat costochondral chondrocytes are the first to show that there are specific membrane effects for at least two vitamin D metabolites and that membrane enzymes, including those involved in phospholipid metabolism, can be differentially regulated by them. Furthermore, these experiments have provided for the first time a clear hypothesis for how cells can regulate events in the extracellular matrix after the matrix vesicles are produced and incorporated into the matrix.
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PMID:In vitro studies on the regulation of endochondral ossification by vitamin D. 173 69

A seventeen-year-old youth was presented with muscle cramps and convulsions. A brain CT scan showed calcification in the region of the ganglia, and a diagnosis of brain tumor was thus made and an anticonvulsant given for two years. At age nineteen, the patient developed pseudohypoparathyroidism owing to low serum calcium and high serum PTH levels. However, serum alkaline phosphatase and serum osteocalcin levels were high, lesion was detected in the femur neck. These data indicated that the bone remodeling response to PTH had remained intact in this patient. Serum osteocalcin is known to increase in primary hyperparathyroidism. However, unlike patients with hyperparathyroidism, those with pseudohypoparathyroidism show no increase in serum 1,25(OH)2D. The present case was thus useful for examining the direct effect of PTH on serum osteocalcin. The patient was administered 1 alpha (OH)D, and his condition monitored for two years. During this period, osteocalcin and PTH levels decreased while that of 1,25(OH)2D increased. Osteocalcin and PTH levels were found to be closely correlated (r = 0.68, p less than 0.01). The present results indicate the possibility that PTH may increase serum osteocalcin independent of Vitamin D.
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PMID:[Serum osteocalcin concentration in a patient with pseudohypoparathyroidism type Ib]. 188 14


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