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)

Vitamin D3 induction of the vitamin-D3-dependent proteins biosynthesis and certain indexes characterizing the rachitic state in animals were studied as affected by potassium orotate. Introduction of potassium orotate to the rachitogenic diet in combination with vitamin D3 is shown to normalize the processess of bone mineralization and to increase intensity of chicken growth. In duodenum mucosa with rachitis orotate normalizes the activity of alkaline phosphatase, raises the content of calcium-binding protein and stimulates the latter formation after administration of vitamin D3; orotate favours redistribution of the purine and pyrimidine nucleotides content. Radioactive orotic acid is subjected to intensive metabolism in mucosa and is converted to nucleotides of pool and RNA.
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PMID:[Effect of potassium orotate on metabolism in chickens under different provision with vitamin D3]. 21 21

Vitamin D3 in rachitic chicks stimulates calcium absorption and induces the synthesis of two pools of intestinal calcium-binding protein (CaBP), one soluble and the other membrane bound. Cortisol acetate caused a decrease in calcium absorption which was accompanied by a decrease in soluble CaBP. Cortisol was similarly effective in 1,25-dihydroxyvitamin D3-dosed chicks, suggesting that the glucocorticoid effect was not entirely due to the defective synthesis of this metabolite. Ca absorption was directly correlated with soluble CaBP and alkaline phosphatase and inversely related to the ratio of bound to soluble CaBP. It was further observed that the slope of the Ca absorption vs. soluble CaBP regression line was greater in chicks given 1,25-dihyroxyvitamin D3 compared to those given vitamin D3, and this is interpreted to mean that another factor or condition, in addition to assayed concentrations of soluble CaBP, determines the degree of calcium absorption.
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PMID:Intestinal calcium-binding protein and calcium absorption in cortisol-treated chicks: effects of vitamin D3 and 1,25-dihydroxyvitamin D3. 22 Nov 83

Cholecalciferol (Vitamin D3) and its metabolites participate in the regulation of Ca and P metabolism in vertebrates. The intermediate (6,7-cis-precalciferol) is formed by a photoreaction at wave length of 250-310 nm from 7-dehydrocholecalciferol in skin tissues. Vitamin D3, 1,25(OH)2 D3 and other metabolites, previously known to be synthesized only in mammalians and avians, have been detected also in plants. The influence of the UV light (6 hrs radiation with 254 nm) in the calcinogenic activity of T. flavescens and N. veitchii was tested. The extracts of the plants were administered to rachitic chicks in two research models: "Alimentation without Vitamin D" and "Strontium added Alimentation". After 25 days the extracts were administered (per os) and the serum was analyzed to determine the level of Ca, P and alkaline phosphatase. The results were compared with those obtained in chicks with standards of vitamin D3, 1,25(OH)2 D3, T. flavescens and N. veitchii not irradiated and also with T. flavescens that has grown in Rio Grande do Sul/Brazil.
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PMID:[The effect of ultraviolet rays and climatic conditions (solar radiation and temperature) on the calcinogenic activity of Trisetum flavescens and Nierembergia veitchii]. 179 Jul 68

Vitamin D3 administered to patients with postoperative hypoparathyroidism increases calcium absorption from the gut and calcium blood levels but leads to hypercalciuria and may produce renal lithiasis. Thiazides decrease calcium excretion with the urine. Therefore, an effect of combined therapy with hydrochlorothiazide, vitamin D3 and calcium on hypoparathyroidism was investigated. Twenty one women were selected out of 135 patients with postoperative hypoparathyroidism. These women were constantly given vitamin D3 (30,000-225,000 IU daily) and calcium. Normocalcemia, hyperphosphatemia and hypercalciuria were noted before the treatment with hydrochlorothiazide. Therapy normalized hypercalciuria but did not change mean differences in calcemia, phosphatemia, magnesemia, blood alkaline phosphatase and phosphates and magnesium clearance factors. Hypercalcemia and necessity to withdraw hydrochlorothiazide together with change of either doses or preparation of vitamin D3 were noted in three patients, including one patient in whom both hypercalcemia and hypercalciuria with the symptoms of vitamin D3 poisoning were observed. The author suggests that combined therapy with hydrochlorothiazide, vitamin D3 and calcium prevents hypercalciuria but may require changes in vitamin D3 dosage and withdrawal of hydrochlorothiazide in some patients.
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PMID:[Effect of hydrochlorothiazide on calcium metabolism in postoperative hypoparathyroidism]. 196 53

Turkey poults were fed a vitamin D-deficient diet and examined for clinical signs and structural changes of bone and parathyroid glands. Vitamin D-deficient poults developed ricketic changes during days 10 to 14. Control poults (deficient diet plus vitamin D) did not develop rickets. In deficient poults, lengths of proliferating-prehypertrophied zones of growth plates increased significantly in the proximal tibiotarsus but were only slightly elongated in the distal tibiotarsus. Unmineralized hypertrophic chondrocyte zones increased in length rapidly in conjunction with a decrease in the length of mineralized hypertrophic degenerative zones; this occurred more rapidly in proximal than in distal tibiotarsus. Other ricketic changes included decreases in bone ash, total femoral bone ash (calcium, phosphorus, magnesium), bone length, and body weight. Plasma alkaline phosphatase was increased, calcium was normal, and phosphorus was normal or elevated. Parathyroids were hyperplastic and had foci of degeneration. Vitamin D3 metabolites 25OHD3, 1,25(OH)2D3, and 24,25(OH)2D3 were rapidly depleted. Increase in bone ash Ca/P ratios in deficient poults suggests that phosphorus may be selectively released from ricketic bone. Low 25OHD3 and 1,25(OH)2D3 of control poults early in the experiment suggests that 1,400 IU of vitamin D3/kg of feed may not be an adequate level of vitamin D3 for growing turkey poults.
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PMID:Pathology of vitamin D deficiency in growing turkeys. 375 Jul 40

Vitamin D3 is known to stimulate the absorption of calcium across the asymmetric intestinal epithelial cells. Efforts to elucidate the mechanism of stimulation of intestinal calcium transport by vitamin D are now focused on evaluating the protein composition and topology of the brush-border membrane and its associated core material. Intestinal brush-border membranes were isolated from vitamin D-replete and vitamin D-deficient chicks. Core material proteins were isolated, by sedimentation, from brush-border membranes which were solubilized with Triton X-100. As determined by polyacrylamide gel electrophoresis, dietary vitamin D3 treatment caused no change in the relative amounts of five major core material proteins with Mr = 101,000, 94,000, 67,000, 42,000 (actin), and 17,000. In contrast, dietary vitamin D3 treatment caused a significant reduction in the levels of two proteins with Mr = 111,000 (sucrase) and 83,000, and an increase in the levels of a protein with Mr = 78,000 (possibly a subunit of alkaline phosphatase). The Mr = 111,000, 83,000, and 78,000 proteins are readily solubilized by Triton X-100 and are located on the extracellular surface of the brush-border membrane, as judged by [125I]diazoiodosulfanilic acid and lactoperoxidase 125I labeling. A significant vitamin D-dependent difference was found with respect to iodination of isolated core material as evidenced by the 125I labeling patterns of the Mr = 42,000 protein (actin). The Mr = 42,000 protein was labeled two to three times more extensively when associated with core material derived from vitamin D-deficient chicks as compared to vitamin D-replete chicks. Increasing the salt concentration (0-125 mM KCl) present during core material isolation from either vitamin D-replete or vitamin D-deficient chicks yields core material actin which is more susceptible to iodination by both [125I]diazoiodosulfanilic acid and lactoperoxidase. This increase in the extent of actin iodination is coupled to a salt-induced decrease in the stability of the core material which is evidenced by a decrease in the percentage of total brush-border membrane actin which is Triton-insoluble. This strongly suggests that the vitamin D-induced decrease in the accessibility of actin to iodination reagents results from a vitamin D-dependent change in the structure of the core material. Collectively, these results implicate a role for dietary vitamin D3 in maintaining a specified composition and topology of both the brush-border membrane proteins as well as its associated cytoskeletal core proteins, which is possibly important for intestinal calcium transport.
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PMID:Vitamin D. Its effect on the protein composition and core material structure of the chick intestinal brush-border membrane. 630 7

Two experiments were conducted on dietary predisposition to rickets in poults. The first experiment compared fat type (corn oil or tallow), level of added fat (3.5 or 7%), vitamin D3 (900 or 2,400 IU/kg feed), and total calcium (.6, 1.2, or 3%) inclusion in the diet. Poults fed diets supplemented with corn oil had higher percentage tibia ash than poults fed tallow-supplemented diets. Vitamin D3 included at 2,400 IU/kg feed increased body weights significantly by 2 and 4 weeks of age and lowered plasma alkaline phosphatase (AP) at 2 and 4 weeks compared with diets containing 900 IU/kg feed. Tibia ash was significantly greater with the higher vitamin D3 supplementation at 2 weeks. At 2 weeks of age both low (.6%) and high (3%) levels of dietary calcium increased plasma AP, decreased tibia ash, and decreased body weight compared with diets containing 1.2% calcium. By 4 weeks of age, diets containing 1.2 and 3% calcium had no significant effects on body weight and plasma AP; however, tibia ash was significantly greater with these levels than with the .6% calcium diets. The second experiment compared level of dietary tallow inclusion (2.5 or 7%) and supplementary vitamin A (4,000, 16,000, or 44,000 IU/kg feed). The high tallow diets decreased tibia ash at 3 weeks, and the maximum supplementation of vitamin A significantly depressed body weight. Clinical rickets were first noted at 18 days of age. By 26 days of age the higher level of dietary fat and the highest level of vitamin A caused a significant increase in severity of rickets. The results suggested that rickets can be induced by high dietary levels of tallow and vitamin A.
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PMID:Dietary level of fat, calcium, and vitamins A and D3 as contributory factors to rickets in poults. 631 10

Rat osteogenic sarcoma cells which have osteoblast properties including the ability to form bone and to mineralize were recently found to possess specific cytoplasmic receptors for 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). We have examined now the effect of 1,25(OH)2D3 and other vitamin D3 metabolites on the alkaline phosphatase of such cell lines. We found in two cell lines cultured in the presence of 10(-7) M 1,25(OH)2D3 a 3-fold increase in intracellular alkaline phosphatase activity and a 6-fold increase in secreted alkaline phosphatase activity. The cellular response occurred in a dose-dependent fashion at a range of 10(-9) to 10(-7) M. In a third cell line, which does not possess the specific receptor for 1,25(OH)2D3, we could not detect stimulation of alkaline phosphatase. Vitamin D3, 25-dihydroxyvitamin D3, and 24,25-dihydroxyvitamin D3 at 10(-7) M had no effect on alkaline phosphatase. The effect of 1,25(OH)2D3 was enhanced in the presence of increased calcium. In view of the postulated role for alkaline phosphatase in calcification, we speculate that the stimulatory effect of 1,25(OH)2D3 on the alkaline phosphatase activity of osteoblast-like cells indicates a direct involvement of 1,25(OH)2D3 in bone mineralization.
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PMID:1,25-Dihydroxyvitamin D3 stimulates the alkaline phosphatase activity of osteoblast-like cells. 694 64

Vitamin D3 metabolites affect the proliferation and differentiation of cartilage cells. Previous reports have shown that rat costochondral cartilage chondrocytes isolated from the growth zone (GC) respond to 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], whereas those from the resting zone (RC) respond to 24,25-(OH)2D3. The aim of the present study was to determine whether 24,25-(OH)2D3 induces differentiation of RC cells into a 1,25-(OH)2D3-responsive GC phenotype. To do this, confluent, fourth passage RC chondrocytes were pretreated for 24, 36, 48, 72, and 120 h with 10(-7) M 24,25-(OH)2D3. The medium was then replaced with new medium containing 10(-10) to 10(-8) M 1,25-(OH)2D3, and the cells were incubated for an additional 24 h. At harvest, DNA synthesis was measured as a function of [3H]thymidine incorporation; cell maturation was assessed by measuring alkaline phosphatase (ALPase) specific activity. Incorporation of [3H]uridine was used as a general indicator of RNA synthesis. Matrix protein synthesis was assessed by measuring incorporation of [3H]proline into collagenase-digestible protein (CDP) and collagenase-nondigestible protein (NCP) as well as 35SO4 incorporation into proteoglycans. When RC cells were pretreated for 24 h with 24,25-(OH)2D3, they responded like RC cells that had received no pretreatment; further treatment of these cells with 1,25-(OH)2D3 had no effect on ALPase, proteoglycan, or NCP production, but CDP production was inhibited. However, when RC cells were pretreated for 36-120 h with 24,25-(OH)2D3, treatment with 1,25-(OH)2D3 caused a dose-dependent increase in ALPase, CDP, and proteoglycan synthesis, with no effect on NCP production. RC cells pretreated with 1,25-(OH)2D3 responded like RC cells that had not received any pretreatment. To determine whether these responses were specific to chondrocytes in the endochondral pathway, cells were isolated from the xiphoid process, a hyaline cartilage. In these cells, 1,25-(OH)2D3 inhibited ALPase, whereas 36 h of pretreatment with 24,25-(OH)2D3 caused these cells to lose their response to 1,25-(OH)2D3. These results indicate that 24,25-(OH)2D3 can directly regulate the differentiation and maturation of RC chondrocytes into GC chondrocytes, as evidenced by increased responsiveness to 1,25-(OH)2D3. 24,25-(OH)2D3 also promotes differentiation of cells derived from xiphoid cartilage, resulting in the loss of 1,25-(OH)2D3 responsiveness. These observations support the hypothesis that 24,25-(OH)2D3 plays a significant role in cartilage development.
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PMID:Treatment of resting zone chondrocytes with 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] induces differentiation into a 1,25-(OH)2D3-responsive phenotype characteristic of growth zone chondrocytes. 753 Jun 45

The bone histology of renal osteodystrophy is classified into osteitis fibrosa, osteomalacia, those of mixed, osteoporosis and low turnover bone. Osteitis fibrosa is the most frequent skeletal abnormality and is caused by various degrees of hyperparathyroidism. The main factors inducing hyperparathyroidism which is a well known complication in patients with renal failure include (a) phosphorus retention: 1) hypocalcemia and 2) decreased levels of 1 alpha, 25(OH)2 Vitamin D3, (b) reduced number of 1 alpha, 25(OH)2 Vitamin D3 receptors in parathyroid tissue, (c) skeletal resistance to set-point for calcium-regulated parathyroid hormone secretion. Serum or plasma levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone, calcitonin and tartrate resistant acid phosphatase are measured to evaluate hyperparathyroidism and metabolic bone disease. Dietary phosphorus restriction in chronic renal insufficiency prevents secondary hyperparathyroidism and renal osteodystrophy. Other treatment of phosphorus binders, Vitamin D metabolites or analogues, carcitonin and bisphosphonate are useful for the management of renal bone disease.
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PMID:[Secondary hyperparathyroidism and tertiary hyperparathyroidism chronic renal failure, uremia]. 775 92


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