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)

Biomaterial implantation in animals is commonly used for biocompatibility studies as well as examination of long-term interaction between tissue and the test material. An in vitro cell culture model is proposed as an alternative which will save animal lives and reduce the pain and discomfort of animals used for such studies. In this study the biomaterial was matched to the cell types typical of the implant site of the particular material: porous calcium phosphate ceramic, used as dental and orthopaedic implants, with periosteal fibroblasts, osteoblasts and chondrocytes. All three cell types attached on to the ceramic and formed multicellular layers. Numbers of periosteal fibroblasts, osteoblasts and chondrocytes increased 29-, 23- and 17-fold, respectively, during the 10 wk period. Osteoblasts retained their phenotypic expression by producing only Type I collagen. Parathyroid hormone (PTH, 50 nM) suppressed the alkaline phosphatase activity of osteoblasts by over 50% and increased cAMP by more than 10-fold over control cultures.
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PMID:Growth of osteoblasts on porous calcium phosphate ceramic: an in vitro model for biocompatibility study. 254 Aug 46

This report describes the case of a 60-year-old woman with severe metabolic bone disease and fractures due to vitamin D deficiency and hyperparathyroidism. 25OHDH3 and 1,25(OH)2D3 serum levels were undetectable and increased immediately following 25OHD3 oral administration. Serum 1,25(OH)2D3 following vitamin D repletion reached values above the normal range, and remained elevated with strict dependence on the serum 25OHD3 levels. Parathyroid hormone and alkaline phosphatase decreased during treatment, without reaching normality during 1 year of observation. Bone biopsies before and after 8-month 25OHD3 treatment showed disappearance of the osteomalacic and hyperparathyroid lesions. During treatment an increase in serum and urine calcium and formation of renal stones were observed. The patient underwent neck exploration with the finding and removal of a lipoadenoma, a rare parathyroid tumor, followed by complete and permanent remission of the disease. In conclusion, this case is suggestive of the key role played by the long-term vitamin D status in the clinical expression of primary hyperparathyroidism.
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PMID:Severe vitamin D deficiency in a case of primary hyperparathyroidism caused by parathyroid lipoadenoma, effect of 25OHD3 treatment. 261 20

Osteocalcin serum levels reflect bone turnover. In renal insufficiency secondary hyperparathyroidism and reduced renal clearance might be responsible for elevated serum levels of osteocalcin. Renal transplantation might improve renal osteodystrophy and therefore could influence osteocalcin serum levels. We determined the influence of renal transplantation on osteocalcin levels in 37 consecutive patients (25m/12f) by RIA. Blood samples were collected prior to, 3 days, 28 days, 6 months and 12 months after renal transplantation. Prior to renal transplantation osteocalcin levels were significantly elevated (mean +/- s: 23.4 +/- 12.8 ng/ml) compared to healthy volunteers (4.1 +/- 1.4 ng/ml). Following renal transplantation osteocalcin decreased significantly (9.4 +/- 8.9 ng ml) 3 days and (7.1 +/- 7.8 ng/ml) 28 days. However, 6 and 12 months following renal transplantation the mean osteocalcin level increased again (8.3 +/- 5.7 ng/ml, 12.1 +/- 15.4 ng/ml). At 6 months 11 and at 12 months only 6 of 37 patients had osteocalcin levels in the normal range. 12 months following renal transplantation 21 out of 37 patients with elevated osteocalcin levels had parathyroid hormone levels above the normal range. Additionally to increased osteocalcin levels patients prior to renal transplantation had elevated alkaline phosphatase. Alkaline phosphatase had following renal transplantation a similar pattern as osteocalcin with initial decrease and secondary increase 6 and 12 months after renal transplantation. Parathyroid hormone was elevated in all patients before renal transplantation. Following renal transplantation mean parathyroid hormone levels tell significantly, however remained above normal range in 57% of these 37 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osteocalcin serum levels in patients following renal transplantation. 265 90

Hypophosphataemic osteomalacia occurred in a 38-year-old woman. The leading clinical symptom was severe bone pain. X-ray studies demonstrated fractures of the iliac crest and pubic and ischiadic bone, as well as Looser's zones and demineralization of the skeleton. Computerized densitometry of the bone revealed a 31% reduction of hydroxyapatite. Histological evaluation showed nearly absence of osteoclasts and extensive demineralisation of the bone. Hypophosphataemia (0.48 mmol/l), increased urinary phosphate clearance (36 ml/min), reduced renal-tubular reabsorption for phosphate (73%) and increased alkaline phosphatase (355 U/l) were present. Parathyroid hormone and 1,25-dihydroxyvitamin D were normal. No inborn errors, disturbances of the calcium metabolism or paraneoplastic signs could be detected. Defective renal tubular reabsorption of phosphate is likely to be the underlying cause of the disease. Phosphate supplementation and intermittent vitamin D administration remains the therapy of choice.
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PMID:[Hypophosphatemic osteomalacia in adults]. 270 31

In order to determine the prevalence of secondary hyperparathyroidism in patients with Paget's disease of bone, we measured serum parathyroid hormone levels (N-terminal assay) in 39 patients with a wide range of pagetic activity. All patients had normal serum calcium levels. A total of 30 patients were either untreated or had received no treatment for 6 months or longer when studied; the other 9 were receiving either salmon calcitonin (3) or EHDP (6). The results showed that in 7 of the 39 patients (18%) parathyroid hormone levels were increased above normal. These were among the most severely affected cases, as manifested by the degree of elevation of three pagetic biochemical indices: serum alkaline phosphatase, plasma bone Gla protein, and 24 h urinary hydroxyproline-creatinine ratios. Levels of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 were normal. We examined the relationships between parathyroid hormone and each of the three pagetic indices as well as serum calcium for the entire group of 39 patients. Parathyroid hormone values did not correlate with serum calcium measurements (r = -0.241, p = NS) but did correlate significantly with serum alkaline phosphatase (r = 0.496, p less than 0.001), plasma bone Gla protein (r = 0.537, p less than 0.001), and urinary hydroxyproline (r = 0.450, p less than 0.011). We conclude that relative or absolute increases in parathyroid hormone may occur in moderately active Paget's disease, possibly in the setting of greater calcium demands during periods of increased pagetic new bone formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid function in Paget's disease of bone. 271 81

The authors evaluated bone mineralization by single photon absorptiometry and mineral homeostasis in 7 patients with anorexia nervosa. The patients with anorexia nervosa showed a reduction of bone mineralization in respect to age-sex matched normal values. Serum levels of calcium, ionized calcium, phosphate, magnesium, alkaline phosphatase, calcitonin and 25-hydroxyvitamin D were normal as well as phosphate and hydroxyproline urinary excretion. Osteocalcin levels were significantly low as compared to normal values (5.0 +/- 3.0 ng/ml vs 14.3 +/- 5.2 ng/ml, p less than 0.01) as well as urinary calcium excretion (0.02 +/- 1.01 vs 0.08 +/- 0.06, p less than 0.05); 1,25-dihydroxyvitamin D values were low only in 4 patients. Parathyroid hormone means levels were increased in respect to normal values (74.1 +/- 12.7 pg/ml vs 38.0 +/- 12.0, p less than 0.02). We confirm that adolescents with anorexia nervosa showed a reduced bone mineral content and alterations of mineral homeostasis that may contribute to the development of bone mineral loss.
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PMID:[Calciotropic hormones in osteoporosis caused by anorexia nervosa]. 278 86

Cell cultures derived from young rat epiphyseal cartilage were grown for approximately 2 wk in BGJb medium supplemented with 10% fetal bovine serum to reach confluence. These cells were identified as chondrocytes as checked by morphology, the presence of alkaline phosphatase, and a positive type II collagen antibody reaction. The cells also responded to different hormonal treatment. Parathyroid hormone (PTH) increased cyclic AMP production by 50% within 15 min of treatment, whereas prostaglandin E2 (PGE2) caused an increase of 160%. Calcitonin (CT) did not affect cAMP production in these cells. DNA synthesis 24 h after hormonal treatment was increased by PTH (2.5-fold) and PGE2 (2-fold), but not by CT. Among the vitamin D metabolites, 24,25(OH)2D3 increased significantly the [3H]thymidine incorporation into DNA, whereas 1,25(OH)2D3 effect was minimal. These results provide evidence for the use of these cell cultures as a model for cartilage in vitro when studying biological and hormonal responsiveness.
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PMID:Rat epiphyseal cells in culture: responsiveness to bone-seeking hormones. 284 Apr 29

Cyclic AMP (cAMP) levels were measured in both isolated and attached osteoclasts. The level of cAMP was 0.1 pmol/10(5) osteoclasts. No change in cAMP level of osteoclasts could be detected following calcitonin treatment. Parathyroid hormone (PTH) and prostaglandin E2 (PGE2) treatment stimulated cAMP production in proportion to alkaline phosphatase levels and divergent to acid phosphatase levels. This indicates that osteoblasts, not osteoclasts, were responsive to PTH and PGE2.
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PMID:The effects of calcitonin, parathyroid hormone and prostaglandin E2 on cyclic AMP levels of isolated osteoclasts. 286 55

Transforming growth factor beta (TGF-beta) is produced by bone cells, is abundant in bone matrix, and regulates bone cell biochemical processes. In osteoblast-enriched fetal rat parietal bone cell cultures, low TGF-beta doses increase DNA synthesis, whereas higher levels are less mitogenic, stimulate collagen production, and decrease alkaline phosphatase activity. Parathyroid hormone by itself has minimal effects on these processes, but it opposes the effects of TGF-beta and alters TGF-beta binding to its receptors in osteoblast-enriched cultures. Some functions ascribed to parathyroid hormone in bone may therefore result from alterations in TGF-beta activity, suggesting that the local effects of TGF-beta in bone are under systemic hormonal control.
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PMID:Parathyroid hormone modulates transforming growth factor beta activity and binding in osteoblast-enriched cell cultures from fetal rat parietal bone. 290 Oct 93

Parathyroid hormone (PTH) and cAMP inhibit sodium, water, and bicarbonate reabsorption in the proximal tubule. We wished to determine whether these agents directly inhibit proximal tubular Na+/H+ exchange. A suspension of rabbit proximal tubules was prepared by enzymatic digestion and Ficoll gradient centrifugation. Oxygen consumption at 37 degrees C was stable over 60 min, averaged 20 nmol X mg protein-1 X min-1, and was inhibited 60% by ouabain. Over 96% of cells excluded trypan blue. From this suspension, brush border membrane vesicles were isolated. The vesicles were enriched 12.7 times in alkaline phosphatase relative to a cortical homogenate and demonstrated pH gradient-stimulated, amiloride-sensitive Na+/H+ countertransport and sodium-phosphate and sodium-D-glucose cotransport. When the tubule suspension was exposed to PTH or dibutyryl cAMP, the activity of Na+/H+ countertransport in the resultant brush border vesicles was inhibited. Neither PTH nor dibutyryl cAMP affected the amiloride-insensitive component of sodium transport or sodium-phosphate or sodium-D-glucose cotransport. The effect of PTH on Na+/H+ counter-transport could not be explained by an alteration in fluidity of the brush border membrane. These experiments demonstrate that PTH and dibutyryl cAMP directly inhibit Na+/H+ countertransport in the brush border membrane of the rabbit proximal tubule.
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PMID:Parathyroid hormone and dibutyryl cAMP inhibit Na+/H+ exchange in renal brush border vesicles. 298 85


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