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)

Parameters of calcium and phosphate metabolism were measured in 27 patients with mild renal failure [glomerular filtration rate (GFR) 40-90 ml/min], 12 patients with moderate renal failure (GFR 20-39 ml/min) and in 12 healthy subjects. GFR was determined by technetium-99m diethylenetriamine penta-acetic acid clearance. Intact parathyroid hormone (PTH) was measured by a sensitive immunochemiluminometric assay and somatomedin-C was determined by radioimmunoassay. Both 1,25-dihydroxyvitamin D [1,25(OH)2D] and vitamin-D-binding protein were measured allowing calculation of the free 1,25(OH)2D index. By linear regression and multivariate analysis, PTH was negatively and independently correlated with GFR, plasma bicarbonate and 25-hydroxyvitamin D [25(OH)D] while free 1,25(OH)2D was positively correlated with GFR. Increased PTH secretion and reductions in 1,25(OH)2D were present in mild renal failure patients before any changes in plasma calcium, phosphate and bicarbonate were noted. Plasma alkaline phosphatase was significantly higher in mild chronic renal failure patients compared to normal subjects, possibly indicating early effects of the secondary hyperparathyroidism on the skeleton. Somatomedin-C did not correlate with the free 1,25(OH)2D index or a measure of 1,25(OH)2D production. It is concluded that the secondary hyperparathyroidism which occurs very early in the onset of chronic renal failure may be due to a reduction in the circulating concentration of 1,25(OH)2D consequent upon the renal failure. Low plasma bicarbonate and 25(OH)D also appear to be determinants of a raised PTH concentration. The compensatory increase in PTH presumably maintains extracellular calcium and phosphate levels constant but with possible deleterious effects on the skeleton.
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PMID:Determinants of intact parathyroid hormone and free 1,25-dihydroxyvitamin D levels in mild and moderate renal failure. 150 39

Fifteen prepubertal short stature children (10 girls, 5 boys), mean age 9.6 years (range 5.2-12.7 years), with normal response to growth hormone stimulation tests (group A) or partial growth hormone deficiency (GHD) of idiopathic nature (group B) were included in a controlled longitudinal study for evaluation of predictive parameters for the long-term growth response after administration of biosynthetic human growth hormone (B-hGH). The average knee-heel length velocity for the first 3 months was significantly correlated to total body height velocity during the following 9 months (p less than 0.0008). By contrast, this association could not be found for height velocity during the same period. The increase in serum values of alkaline phosphatase and insulin-like growth factor I (IGF-1) during the first month of treatment was not significantly correlated to height velocity during the first year. During one year of treatment with B-hGH the mean height velocity for groups A and B increased from 4.4 cm/year (range 2.5-6.5) to 7.6 cm/year (range 4.7-10.6). Bone age advanced by 1.08 +/- 0.60 per chronological year. The ratio between total height and knee-heel length prior to treatment was 3.34 +/- 0.10 and after one year 3.33 +/- 0.10, suggesting a proportional linear growth. An inverse relationship was observed between the ratio and chronological age. In conclusion, early knee-heel measurement may be a useful non-invasive predictor of long-term linear growth in children during treatment with growth hormone, and the ratio of total height to lower leg length may be of importance in detecting dysproportional growth.
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PMID:Predicting and monitoring of growth in children with short stature during the first year of growth hormone treatment. 178 87

This article reports the efficacy and safety of treatment with Somatonorm in 9 children with idiopathic growth hormone (GH) deficiency in China. The growth velocity increased from 2.6 +/- 0.2 cm/year before treatment to 10.7 +/- 0.5 cm/year at the end of 1-year treatment. The increment of human growth hormone (hGH) level and area under the response curve above the baseline level were larger after one injection of Somatonorm at the dose of 0.1 IU/kg sc than that of 0.17 IU/kg im. Increments of delayed bone age were not significant. There was no correlation between the increase of height growth velocities and the serum Somatomedin-C (SMC) levels during hGH therapy (r = -0.055). Blood sugar levels and blood alkaline phosphatase concentrations increased significantly after therapy. There were no significant side effects. Serum T4 levels of 3 patients dropped below normal after treatment. Serum anti-hGH antibody appeared at 3-12 month in 2 patients, but it did not attenuate the growth velocity.
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PMID:Clinical trial with somatonorm in idiopathic growth hormone deficiency in children. 211 59

Cytochemical staining of normal human bone cells in monolayer cultures for alkaline phosphatase (ALP) indicated that the cultures contained mixed-cell populations. Time course evaluations of the cytochemical staining revealed, in addition to the ALP-negative cell population, at least two subpopulations of ALP-positive human bone cells with different levels of ALP. A cytochemical method has been developed which separates the ALP-positive cells into high and intermediate ALP subpopulations. In this method, human bone cells were stained for ALP using an azo-dye method and incubating at 4 degrees C for 10 and 30 minutes, respectively. We defined the cell population that stained positively for ALP at 10 minutes as strong ALP-positive cells, and both strong and intermediate cells were stained at 30 minutes. The intermediate cells were determined from the difference between the values at the two time points. The intra- and interassay variations of the assay, with the same investigator in blinded investigations, were both less than 10% and the interobserver variation was approximately 25%. Analysis of the distribution of ALP levels in cells with a laser densitometer confirmed the presence of at least three cell subpopulations. 1,25(OH)2D3 treatment increased the proportions of both ALP-positive cell populations, whereas TGF-beta treatment increased only the intermediate ALP-positive cell population. On the contrary, fluoride increased the proportion of the strong ALP cells, and IGF-1 had no effect on the proportions of either ALP-positive subpopulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monolayer cultures of normal human bone cells contain multiple subpopulations of alkaline phosphatase positive cells. 225 20

IGF-1 has been shown to be locally produced in several tissues and to play a role in the regulation of cellular activity. We have investigated its production in short-term cultures of human bone derived cells, and the regulation of this production by growth hormone (GH) and by 1,25 dihydroxyvitamin D3 (1,25(OH)2D3). Bone cells obtained from surgical bone biopsies produced and secreted IGF-1 in their culture media. In four days cultures of bone-derived cells recombinant human r-IGF-1 at 20 ng/mL increased the alkaline phosphatase activity and the osteocalcin (bone gla protein) secretion, two specific markers of bone formation. This stimulation occurred only in the presence of 1,25(OH)2D3. Human bone cells exposed to GH increased their alkaline phosphatase activity, but no osteocalcin was detectable. However, in the presence of 1,25(OH)2D3 (1 nM), GH in concentrations of 8 to 40 nM increased by 30-50% the alkaline phosphatase activity and by 50 to 100% the osteocalcin secretion of human bone cells. At the same concentrations, GH also increased by 140% endogenous IGF-1 levels in cell culture supernatants, 1,25(OH)2D3 (10 nM) also increased time- and dose-dependently, IGF-1 levels in human bone cell supernatants, and stimulated dose-dependently alkaline phosphatase activity and osteocalcin secretion. It is therefore suggested that by regulating local production of growth factors such as IGF-1, GH and 1,25(OH)2D3 may modulate the metabolism of human bone cells.
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PMID:Insulin like growth factor I hormonal regulation by growth hormone and by 1,25(OH)2D3 and activity on human osteoblast-like cells in short-term cultures. 235 26

The effect of the bone resorptive cytokines IL-1 alpha, IL-1 beta, and TNF on bone formation was studied in an in vitro system. All three cytokines were profoundly inhibitory, with the rank order of potency IL-1 beta greater than IL-1 alpha greater than TNF. Inhibition was mediated by a depression of differentiated osteoblast functions, including alkaline phosphatase expression and matrix synthesis. Osteoblast proliferation was not affected. Bone formation inhibition was independent of PGE2 production, indicating a direct effect of cytokines on osteoblasts. High concentrations of IL-1 beta (10 U/ml) abrogated IGF-1-stimulated bone formation, providing evidence for the hypothesis that cytokines act as 'uncoupling factors'. Conversely, high concentrations of IGF-1 circumvented inhibition by IL-1 beta (0.1-1.0 U/ml). The interaction of cytokines and bone growth factors with osteoblasts are likely to be of critical importance in the regulation of bone mass at local inflammatory sites.
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PMID:Effect of immune cytokines on bone. 265 11

The non-collagen proteins of bone are a complex set of molecules that arise from local or exogenous sources. Because bone mineral is an excellent adsorbent, many circulatory and/or cell surface proteins bind to bone, where they may have immediate or subsequent effects. These include the alpha 2-HS-glycoprotein from blood and the potent growth factors TGF-beta, PDGF, IGF-1, FGF-a and -b, and IL-1, derived from both bone and non-bone cells. Furthermore, bone cell membrane proteins such as alkaline phosphatase may be cleaved from the cell surface and entrapped in the bone matrix. Bone is enriched in a variety of enzymes and their inhibitors by similar adsorption processes. Even osteocalcin, a bone cell product, is adsorbed to bone via mineral-binding (Gla) groups. The bone sialoproteins (BSP-I or osteopontin and BSP-II) also bind to the mineral via acidic groups. Because of this phenomenon it is difficult to distinguish whether a given protein's presence in bone is advantageous or merely fortuitous. The bone matrix proper consists of type I collagen and other osteoblast products such as osteonectin (a phosphorylated glycoprotein) and small proteoglycans (PG-I and/or PG-II) which are incorporated into bone collagen fibrils. These proteins may have additional roles in tissue morphogenesis and/or differentiation.
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PMID:Non-collagen proteins in bone. 306 9

A study of 31 children with short stature was initiated in 1982. They received subcutaneous injections of pituitary hGH, 0.1 IU/kg/day; no adverse effects were seen and none of the patients acquired antibodies. Only the results of the first year are presented, as final height has not yet been attained. A high growth response was seen in 29 of the 31 children; they experienced an initial rise of IGF-1, IGF-2, alkaline phosphatase and procollagen III. The best response was obtained in the child with the lowest levels of endogenous pulsatile hGH secretion.
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PMID:Growth hormone treatment in short children. 329 40

Estrogen has been shown to modify calcium and skeletal homeostasis. In this study, we tested the ability of estrogen to influence the effects of short-term 1,25(OH)2D administration on biochemical indices of bone formation and resorption in a cross-sectional analysis of untreated (n = 10) and estrogen-treated (n = 14) osteoporotic women. Patients were given oral 1,25(OH)2D (Rocaltrol) 0.5 microgram twice a day for 5 days. Serum and urine were sampled at baseline and then 1 h after the first daily Rocaltrol dose for the 5 days of the study. 1,25(OH)2D levels rose similarly in both groups with plateaus reached by the third day of the investigation. Serum PTH levels decreased by the first sampling period (1 h after first Rocaltrol dose; p < 0.008 both groups) and continued to fall gradually in both groups. There were no changes in serum calcium but serum phosphorus rose by the second day (p < 0.05 both groups) and remained elevated throughout the remainder of the protocol. Serum bone Gla protein increased approximately 40% (p < 0.05) with no group differences. In contrast, total alkaline phosphatase and carboxy-terminal propeptide of type I collagen did not increase in either group. Furthermore, there were no significant increments in any bone resorption indicators, including serum tartrate-resistant acid phosphatase and cross-linked carboxy-terminal telopeptide of type I collagen, as well as urine hydroxyproline and pyridinoline. Serum IGF-1 levels also remained unchanged in both groups. We conclude that oral 1,25(OH)2D administration decreased 1-84PTH levels, probably due to a suppression of parathyroid production, and did not stimulate bone resorption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral 1,25-dihydroxyvitamin D administration in osteoporotic women: effects of estrogen therapy. 761 Sep 30

The study described here investigates the influence of a specific alimentary Zn deficiency on the concentration of growth hormone (GH), insulin-like growth factor I (IGF-I) and insulin in the serum of force-fed rats. For this purpose 24 male Sprague-Dawley rats with an average bodyweight of 108 g were divided into 2 groups of 12 animals each. The Zn-deficient group and the control group received for 12 days a semi-synthetic casein diet with a Zn content of 1.3 and 25 ppm respectively. In order to prevent the reduced feed intake which occurs in Zn deficiency and the associated energy and protein shortage from interfering with the experimental parameters, all animals were fed 4 times daily by gastric tube. This made it possible to supply all animals with adequate-nutrients and to synchronise the feed intake exactly. After 12 days the depleted rats were in a severe state of Zn deficiency, as demonstrated by the reduction of Zn in the serum and the femur by 62% and 44% respectively and the 70% lower serum activity of alkaline phosphatase. In the Zn-deficient rats the concentration of GH in the serum was significantly increased by 78%, while IGF-1 and insulin were significantly reduced by 28% and 25% respectively. It is thought that the growth depression observed in the Zn-deficient rats in this study despite their identical feed intake is probably due to a reduced concentration of IGF-I and insulin and that the biological activity or the binding of GH to receptors is impaired in specific alimentary Zn deficiency.
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PMID:Influence of alimentary zinc deficiency on the concentration of growth hormone (GH), insulin-like growth factor I (IGF-I) and insulin in the serum of force-fed rats. 783 22


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