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)

Four clonal cell lines derived from a rat osteosarcoma were tested for the ability to secrete the gamma-carboxyglutamic acid-containing protein of bone (BGP) using a specific radioimmunoassay for this protein. Two cell lines secreted BGP into culture media while the other two did not. Other investigators have shown that these two cell lines are also the only ones with the high parathyroid hormone responsiveness and alkaline phosphatase activity expected for osteoblast cells in culture. Both cell lines also form a mineralized sarcoma when implanted in rats. The BGP in culture media is identical in molecular weight and in electrophoretic mobility with the 5800-dalton BGP purified from rat bone. Thus, BGP is probably secreted by osteosarcoma cells directly and not derived from an extracellular precursor by proteolytic cleavage. There are two immunoreactive components within osteosarcoma cells which secrete BGP. One component is identical in molecular weight and electrophoretic mobility with BGP from rat bone. The other component has a higher molecular mass (approximately 9000 daltons) and about half the electrophoretic mobility of BGP from bone. The presence of both components within these cells raises the possibility that the larger component may be an intracellular precursor which is processed to BGP prior to secretion.
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PMID:Secretion of the vitamin K-dependent protein of bone by rat osteosarcoma cells. Evidence for an intracellular precursor. 696 67

We evaluated the effects of low-dose ethinylestradiol administration in the prevention of the rapid bone loss that follows ovariectomy in women. After 10-30 days from surgery, patients received either a sole calcium supplementation 500 mg/day (n = 20) or ethinylestradiol 20 micrograms/day in addition to the same daily calcium supplement (n = 21), for 12 months. In the control group, urinary hydroxyproline excretion, serum alkaline phosphatase and plasma bone Gla protein levels presented a substantial (p < 0.05) increase, while radial bone density significantly (p < 0.05) decreased 6 months after surgery. In the ethinylestradiol-treated group, the patterns of biochemical markers indicated that ethinylestradiol can restrain the bone remodelling processes. Radial bone density showed no significant modification during the 12 months' study period. In conclusions, these results demonstrate that the administration of 20 micrograms/day of ethinylestradiol can prevent the rapid bone loss that follows ovariectomy.
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PMID:Prospective evaluation of calcium and estrogen administration on bone mass and metabolism after ovariectomy. 750 89

Bone mineral metabolism and mineralization before and during treatment were studied in 10 girls aged 6.9-8.4 years affected by central precocious puberty and treated with gonadotrophin-releasing hormone agonist (GnRHa) leuprolide acetate depot, in order to understand better the consequences of oestrogen deficiency and the reduction of growth hormone (GH)-insulin-like growth factor I (IGF-I) axis activity. Before and after 12 months of therapy, the patients underwent a clonidine stimulation test and a 4-day calcitriol osteoblast stimulation test. On day 0, day 5 and at 3-month intervals thereafter, serum calcium, phosphate, alkaline phosphatase, IGF-I, IGF binding protein 3 (IGFBP-3), GH, GH binding protein and osteocalcin levels were measured; urinary calcium, phosphate and hydroxyproline levels were evaluated in fasting spot samples. Trabecular and cortical bone mass variations, measured by dual X-ray absorptiometry in the lumbar spine and by dual photon absorptiometry in the radius, respectively were evaluated before the start and after 12 months of therapy. During treatment, a decrease of serum oestradiol levels from pubertal to prepubertal levels was observed. The GH peak following clonidine diminished significantly after 1 year. Growth hormone binding protein showed a slight increase, and IGF-I and IGFBP-3 decreased, although not significantly. Osteocalcin levels decreased significantly after 9 and 12 months of treatment, but they did not change significantly after calcitriol load, either before or after GnRHa therapy. Urinary hydroxyproline decreased significantly after 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone mineral metabolism in girls with precocious puberty during gonadotrophin-releasing hormone agonist treatment. 758 63

The purpose of this study was to define the bone metabolic properties during the postfracture period in elderly women with hip fracture. Osteocalcin (Oc), a marker of bone formation, was measured in 58 women with hip fracture (77 +/- 7 years) admitted to the hospital from their own homes. Serum samples were taken on average 5 h (range 1-21) from fracture and at follow-up, on average 4.6 months later. Comparison was made with 58 age-matched (79 +/- 5 years) women. Women with hip fracture had initially 30% lower Oc levels compared to the controls (p = 0.0001). The Oc level was independent of time elapsed from trauma, within 18 h, after which the level further decreased. At follow-up, Oc showed a 44% increase (p = 0.0001) and had reached the level of the controls, but not beyond it. A concomitant, but less marked increase was noted for alkaline phosphatase (ALP) (p = 0.0001). We conclude that although the bone formation, as assessed by Oc, is apparently lower in elderly women who sustain a hip fracture, the ability to induce a fracture response, with an increased bone turnover during fracture healing is intact. Subsequently, it is essential that a time perspective is applied, as the bone metabolic changes in patients having sustained a fracture are related to the time elapsed from fracture.
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PMID:Serum osteocalcin increases during fracture healing in elderly women with hip fracture. 760 2

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

In order to clarify the effects of longterm inhaled steroid therapy on bone metabolism, we examined 72 patients with bronchial asthma treated mainly with BDP (beclomethasone dipropionate). Multiple scanning X-ray photodensitometry was used to evaluate the degree of bone mineral loss. Osteocalcin, alkaline phosphatase (total and type III) was measured as a marker of bone synthesis and urinary pyridinoline, and deoxy-pyridinoline was measured as a marker of bone resorption. There was age related bone mineral loss. Urinary pyridinoline increased with aging. Treatment related bone mineral loss was not observed either in cases treated with BDP or in cases treated with continual oral steroids. Urinary pyridinoline and deoxy-pyridinoline decreased in patients treated with larger doses of for longer periods with BDP. Serum osteocalcin levels were lower in patients on continual oral corticosteroids. We conclude that inhaled steroid do not deteriorate bone metabolism in patients with bronchial asthma, when used appropriately.
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PMID:[Effect of inhaled steroid on bone metabolism in the treatment of bronchial asthma]. 769 81

Osteocalcin is a vitamin K-dependent bone protein synthesized by osteoblasts. In generalized bone disorders serum osteocalcin correlates with osteoblast activity. Bone resorption and new bone formation occur in chronic osteomyelitis, dependent on the level of inflammatory activity. In 17 patients with active chronic osteomyelitis undergoing surgery, the serum levels of osteocalcin, alkaline phosphatase and C-reactive protein were measured before and after treatment. The osteocalcin levels were within the normal range preoperatively (10.8 +/- 11.0 micrograms/l), in the early postoperative period, and at discharge. It is therefore not a helpful marker in the clinical management of this condition.
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PMID:Osteocalcin levels in chronic osteomyelitis. 769 52

Hind limb elevation of the growing rat provides a good model for the skeletal changes that occur during space flight. In this model the bones of the forelimbs (normally loaded) are used as an internal control for the changes that occur in the unloaded bones of the hind limbs. Previous studies have shown that skeletal unloading of the hind limbs results in a transient reduction of bone formation in the tibia and femur, with no change in the humerus. This fall in bone formation is accompanied by a fall in serum osteocalcin (bone Gla protein, BGP) and bone BGP messenger RNA (mRNA) levels, but a rise in bone insulin-like growth factor-I (IGF-I) protein and mRNA levels and resistance to the skeletal growth-promoting actions of IGF-I. To determine whether skeletal unloading also induced resistance to GH, we evaluated the response of the femur and humerus of sham and hypophysectomized rats, control and hind limb elevated, to GH (two doses), measuring mRNA levels of IGF-I, BGP, rat bone alkaline phosphatase (RAP), and alpha 1(1)-procollagen (coll). Hypophysectomy (HPX) decreased the mRNA levels of IGF-I, BGP, and coll in the femur, but was either less effective or had the opposite effect in the humerus. GH at the higher dose (500 micrograms/day) restored these mRNA levels to or above the sham control values in the femur, but generally had little or no effect on the humerus. RAP mRNA levels were increased by HPX, especially in the femur. The lower dose of GH (50 micrograms/day) inhibited this rise in RAP, whereas the higher dose raised the mRNA levels and resulted in the appearance of additional transcripts not seen in controls. As for the other mRNAs, RAP mRNA in the humerus was less affected by HPX or GH than that in the femur. Hind limb elevation led to an increase in IGF-I, coll, and RAP mRNAs and a reduction in BGP mRNA in the femur and either had no effect or potentiated the response of these mRNAs to GH. We conclude that GH stimulates a number of markers of bone formation by raising their mRNA levels, and that skeletal unloading does not block this response, but the response varies substantially from bone to bone.
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PMID:The molecular response of bone to growth hormone during skeletal unloading: regional differences. 772 Jun 59

Osteocalcin in the serum reflects bone turnover. It is known that prolonged therapy with glucocorticoids inhibits bone turnover. The aim of this study was to evaluate the osteocalcin level in children with congenital adrenal hyperplasia treated by glucocorticoids and mineralocorticoids and to assess the influence of 1,25(OH)2D3. The subjects were 75 children with congenital adrenal hyperplasia, aged 1-18 years, treated with glucocorticoids and mineralocorticoids in substitution doses from birth. These children demonstrated low levels of osteocalcin and alkaline phosphatase, whereas calcium and phosphate were in the normal ranges. Despite these abnormalities, no osteoporosis was detectable and a normal growth rate was confirmed, most probably because of higher levels of androgens; 17-OH progesterone averaged 11.8 nmol/l. After treatment with 1,25(OH)2D3, the osteocalcin levels increased, followed later by increases of alkaline phosphatase and bone isoenzyme.
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PMID:Osteocalcin in congenital adrenal hyperplasia. 774 84

We investigated the sequence of expression of osteoblast gene markers during bone formation in vivo by in situ hybridization. Cylindrical lesions were induced in the femora of sheep with titanium analytic bone implants that allow removal of serial core samples to study bone formation. At 2 weeks (2W), granulation tissue made up of spindle-shaped cells had partially replaced the blood clot. Islands of osseous tissue, first noted in the periphery of the ingrowing tissue at 3W, became the predominant tissue by 6W. The surfaces of newly forming bone at 3W were apposed by cuboidal cells, which in some areas were several layers thick. By 6W, most of the cells lining bone trabeculae had assumed a flattened morphology. The temporal and spatial distribution of osteoblast gene markers was examined by in situ hybridization with nonradioactive digoxigenin probes for alpha 1(I) procollagen, alkaline phosphatase (ALP), osteopontin (OP), and bone Gla protein (BGP). The spindle-shaped cells in the granulation tissue expressed mRNA for alpha 1(I) procollagen, ALP, and OP but not BGP, suggesting that they may be osteoblast precursor cells. alpha 1(I) procollagen mRNA was strongly expressed by all cells on the surface of bone, with a peak intensity at 3W and then reducing sharply by 6W. Initially, only pockets of cuboidal cells on bone surfaces expressed ALP mRNA, with a peak intensity at 5W. Similarly, only a proportion of cuboidal cells expressed OP mRNA early in bone formation, but the number of cells expressing OP mRNA increased with time. Clumps of cuboidal cells expressed BGP mRNA only when bone was present, and the degree of expression increased with the amount of bone formed. This model allows the study of temporal and spatial sequence of gene expression in cells participating in osteogenesis. The temporal sequence is similar to that shown in vitro in other models of mineralization. The geographic localization of cells expressing mRNA for alpha 1(I) procollagen, ALP, OP, and BGP implies subspecialization of osteoblasts in bone formation.
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PMID:In situ hybridization to show sequential expression of osteoblast gene markers during bone formation in vivo. 781 34


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