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)

The purpose of the present study was to determine the effects of oral contraceptive therapy on bone density and serum markers of bone metabolism in a prospective, longitudinal study of young adult female cynomolgus monkeys. Two hundred and seven intact cynomolgus monkeys were randomized to two groups, and fed an atherogenic diet containing either no drug (Control) or a triphasic oral contraceptive regimen (Contraceptive). Measurements of bone density were carried out by dual-energy X-ray absorptiometry at 10-month intervals (0, 10, and 20 months) and serum bone biomarkers were determined at 5-month intervals over the 20-month time course. No significant differences in these variables were observed prior to treatment. Both groups of animals gained bone mineral during the study, indicating that peak bone mass had not been reached at baseline. Contraceptive-treated animals gained less spinal (lumbar vertebrae 2-4) bone mineral content and density and less whole-body bone mineral content than Controls over the course of the study. Significant depressive effects of contraceptive treatment on gains in BMC and BMD were observed during each 10-month interval of the study. Bone metabolism was inhibited in the Contraceptive group, as reflected by marked reductions (approximately 40%) in serum osteocalcin and alkaline phosphatase levels along with moderate reductions in serum acid phosphatase and calcium. The results suggest that triphasic oral contraceptive treatment of young adult female monkeys that have not reached peak bone mass inhibits net bone accretion and/or growth by reducing bone metabolism. Thus, prolonged continuous oral contraceptive use in skeletally immature females may lead to a lower peak bone mass--an effect which could increase the risk of fractures in later life.
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PMID:Oral contraceptive treatment inhibits the normal acquisition of bone mineral in skeletally immature young adult female monkeys. 937 69

In general, physical exercise appears to have favorable effects on the skeleton. However, a few recent reports have described negative effects, including reduced bone density (BMD) and high bone turnover in runners. The aim of our study was to compare endurance runners to controls with respect to BMD at different sites and ultrasound transmission through the peripheral skeleton, and to use PTH, total serum calcium, and biochemical markers of bone metabolism as a complement in evaluating the effects of endurance running on bone. Thirty runners (mean age 32 years, range 19-54 years) participated in the study. Their main form of training consisted of endurance running at moderate intensity for about 7 hours (range 2-12 hours) per week, and they had been active in their sport for about 12 years (range 1-21 years). For a comparison, 30 age- and sex-matched population based controls were investigated. BMD values, measured by dual energy X-ray absorptiometry (DXA), were higher in runners than in controls for the total body (3.6%; P = 0.03), legs (9.6%; P = 0. 001), femoral neck (10.0%; P = 0.01), trochanter (9.9%; P = 0.01), and Wards triangle (11.8%; P = 0.02), but not in the lumbar spine or in the forearm measured by single energy X-ray absorptiometry (SXA). The quantitative ultrasound measurement of the calcaneus also revealed higher values in runners than in controls for both broadband ultrasound attenuation (9.2%; P = 0.002) and speed of sound (3.1%; P = 0.0001). At all sites, BMD was related to ultrasound measurements in controls, but no such relationship was evident in runners. Concentrations of parathyroid hormone (PTH) were lower (23.2%; P = 0.02) in runners than in controls, whereas total serum calcium concentrations were slightly higher (3.0%; P = 0.003). The levels of PICP (bone formation) and ICTP (bone resorption) in serum were lower (18.0%; P = 0.03 and 22.2%; P = 0.004, respectively) in runners than in controls, but no differences were seen for osteocalcin or bone specific alkaline phosphatase (b-ALP). In conclusion, BMD at the focus of strain for running, that is, the legs, is higher in endurance runners when compared to matched controls. Low bone turnover in runners, indicated by lower levels of PTH and biochemical markers of bone metabolism, point to an influence of endurance running at the cellular level.
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PMID:Bone metabolism in endurance trained athletes: a comparison to population-based controls based on DXA, SXA, quantitative ultrasound, and biochemical markers. 1059 70

Several studies have shown that bone mass and bone turnover are genetically determined. This genetic component is thought to be mediated in part by polymorphisms at the vitamin D receptor (VDR) locus, even though the underlying molecular mechanisms are still unknown. To evaluate a possible site of differential action of the VDR gene alleles we examined their correlation with intestinal calcium absorption in 120 Caucasian postmenopausal women (aged 61 +/- 0.6 years). VDR gene polymorphisms for Apa I, Bsm I, and Taq I restriction endonucleases were assessed by Southern blotting analysis. The most common genotypes observed in our population were AaBbTt (37%), AABBtt (20%), aabbTT (15%), AabbTT (15%), and AABbTt (9%). Although there was some evidence of 13% higher lumbar BMD values in aabbTT genotype with respect to AABBtt genotype, this difference of approximately 0.1 g/cm2 did not reach statistical significance, possibly because of the limited number of observations. On the contrary, no relationship was found between genotypes and femoral neck BMD values. Intestinal calcium absorption was significantly lower in BB and tt genotypes than, in bb and TT genotypes, respectively, and in AABBtt genotype than in either aabbTT or AaBbTt genotypes (P = 0.0015 ANOVA). No significant differences in intact PTH, alkaline phosphatase, 25OHD3, and 1, 25(OH)2D3 were found among subjects with different VDR genotypes. These results are consistent with a possible role of VDR alleles on intestinal calcium absorption.
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PMID:Vitamin D receptor genotypes and intestinal calcium absorption in postmenopausal women. 938 72

Intranasal administration of calcitonin (CT) avoids the problem of daily injections in the long-term treatment of osteoporosis. We examined the effect of nasal CT on bone and calcium metabolism in postmenopausal osteoporotic women in a double-blind design. 46 women, 55-75 years in age, and in good general health were included in the study. All patients were at least 6 months postmenopausal and had at least 1 vertebra fracture, bone mineral density (BMD; g/cm2) lower than 0.850 in L2-L4 in a dual energy x-ray absorptiometry (DEXA) AP view of the spine and showed biochemical indications of a fast bone loser. The patients were randomly treated with either nasal CT 200 IU per day, divided in 2 doses (n = 23) or placebo (n = 23) for 1 year. All participants received a daily calcium supplement of 1 g. Clinical and laboratory follow-up every 3 and 6 months, respectively, assessed the clinical picture, bone mineral density measured by DEXA, serum alkaline phosphatase, fasting urinary calcium, creatinine and hydroxyproline. BMD was measured in 4 sites (spine and cervical, Ward's triangle, and the trochanteric area of the hip) before treatment and after 6 and 12 months of treatment. In the placebo group, mean values at the 4 sites showed a 3.3% decrease in BMD after 6 months and a 5.0% decrease after 12 months. In contrast, the calcitonin group showed a 6.8% increase in BMD after 6 months and 11% increase after 12 months (p < or = 0.005). No patient experienced side-effects and there were no complaints of local irritation. We conclude that nasal administration of 200 IU calcitonin daily, continuously for 1 year had a positive effect on the bone mass density in osteoporotic postmenopausal women.
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PMID:A double blind study of intranasal calcitonin for established postmenopausal osteoporosis. 938 82

Osteoporosis is a complication of adult celiac disease. The gluten-free diet improves but does not normalize bone mineral density. Only few and conflicting data are known about the influence of the disease and diet on bone mineralization in children. The aim of this study was to evaluate the radial bone mineral content (BMC) and density (BMD) in children and adolescents who are asymptomatic on gluten-free diet. The BMD and BMC values of non-dominant radius midshaft in ninety-one children (53 girls and 38 boys, mean age: 11.7 years, mean duration of disease: 8.7 years) were determined by single photon absorptiometry. At the diagnosis and at least three years after gluten-free diet, serum calcium, phosphorous and albumin concentrations and alkaline phosphatase activities were determined in all, and additionally intact parathormone concentrations in 16 patients. The mean BMC Z-score value in the entire study population did not differ from the value of normal age-matched population (mean Z-score: -0.27), but in female adolescent group was significantly lower than the normal value (mean Z-score: -1.04, p < 0.01). In contrast, the mean BMC Z-score value was significantly higher than in normal value in girls (mean Z-score: +1.36, p < 0.001), in boys (mean Z-score: +0.53, p < 0.02) as well as in the total patients group (mean Z-score: +1.01, p < 0.001). The diameter of radius midshaft was significantly smaller in all age group than the normal mean value. Serum laboratory parameters of asymptomatic patients were in the normal range. The serum parathormone value in treated patients was significantly lower than in untreated celiac children (mean +/- SD: 3.77 +/- 1.07 versus 7.89 +/- 2.54, p < 0.01), but significantly higher compared to controls (2.89 +/- 0.9, p < 0.05). The data indicate that the gluten-free diet alone is not able to normalize bone mineralization in children. The significant increase of serum parathormone level in treated asymptomatic patients may be explained by the lower calcium content of gluten-free diet. The authors suppose that low calcium supply in children similarly to adult patients can lead to increased parathormone secretion, which can cause the retardation of bone growth even in treated patients with celiac disease.
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PMID:[Mineral content in bones of children with symptomless celiac disease and gluten-free diet]. 945 2

In order to assess the relative roles of the androgenic and/or estrogenic components in the stimulatory effect of dehydroepiandrosterone (DHEA) on bone mineral content (BMC) and density (BMD), ovariectomized (OVX) female rats received DHEA administered alone or in combination with the antiandrogen flutamide (FLU) or the antiestrogen EM-800 for 12 months. We also evaluated, for comparison, the effect of estradiol (E2) and dihydrotestosterone (DHT) constantly released by Silastic implants as well as medroxyprogesterone acetate (MPA) released from poly(lactide-co-glycolide) microspheres. Femoral BMD was decreased by 11% 1 year after OVX, but treatment of OVX animals with DHEA increased BMD to a value 8% above that of intact animals. The administration of FLU reversed by 76% the stimulatory effect of DHEA on femoral BMD and completely prevented the stimulatory effect of DHEA on total body and lumbar spine BMD. Similar results were obtained for BMC. On the other hand, treatment with the antiestrogen EM-800 did not reduce the action of DHEA on BMD or BMC. At the doses used, MPA, E2 and DHT increased femoral BMD, but to a lesser degree than observed with DHEA. Bone histomorphometry measurements were also performed. While DHEA treatment partially reversed the marked inhibitory effect of OVX on the tibial trabecular bone volume, the administration of FLU inhibited by 51% (P < 0.01) the stimulatory effect of DHEA on this parameter. The addition of EM-800 to DHEA, on the other hand, increased trabecular bone volume to a value similar to that of intact controls. DHEA administration markedly increased trabecular number while causing a marked decrease in the intertrabecular area. The above stimulatory effect of DHEA on trabecular number was reversed by 54% (P < 0.01) by the administration of FLU, which also reversed by 29% the decrease in intertrabecular area caused by DHEA administration. On the other hand, the addition of EM-800, while further decreasing the intertrabecular space achieved by DHEA treatment, also led to a further increase in trabecular number to a value not significantly different from that of intact control animals, suggesting an additional effect of EM-800 over that achieved by DHEA. Treatment with DHEA caused a 4-fold stimulation of serum alkaline phosphatase, a marker of bone formation, while the urinary excretion of hydroxyproline, a marker of bone resorption, was decreased by DHEA treatment. Treatment with DHEA and DHEA + EM-800 decreased serum cholesterol levels by 22 and 65% respectively, while the other treatments had no significant effect on this parameter. The present data indicate that the potent stimulatory effect of DHEA on bone in the rat is mainly due to the local formation of androgens in bone cells and their intracrine action in osteoblasts.
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PMID:Predominant androgenic component in the stimulatory effect of dehydroepiandrosterone on bone mineral density in the rat. 969 76

Alendronate is an antiresorptive therapy for osteoporosis and results in a decrease in bone turnover. To choose the optimal measurement for monitoring this therapy, the size of the change needs to be compared with the variability of the measurement. We studied 26 women with postmenopausal osteoporosis (bone mineral density [BMD] T score < -2.5), who were randomized in a 2:1 ratio to receive alendronate (10 mg/day) and calcium carbonate (500 mg/day) or calcium carbonate alone for 6 months. We measured serum markers of bone formation (osteocalcin [OC], bone isoform of alkaline phosphatase [BAP], and collagen type I C-terminal propeptide [CICP]) and urinary markers of bone resorption (cross-linked N-telopeptide [NTx], free deoxypyridinoline [iFDpd], and free pyridinolines). All subjects had two measurements 1 week apart at baseline to calculate the short-term variability. Biochemical measurements were then made at 4, 8, 12, 24, and 25 weeks. Measurements of bone mass were made by dual-energy X-ray absorptiometry (DXA) at the lumbar spine and proximal femur twice at baseline and then at 24 and 25 weeks. The mean difference in change in BMD and markers between both groups at the end of the study that were significant were (short-term variability in brackets): DXA total hip 4.3% (2.5%), NTX 49% (10%), iFDpd 22% (12%), OC 28% (13%), BAP 31% (13%), and CICP 31% (11%). Five of the six markers showed significant responses to alendronate therapy, but they differed in the relationship between size of response and variability. These biochemical markers performed better than DXA for monitoring alendronate therapy over 6 months.
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PMID:Monitoring alendronate therapy for osteoporosis. 1023 82

We tested the hypothesis that biomarkers of bone resorption are increased in hyperprolactinemic amenorrheic patients with estrogen (E) deficiency, augmenting the possible risk of developing osteoporosis. Fifty hyperprolactinemic patients with amenorrhea of more than 12 months and with low serum E2, as well as 30 healthy fertile women (controls), matched for age and body mass index, participated in this study. Bromocriptine was administered orally to hyperprolactinemic patients and blood and urine samples were collected before and 12 weeks after treatment. Serum osteocalcin (OC) and bone-specific alkaline phosphatase (B-ALP), reflecting bone formation, and urinary deoxypridinoline (D-Pyr) and N-telopeptide of type 1 collagen (NTX) excretion, reflecting bone resorption, were measured using direct immunoassays. Hyperprolactinemic patients had higher (p < 0.0005) levels of all the biomarkers compared to control values: (OC, 22+/-1.2 [SE] vs. 14+/-.99 ng/ml (+57 %); B-ALP, 14.2+/-0.7 vs. 7.5+/-0.8 ng/ml (+89 %); D-Pyr, 8.8+/-0.6 vs. 3.2+/-0.3 nmol/mmol creatinine (+175%) and NTX, 65+/-5.1 vs. 25+/-3.2 nmol bone collagen equivalent (BCE)/mmol creatinine (+160%)). These results were associated with significantly decreased lumbar spine bone mineral density (LS-BMD), measured by dual energy X-ray absorptiometry (DEXA). Treatment of hyperprolactinemia with bromocriptine restored normal values of bone formation and resorption markers. In conclusion, hyperprolactinemia with estrogen deficiency exhibits a significant increase of bone resorption which is associated with a significant decrease of LS-BMD. These changes may subject the patient to the possible risk of developing osteoporosis.
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PMID:Biomarkers of bone turnover and bone mineral density in hyperprolactinemic amenorrheic women. 1036 15

We studied 21 patients (11 men and 10 women) with osteogenesis imperfecta (OI) and 21 age- and sex-matched controls. In all patients we measured serum levels of total alkaline phosphatase (ALP), type I procollagen carboxy-terminal propeptide (PICP), osteocalcin (BGP), urinary excretion of hydroxyproline (HOP/Cr), and pyridinoline crosslinks (Pyr/Cr). Bone mineral density was measured at the distal radius (BMD-R) and at the lumbar spine (BMD-LS) by dual X-ray absorptiometry (DXA). Ultrasound parameters were also performed at the calcaneous with the Achilles device and at the phalanxes with DBM Sonic 1200. A significant reduction (P < 0.001) in BMD and in ultrasound parameters was found in OI patients compared with normals. PICP was significantly reduced in the OI patients compared with controls (P < 0.001); other markers of bone turnover were higher in OI than in controls, but the difference did not reach the statistical significance. A significant correlation (P < 0.05) was found between PICP and BMD at the lumbar spine and between PICP and ultrasound parameters at the calcaneous. On the basis of our data, we conclude that patients with OI show low values of BMD and ultrasound parameters; therefore in these patients, not only is bone mass disturbed but also bone quality. The reduced levels of PICP in OI patients confirm that most OI patients have defects in collagen I biosynthesis. These defects may contribute to the fragility of OI bone by interfering with complete mineralization and/or normal tissue structure. PICP may be considered a useful marker in the clinical management of OI.
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PMID:Osteogenesis imperfecta: bone turnover, bone density, and ultrasound parameters. 1043 Jun 45

Changes in skeletal remodeling (biochemical bone markers) and regional bone mineral density (spine, hip, and forearm bone mineral density [BMD]) were observed for 3 years in 20 patients (15 women and 5 men; age 54 +/- 11 years, range 29-69 years) after successful surgery for primary hyperparathyroidism (PHPT). Fifteen PHPT patients were compared with 15 normal controls who were exactly matched with respect to age, gender, and menopausal status (10 women and 5 men; age 53 +/- 12 years, range 29-65 years [PHPT] and 29-66 years [controls]). All bone markers (serum osteocalcin, bone alkaline phosphatase, and type I collagen telopeptide [ICTP], and urinary hydroxyproline and NTx/creatinine ratio) declined significantly and reached normal levels within 6 months. No major changes took place during the remaining 2.5 years, apart from urine hydroxyproline, which disclosed a small peak around 12 months with a further decline towards study end (p < 0.05). Bone mineral density increased significantly in all regions (p < 0.001). At all locations, except the intertrochanteric region of the hip, the increase continued from 6 months until study end (p < 0.05). The increase in BMD was unequally distributed among regions (p < 0.001). The increase at the proximal forearm was less than in the spine (p < 0.05), the trochanteric region of the hip (p < 0.05), and the distal forearm (p < 0.05). No difference in BMD increase was observed between men, and pre- and postmenopausal women. Compared with the matched control group, PHPT patients had significantly lower BMD at baseline in the proximal (p < 0.02) and distal (p < 0.05) forearm. Furthermore, during the 3-year follow-up period, the PHPT patients showed a significant increase in BMD compared with controls in the spine (p < 0.005), the trochanteric and intertrochanteric regions of the hip (p < 0.005 and p < 0.05, respectively), and the distal forearm (p < 0.005). In conclusion, bone remodeling is normalized within the first 6 months after successful parathyroid surgery, with no major changes during the following 2.5 years. Bone mineral density increases at both cancellous and cortical sites, but in predominantly cortical bone, the recovery in BMD is less than in cancellous bone-rich areas.
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PMID:Primary hyperparathyroidism: effect of parathyroidectomy on regional bone mineral density in Danish patients: a three-year follow-up study. 1057 80


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