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)

This study sought to confirm that osteoblasts of C3H/HeJ (C3H) mice, which have higher differentiation status and bone-forming ability compared to C57BL/6J (B6) osteoblasts, also have a lower apoptosis level and to test whether the higher differentiation status and bone-forming ability of C3H osteoblasts were related to the lower apoptosis. C3H mice had 50% fewer (P < 0.01) apoptotic osteoblasts on the endocortical bone surface than B6 mice as determined by the TUNEL assay. Primary C3H osteoblasts in cultures also showed a 50% (P < 0.05) lower apoptosis level than B6 osteoblasts assayed by acridine orange/ethidium bromide staining of apoptotic osteoblasts. The lower apoptosis in C3H osteoblasts was accompanied by 22% (P < 0.05) and 56% (P < 0.001) reduction in the activity of total caspases and caspases 3/7, respectively. C3H osteoblasts also displayed greater alkaline phosphatase (ALP) activity (P < 0.001) and higher expression of Cbfa1, type-1 collagen, osteopontin, and osteocalcin genes (P < 0.05 for each). To assess if an association existed between population apoptosis and the differentiation status (ALP-specific activity) and/or bone-forming activity (insoluble collagen synthesis), C3H and B6 osteoblasts were treated with several apoptosis enhancers (tumor necrosis factor-alpha, dexamethasone, lipopolysaccharide, etoposide) and inhibitors (parathyroid hormone, insulin-like growth factor I, transforming growth factor beta1, estradiol). Both ALP (r = -0.61, P < 0.001) and insoluble collagen synthesis (r = -0.61, P < 0.001) were inversely correlated with apoptosis, suggesting that differentiation (maturation) and/or bone-forming activity of these mouse osteoblasts were inversely associated with apoptosis. In conclusion, these studies support the premise that higher bone density and bone formation rate in C3H mice could be due in part to lower apoptosis in C3H osteoblasts.
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PMID:High osteoblastic activity in C3H/HeJ mice compared to C57BL/6J mice is associated with low apoptosis in C3H/HeJ osteoblasts. 1660 80

There is an increasing body of evidence supporting the idea that nonsteroidal antiinflammatory drugs can effectively suppress ovariectomy-induced bone loss in adult rats. The present study investigated the effects of supplementation of selective cyclooxygenase-2 inhibitor [5,5-dimethyl-3-(3 flurophenyl)-4-(4 methylsulphonal) phenyl-2 (6H) furanone, DFU] to diets on bone metabolism, bone mineral density (BMD), and histomorphometry in middle-aged male rats. Forty 16-month-old male rats (n = 8/group) were fed diets containing 0 (control), 5, 10, 15, or 20 mg/kg DFU body weight/day for 4 weeks. Supplementation of DFU resulted in higher plasma levels of pyridinoline, insulin-like growth factor I, and parathyroid hormone, but lower bone-specific alkaline phosphatase activity, prostaglandin E(2,) and 1,25-(OH)(2) vitamin D(3). Compared to the control, DFU supplementation at 20 mg/kg did not affect total scanned area, BMD, and bone mineral content as determined by DEXA. Histomorphometric data showed that rats fed DFU at 20 mg/kg had lower values of mineralizing surface, eroded surface, mineral apposition rate, and bone formation rate, but no difference in trabecular thickness, number, and separation compared to the control. The present data demonstrate that the short-term supplementation of selective COX-2 inhibitor to gonad-intact middle-aged male rats resulted in suppression of bone formation and increased bone resorption, and thereby suppressed bone turnover rate, without significant loss of bone. Such action was through modulating local factors and systemic hormones.
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PMID:Short-term supplementation of COX-2 inhibitor suppresses bone turnover in gonad-intact middle-aged male rats. 1707 38

Intermittent administration of the N-terminal fragment of parathyroid hormone (PTH) and PTH-related protein (PTHrP) induces bone anabolic effects. However, the effects of the C-terminal domain of PTHrP on bone turnover remain controversial. We examined the putative mechanisms whereby this PTHrP domain can affect osteoblastic differentiation, using human osteosarcoma MG-63 cells and osteoblastic cells from human trabecular bone. Intermittent exposure to PTHrP (107-139), within 10-100 nM, for only <or=24 hours during cell growth stimulated alkaline phosphatase (ALP) and Runt homology domain protein (Runx2) activities as well as osteocalcin (OC) and osteoprotegerin (OPG) expression but inhibited receptor activator of nuclear factor kappaB (NF-kappaB) ligand. Continuous exposure to this PTHrP peptide reversed these effects. The stimulatory effects of transient treatment with PTHrP (107-139) on OC mRNA and/or OPG protein expression were unaffected by a neutralizing anti-insulin-like growth factor I antibody or [Asn(10), Leu(11), d-Trp(12)]PTHrP (7-34) in these cells. On the other hand, the former antibody and the latter PTHrP antagonist abrogated the PTHrP (1-36)-induced increase in these osteoblastic products. Transient exposure to PTHrP (107-139), in contrast to PTHrP (1-36), stimulated vascular endothelial growth factor receptor 2 (VEGFR2) mRNA levels in these cells. Moreover, induction of ALP activity as well as OC and OPG expression by PTHrP (107-139) was blunted by SU5614, a permeable tyrosine kinase inhibitor of VEGFR2. Protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) inhibitors abolished the PTHrP (107-139)-stimulated VEGFR2 and OPG mRNA levels in these cells. These results indicate that intermittent exposure to PTHrP (107-139) exerts potential anabolic effects through the PKC/ERK pathway and, subsequently, VEGFR2 upregulation in vitro in human osteoblastic cells.
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PMID:Transient exposure to PTHrP (107-139) exerts anabolic effects through vascular endothelial growth factor receptor 2 in human osteoblastic cells in vitro. 1712 Jan 84

We investigated the impact of weight-bearing, aerobic exercise- and diet-induced weight loss on markers of bone turnover during a larger study of changes in metabolic fitness during short-term weight reduction using a repeated-measures, within-subject experimental design. Subjects (N = 19) underwent 6 weeks of energy restriction (reduced by approximately 3140 kJ/d) and aerobic exercise ( approximately 1675 kJ/d, walking or jogging at 60% maximum oxygen consumption) to induce a 5% reduction in body weight. Bone turnover markers and hormones were measured in serum collected at baseline and after 6 weeks of weight loss. Despite a 5% reduction in body weight at week 6, markers of bone formation, osteocalcin, and bone alkaline phosphatase, were significantly increased, and resorption markers, C-terminal cross-links of type I collagen and soluble receptor activator of nuclear factor kappaB ligand, were unchanged after 6 weeks of energy restriction and exercise. The concentration of leptin was significantly reduced after weight loss, but insulin-like growth factor I (IGF-I) and cortisol levels were unaffected. In conclusion, weight-bearing, aerobic exercise training may favorably affect the balance between bone resorption and formation during weight loss.
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PMID:Weight-bearing, aerobic exercise increases markers of bone formation during short-term weight loss in overweight and obese men and women. 1714 33

We assessed the effect of chronic hyperglycemia on bone mineral density (BMD) and bone remodeling in patients with type 2 diabetes mellitus. We investigated 42 patients with type 2 diabetes under stable control for at least 1 year, 22 of them with good metabolic control (GMC: mean age = 48.8 +/- 1.5 years, 11 females) and 20 with poor metabolic control (PMC: mean age = 50.2 +/- 1.2 years, 8 females), and 24 normal control individuals (CG: mean age = 46.5 +/- 1.1 years, 14 females). We determined BMD in the femoral neck and at the L2-L4 level (DEXA) and serum levels of glucose, total glycated hemoglobin (HbA1), total and ionic calcium, phosphorus, alkaline phosphatase, follicle-stimulating hormone, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor I (IGFI), osteocalcin, procollagen type I C propeptide, as well as urinary levels of deoxypyridinoline and creatinine. HbA1 levels were significantly higher in PMC patients (12.5 +/- 0.6 vs 7.45 +/- 0.2% for GMC and 6.3 +/- 0.9% for CG; P < 0.05). There was no difference in 25-OH-D, iPTH or IGFI levels between the three groups. BMD values at L2-L4 (CG = 1.068 +/- 0.02 vs GMC = 1.170 +/- 0.03 vs PMC = 1.084 +/- 0.02 g/cm(2)) and in the femoral neck (CG = 0.898 +/- 0.03 vs GMC = 0.929 +/- 0.03 vs PMC = 0.914 +/- 0.03 g/cm(2)) were similar for all groups. PMC presented significantly lower osteocalcin levels than the other two groups, whereas no significant difference in urinary deoxypyridine was observed between groups. The present results demonstrate that hyperglycemia is not associated with increased bone resorption in type 2 diabetes mellitus and that BMD is not altered in type 2 diabetes mellitus.
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PMID:Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus. 1727 58

In our previous study, it was demonstrated that the administration of anion salts, which slightly lower the dietary cation-anion difference (DCAD), in the prepartum period is safe and effective for preventing milk fever in multiparous cows. In the present study, several biomarkers, which might show activation of Ca metabolism, were analyzed using stored samples in the previous study to investigate the mechanism of the preventive effect on milk fever by lowering DCAD. Changes in bone-specific alkaline phosphatase activity, osteocalcin and insulin-like growth factor I concentrations in serum were almost the same among the three groups of multiparous cows with or without the oral administration of anion salts, while the levels of these serum biomarkers in the group of primiparous cows (heifer group) were much higher compared with those in the three multiparous groups throughout the experimental period. Urinary deoxypyridinoline excretion was not a useful biomarker for dairy cows because it hardly changed during the peripartum period in all groups. However, serum tartrate-resistant acid phosphatase (TRAP) activity, which is known as a biomarker of osteoclast activity, was well associated with the administration of anion salts lowering DCAD because among the three multiparous groups, only the group of multiparous cows fed the anion salts (anion group) showed an increased level, which rose to the level in the heifer group, and was markedly higher than those in the other control groups of multiparous cows. The increased activity of serum TRAP in the anion group suggested that Ca in the plasma pool was mobilized smoothly from bone-bound Ca via mature osteoclasts at parturition, which might be due to prior activation under mild acidosis induced by slightly lowering DCAD. Therefore, TRAP was the best biomarker to monitor the activation of Ca metabolism in dairy cows fed anion salts.
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PMID:Biomarkers for the activation of calcium metabolism in dairy cows: elevation of tartrate-resistant acid phosphatase activity by lowering dietary cation-anion difference is associated with the prevention of milk fever. 1740 42

The purpose of this cross-sectional study was to assess the extent of and mechanisms involved in bone loss in anorexia nervosa patients. We compared 113 anorexia nervosa patients (mean age 25 +/- 8 years, mean duration of disease 5.7 +/- 6.1 years) with 21 age-matched controls. Mean duration of amenorrhea was 3.2 +/- 4.7 years. We measured serum calcium and phosphate; bone remodeling markers (osteocalcin, bone-specific alkaline phosphatase [BSAP], serum crosslaps [CTX], and carboxyl-terminal telopeptide of type I collagen [ICTP]); follicle-stimulating hormone and luteinizing hormone levels; and estradiol (ultrasensitive assay), cortisol, urinary free cortisol, thyroid function, prolactin, and nutritional factors (insulin-like growth factor I [IGF-I], IGF binding protein 3 [IGFBP3]). In controls, only bone remodeling markers and nutritional factors were measured. Osteodensitometry was also performed on both patients and controls. Weight and body mass index (BMI) were significantly lower in anorexia nervosa patients than in controls (P < 0.0001). No significant differences were observed in biological indicators except for IGF-I, which was lower in anorexia nervosa patients (0.9 +/- 0.4 UI/mL) than in controls (1.5 +/- 0.4 UI/mL) (P < 0.0001). Densitometric measurements at three sites were significantly lower in anorexia nervosa patients and correlated with duration of disease and amenorrhea and with IGF-I at the hip only (P < 0.01). In the study population, osteoporosis was observed in 24 patients (21%) and osteopenia in 54 patients (48%). Patients with osteoporosis were significantly older and had longer disease and amenorrhea durations; lower weight and BMI; higher alkaline phosphatase, BSAP, and osteocalcin; and lower serum ICTP, IGF-I, and IGFBP3. All of these differences were significant and remained so even after multiple adjustments were made, except for IGF-I (P = 0.21). When multivariate analysis was performed, we found that age at onset of amenorrhea, weight, alkaline phosphatase, urinary free cortisol, and serum estradiol concentration accounted for 54% of the variance in spinal bone mineral density (BMD). Duration of amenorrhea, alkaline phosphatase, and weight explained 46.6% of the variance in femoral neck BMD. Duration of amenorrhea, IGF-I, and ICTP levels accounted for 38.6% of the variance observed in total hip BMD. The etiology of bone loss in patients with anorexia nervosa is multifactorial. Hypoestrogenia alone cannot account for this loss, and nutritional factors, IGF-I concentrations in particular, seem to play an important role.
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PMID:Evaluation of bone loss and its mechanisms in anorexia nervosa. 1766 43

The objective of the study was to determine the degree of linear growth retardation of patients with vitamin D deficiency rickets at presentation and the magnitude of catch-up growth in relation to their calcium (Ca) homeostasis and hormones affecting it before and after treatment. This prospective study recorded the anthropometric data and measured the circulating 25-hydroxy vitamin D (25-OH-D), insulin-like growth factor I (IGF-I), parathyroid hormone, Ca, phosphate, and alkaline phosphatase concentrations in 46 infants and children with nutritional (vitamin D deficiency) rickets before and 6 months or more after treatment with one intramuscular injection of vitamin D3 megadose (300000 IU). Forty normal age- and sex-matched children were included as controls for the auxological data. At presentation, patients' mean age = 13.1 +/- 1.1 months, length standard deviation scores (LSDS) = -1.5 +/- 0.2, and body mass index = 16.3 +/- 0.85. They were significantly shorter and had markedly lower growth velocity standard deviation scores (GVSDS) compared with normal controls (LSDS = 0.25 +/- 0.18 and 0.31 +/- 0.22, respectively). Six months after treatment, the LSDS increased significantly in patients to -0.45 +/- 0.13, with a significantly increased GVSDS (2.76 +/- 0.45) and body mass index (16.9 +/- 0.65). They were still shorter but with significantly higher GVSDS compared with normal controls. Serum Ca and phosphate concentrations increased from 2.07 +/- 0.25 and 1.23 +/- 0.24 mmol/L, respectively, before treatment to 2.44 +/- 0.2 and 1.94 +/- 0.2 mmol/L, respectively, after treatment. Serum alkaline phosphatase and parathyroid hormone concentrations decreased from 1183 +/- 219 U/L and 294 +/- 87 pg/mL, respectively, before treatment to 334 +/- 75 U/L and 35.2 +/- 15.2 pg/mL, respectively, after treatment. The 25-OH-D level increased from 4.5 +/- 0.56 ng/mL before treatment to 44.5 +/- 3.7 ng/mL after treatment. Circulating concentrations of IGF-I increased significantly after treatment (52.2 +/- 18.9 ng/mL) vs before treatment (26.6 +/- 12.8 ng/mL). The 25-OH-D concentrations were correlated significantly with the IGF-I levels before and after treatment (r = 0.603 and r = 0.59, respectively; P < .001). The GVSDS after treatment was correlated with the increase of IGF-I and 25-OH-D levels (r = 0.325 and r= 0.314, respectively; P < .01). These data denote that the accelerated linear growth after treatment of nutritional vitamin D deficiency is mediated through activation of the growth hormone/IGF-I system and suggests an important role of vitamin D as a link between the proliferating cartilage cells of the growth plate and growth hormone/IGF-I secretion. Three different sequential stages of vitamin D deficiency can be recognized according to the clinical/radiological, biochemical, and hormonal data of patients at presentation.
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PMID:Linear growth in relation to the circulating concentrations of insulin-like growth factor I, parathyroid hormone, and 25-hydroxy vitamin D in children with nutritional rickets before and after treatment: endocrine adaptation to vitamin D deficiency. 1807 65

Safflower (Carthamus tinctorius L.) seeds are used as a folk medicine to enhance bone formation or to prevent osteoporosis in Korea. Therefore, the methanolic extract of safflower seeds (MESS) containing high mineral content, such as calcium (Ca), potassium (K) and phosphorous (P), was evaluated for the role on osteoblast (Ob) markers of Sprague-Dawley rats. In serum of 3 to 11 weeks (wks) old rats, both osteocalcin (OC) content and bone-specific alkaline phosphatase (B-ALP) activity increased to their maximum levels in 4-7 wks. Hence, 3 wks old rats were selected for 8 wks oral treatment of MESS, resulted in the significant increase of Ob markers in serum such as OC content (4-8 wks), B-ALP activity (1-2 wks) and insulin-like growth factor I (IGF-I) level (1 wk), and the growth parameter such as the length of femur (2-8 wks) and tibia (4 wks). On the basis of Pearson's correlation coefficient, there were a moderate correlation between OC and B-ALP at 8 wks, a low correlation between OC and IGF-I at 1, 4 and 8 wks, a moderate correlation between OC and femur length at 1, 2 and 8 wks, and a moderate correlations between OC and tibia length at 1 and 8 wks of MESS-treated groups. The result reveals that the changes of OC correlated at low to moderate level with the changes of B-ALP activity, IGF-I content and femur and tibia length in the MESS-treatment period. On the other hand, there were a strong correlation between IGF-I and femur length at 2 wks and moderate correlation between IGF-I and tibia length at 1, 2 and 8 wks of MESS-treated groups. Therefore, the effect of MESS on bone formation likely appears to be mediated by IGF-I at the early stage of treatment.
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PMID:Determination of mineral content in methanolic safflower (Carthamus tinctorius L.) seed extract and its effect on osteoblast markers. 1933 46

A 16-year-old boy with transfusion-dependent thalassemia major presented with tetany, numbness, bone pain, short stature and pubertal delay. His height SDS score=-2.6, BMI=22.4, spleen was palpable 5 cm and liver 7 cm below the costal margins. The cardio-vascular examination was normal. Laboratory investigations showed a hemoglobin level (8 g/dL), hypocalcemia, hyperphosphatemia and elevated alkaline phosphatase (ALP) with serum 25-OH D below 3 ng/ml and a normal magnesium level. Serum parathyroid hormone (PTH) level was lower (21 pg/mL; normal 16-70 pg/mL) than expected for the degree of hypocalcemia. Serum ferritin concentration was 4442 ug/L, insulin-like growth factor I (IGF-I) was 31 microg/L (normal 122- 286 microg/L), free T4 was 13.1 microg/dL, TSH 1.2 mIU/ml. These results revealed a combined vitamin D-parathyroid defect. Peak growth hormone (GH) responses to clonidine and glucagon tests were 7.6 ng/ml and 6.2 ng/ml, respectively. Serum LH and FSH concentrations were below 0.5 U/L and testosterone was below 10 ng/dl. Radiographs revealed osteopenia of the phalanges and long bones and DXA scanning revealed low BMD Z-score of the femoral neck and 4th and 5th lumbar spines. MRI showed evidence of hemosiderin deposition in the pituitary. The patient was started on oral daily calcium carbonate (1500 mg elemental calcium) and vitamin D2 (calciferol) 25,000 IU/day and intensive iron chelation therapy. A low dose of IM testosterone enanthate (1 mg/kg/month) was injected for 6 months. Follow-up after 4, 8 and 12 months revealed normal Ca, PO4, ALP, and 25-OH D concentrations and disappearance of spasms and numbness and increased growth velocity. In conclusion, investigating calcium homeostasis at regular intervals and early management of any abnormality can preclude the occurrence of complications.
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PMID:An adolescent boy with thalassemia major presenting with bone pain, numbness, tetanic contractions and growth and pubertal delay: panhypopituitarism and combined vitamin D and parathyroid defects. 1933 71


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