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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 clinical study of treated subjects and nontreated controls was made in healthy eumenorrheic young postadolescent women volunteers in the Department of Obstetrics and Gynaecology at Cagliari University, to investigate whether an oral contraceptive (OC) containing drospirenone (3 mg) plus
ethinyl estradiol
(30 microg) (DRSP+EE) can affect bone metabolism. Control group (n = 26) and OC group (n = 28) women did not differ in age, body mass index, waist-to-hip ratio and main outcome measures [urinary levels of deoxypyridinoline and pyridinoline, serum levels of osteocalcin, bone specific
alkaline phosphatase
(bSAP), total testosterone (total-T), sex hormone-binding globulin (SHBG), progesterone and bone mineral density (BMD) at the heel]. The control group was studied at the luteal phase (LP) during both the first and the sixth menstrual cycle; the OC group was studied during the first cycle at the LP, and on days 16-18 of the sixth cycle of DRSP+EE treatment. At the sixth cycle, in the control group, the main outcome measures did not change compared to baseline. In the OC group, deoxypyridinoline, pyridinoline, osteocalcin, bSAP, total-T and progesterone levels were reduced, whereas SHBG levels were increased. The BMD was unchanged compared to baseline. The results suggest that 6-month DRSP+EE treatment decreases bone turnover.
...
PMID:Short-term variations in bone remodeling markers of an oral contraception formulation containing 3 mg of drospirenone plus 30 microg of ethinyl estradiol: observational study in young postadolescent women. 1545 33
The aim of this study was to compare metabolic changes during use of low-dose combined oral contraceptives (COCs) and those of nonhormonal contraceptives in perimenopausal women. Thirty-nine healthy women over 40 years old who attended the Family Planning Clinic of the King Chulalongkorn Memorial Hospital, Bangkok, Thailand, were recruited, 20 in the COC group received COC preparations containing 30 microg of
ethinyl estradiol
and 150 microg of levonorgestrel and 19 in the nonhormonal group were intrauterine device users. Blood samples were taken upon admission and 6 months later. Minor biochemical changes associated with low-dose COC use included an increase in glucose tolerance, triglycerides, serum albumin, serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) levels but a decrease in fasting plasma glucose, total cholesterol, high-density lipoprotein cholesterol, total bilirubin and
alkaline phosphatase
levels. There was no clinical significance for the metabolic changes. Low-dose COCs can be a satisfactory contraceptive choice for healthy perimenopausal women.
...
PMID:Comparison of the metabolic effects of oral contraceptive and nonhormonal contraceptive use in women over 40 years old. 1572 67
This study examines the application of Ishikawa human endometrial adenocarcinoma cells to measure the estrogenic activity of fractionated extracts of sediments from Tokyo Bay, Japan.
Estrogen
stimulates
alkaline phosphatase
activity in this cell line. The results of these assays were compared with those of a yeast estrogen screen (YES) assay. The Ishikawa cell line bioassay showed higher sensitivity to 17beta-estradiol (median effective concentration [EC50], 10.7 pM) than did the YES assay (EC50, 480 pM). Fractionation of sediment extracts (all samples collected from 5 sites) showed that the nonpolar fraction was poisonous to yeast cells; the estrogenic activity of this fraction, therefore, could not be measured by YES. However, the nonpolar fraction did not kill the Ishikawa cells. The 17beta-estradiol-equivalent values of 15 extracts (3 fractions from each of 5 sediment samples) ranged from 5.7 to 697 pg/g dry weight according to the Ishikawa cell line bioassay. Chemical analysis using gas chromatography-mass spectrometry revealed that the highest concentrations of endocrine-disrupting chemicals were observed at the sampling station near the sewage treatment plant. The results support that the Ishikawa cell line bioassay is suitable for measuring the estrogenic activity of sediment samples.
...
PMID:Evaluation of the Ishikawa cell line bioassay for the detection of estrogenic substances from sediment extracts. 1605 May 73
Puberty has a key role in bone development. During puberty, several nutritional and hormonal factors play a major role in this process. The aim of this study was to determine the changes in areal bone mineral density (BMD), gonadal steroids, bone formation markers, and growth parameters in healthy Turkish pubertal girls and boys at different pubertal stages. In additional, we aimed to detect the relationship between BMD, sex steroids, and growth parameters, and to reveal the most important determinant of BMD in the pubertal period. BMD of the lumbar spine and total body was performed by dual-energy X-ray absorptiometry (Lunar DPX series) in 174 healthy pubertal children (91 girls, 83 boys), aged 11-15 years. Height and weight were measured. Pubertal stages were assesed. Bone formation markers and gonadal steroids were measured. BMD values significantly increased until stage IV in girls. In boys, BMD values also increased during puberty (P < 0.05), but it was significantly higher in stage IV compared with that in other pubertal stages (P < 0.01). Testosterone levels increased until stage IV in both sexes, particularly in boys.
Estrogen
levels significantly increased during puberty in girls, whereas it was significantly higher at stage IV in boys (P < 0.001). Bone-specific
alkaline phosphatase
(BAP) level was higher in early and midpuberty, and decreased in late puberty in girls (P < 0.001). BAP level was higher in stage IV in boys. Osteocalcin level was shown not to change significantly in pubertal stages. There was a modest correlation between BMD values and estrogen and testosterone levels in boys. In girls, there was a correlation between BMD values and estrogen levels only (P < 0.05). Weight was significantly associated with BMD in both sexes (P < 0.05).
Estrogen
had a significant influence on BMD in boys and girls. In conclusion, bone mass increased throughout puberty in both sexes. Peak bone mass was not achieved in girls, but was obtained at stage IV in boys. Bone formation markers were good predictors of bone mass in girls, but not in boys.
Estrogen
level made the greatest contribution to bone mineral acquisition in boys and girls. The achievement of peak bone mass was sustained by estrogen in boys. The major independent determinant of BMD in both sexes was weight.
...
PMID:Bone mineral density in girls and boys at different pubertal stages: relation with gonadal steroids, bone formation markers, and growth parameters. 1626 55
Ethinylestradiol
(EE) induces intrahepatic cholestasis in experimental animals being its derivative, ethinylestradiol 17beta-glucuronide, a presumed mediator of this effect. To test whether glucuronidation is a relevant step in the pathogenesis of cholestasis induced by EE (5 mg/kg b.wt. s.c. for 5 consecutive days), the effect of simultaneous administration of galactosamine (200 mg/kg b.wt. i.p.) on biliary secretory function was studied. A single injection of this same dose of galactosamine was able to decrease hepatic UDP-glucuronic acid (UDP-GA) levels by 85% and excretion of EE-17beta-glucuronide after administration of a tracer dose of [3H]EE by 40%. Uridine (0.9 g/kg b.wt. i.p.) coadministration reverted the effect of galactosamine on hepatic UDP-GA levels and restored the excretion of [3H]EE-17beta-glucuronide. When administered for 5 days, galactosamine itself did not alter any of the serum markers of liver injury studied (aspartate aminotransferase, alanine aminotransferase, and
alkaline phosphatase
) or biliary secretory function. When coadministered with EE, galactosamine partially prevented the impairment induced by this estrogen in total bile flow, the bile-salt-independent fraction of bile flow, basal bile salt secretion, and the secretory rate maximum of tauroursodeoxycholate. Uridine coadministration partially prevented galactosamine from exerting its anticholestatic effects. In conclusion, galactosamine administration partially prevented EE-induced cholestasis by a mechanism involving decreased UDP-GA availability for subsequent formation of EE 17beta-glucuronide. The evidence thus supports the hypothesis that EE 17beta-glucuronide is involved in the pathogenesis of EE cholestasis.
...
PMID:Galactosamine prevents ethinylestradiol-induced cholestasis. 1655 70
Estrogen
stimulates endothelial nitric oxide (NO) production and attenuates endothelial dysfunction in ischemia/repurfusion and menopause. Recent studies have shown that phytoestrogens from dietary sources improve endothelial function and reduce cardiovascular risks. The Thai medicinal plant Pueraria mirifica (PM) contains many potent phytoestrogens including miroestrol and deoxymiroestrol but no study on vascular function has been established. Ground powder of PM was orally given to ovariectomized White New Zealand rabbits (OVX + PM group) (n = 4) weighing 3.2-4.0 kg at the dose of 100 mg/kg for 90 days. Saline-treated ovariectomized rabbits were assigned as a control group (OVX group) (n = 5). At the end of treatment thoracic aorta was isolated for functional evaluation. Maximal relaxant response to acetylcholine (ACh) was significantly increased (24%) with 3.5-fold decrease in EC50 while no change in relaxant response to sodium nitroprusside was observed Minimal and maximal responses to 17beta-estradiol (E2) were increased in the OVX + PM group and L-NAME (100 mM) attenuated Emax of E2. PM significantly decreased maximal contractile responses to norepinephrine (NE), but no change in EC50 was observed. In addition to vascular study, the authors found no significant alteration in serum cholesterol, LDL, triglyceride, HDL, ALT AST
alkaline phosphatase
, and lipid peroxidation in OVX + PM rabbits. These data demonstrate that PM (100 mg/kg/d) improved endothelial function through NO-dependent pathway and increased response to E2 while sensitivity to NE was reduced. In addition, it had no impact on lipid profile, liver enzymes, and ALP activities. PM is a potential source of phytoestrogens for postmenopausal women to improve cardiovascular function or reduce cardiovascular risks.
...
PMID:Effects of Pueraria mirifica on vascular function of ovariectomized rabbits. 1686 67
Estrogens cause intrahepatic cholestasis in susceptible women during pregnancy, after administration of oral contraceptives, or during postmenopausal hormone replacement therapy.
17alpha-Ethinylestradiol
(EE) is a synthetic estrogen widely used to cause experimental cholestasis in rodents with the aim of examining molecular mechanisms involved in this disease. EE actions on the liver are thought to be mediated by estrogen receptor alpha (ERalpha) and pituitary hormones. We tested this hypothesis by analyzing metabolic changes induced by EE in livers from hypophysectomized (HYPOX) and hypothyroid rats. Microarray studies revealed that the number of genes regulated by EE was increased almost 4-fold in HYPOX rat livers compared with intact males. Little overlap was apparent between the effects of EE in intact and HYPOX rats, demonstrating that pituitary hormones play a critical role in the hepatic effects of EE. Consistently, hypophysectomy protects the liver against induction by EE of serum bilirubin and
alkaline phosphatase
, two markers of cholestasis and hepatotoxicity and modulates the effects of EE on several genes involved in bile acid homeostasis (e.g., FXR, SHP, BSEP, and Cyp8b1). Finally, we demonstrate a novel mechanism of action of EE through binding and negative regulation of glucocorticoid receptor-mediated transcription. In summary, pituitary- and ERalpha-independent mechanisms contribute to development of EE-induced changes in liver transcriptome. Such mechanisms may be relevant when this model of EE-induced cholestasis is evaluated. The observation that the pharmacological effects of estrogen in liver differ in the absence or presence of the pituitary could be clinically relevant, because different drugs that block actions of pituitary hormones are now available.
...
PMID:Role of pituitary hormones on 17alpha-ethinylestradiol-induced cholestasis in rat. 1710 34
Estrogen
replacement therapy has been shown to reduce postmenopausal osteoporosis. In the present study, we examined the effects of the phytoestrogen coumestrol on neonatal and adult osteoblasts metabolism. Two different sources of osteoblast cells (neonatal mice calvaria and adult mice long bone) cultures were used in this study. The effects of coumestrol on the cellular activities were analyzed by the mitochondrial tetrazolium (MTT) assay, secretion of
alkaline phosphatase
(
ALP
), intracellular calcium content (Ca), and the gene expression of bone matrix protein, estrogen receptors (ER-alpha, ER-beta), and osteoprotegerin (OPG) and osteoprotegerin ligand (OPGL). The results showed that the proliferation of neonatal mice osteoblast cells was enhanced by treatment of coumestrol. In the presence of 10(-9)M coumestrol, the osteoblast proliferation attained 139.5% of the control and that the coumestrol can increase the intracellular calcium contents. Type I collagen gene expression was upregulated 167% at the 1st day's culture;
ALP
gene expression was upregulated 360% at the 7th day's culture; while the osteocalcin gene expression was upregulated 222% at the 14th day's culture. When adult mice osteoblasts were cultured in the presence of 10(-9)M coumestrol, the osteoblasts population increased significantly earlier and attained its maximal effect at the 21st day's culture with 207.4% of control group. The content of ER-beta and osteoprotegerin secretion by neonatal mice control cells gradually increased during osteoblasts differentiation, whereas the ER-alpha and OPGL content were decreased in this study. The cellular responses to the estradiol and counmestrol were quite different in the osteoblasts derived from different age.
...
PMID:Effects of coumestrol on neonatal and adult mice osteoblasts activities. 1712 Feb 6
Adipose-derived stromal cells (ASCs) possess multiple differentiation potentials and may serve as a cell source, if effectively modulated, for regenerative medicine and tissue engineering. Due to estrogen's function in tissue and organ development through regulating cell proliferation and differentiation, we hypothesized that an estrogen supplement may effectively enhance the multiple differentiation potentials of human ASCs. 17-Beta estradiol (E2) was investigated for modulating in vitro osteogenic and adipogenic differentiation in human ASCs isolated from a healthy female donor. After ASCs' exposure to osteogenic and adipogenic differentiation medium supplemented with different concentrations of E2, osteogenic markers (
alkaline phosphatase
activity, extracellular matrix, calcium deposition, and osteocalcin expression) and adipogenic parameters (lipid accumulation and differentiated cell population) significantly improved.
Estrogen
's enhancement is dose dependent and linked to differing alpha and beta estrogen receptors. Our data preliminarily demonstrate that estrogen can modulate the differentiation, and potentially improve the efficiency of ASCs in stem cell-based tissue engineering and regeneration. However, further study is needed to verify the regulatory functions of estrogen on ASC differentiations of donors with different ages and genders.
...
PMID:17-Beta estradiol enhances osteogenic and adipogenic differentiation of human adipose-derived stromal cells. 1751 37
Hyperprolactinemia leads to high bone turnover as a result of enhanced bone formation and resorption. Although its osteopenic effect has long been explained as hyperprolactinemia-induced hypogonadism, identified prolactin (PRL) receptors in osteoblasts suggested a possible direct action of PRL on bone. In the present study, we found that hyperprolactinemia induced by anterior pituitary transplantation (AP), with or without ovariectomy (Ovx), had no detectable effect on bone mineral density and content measured by dual-energy X-ray absorptiometry (DXA). However, histomorphometric studies revealed increases in the osteoblast and osteoclast surfaces in the AP rats, but a decrease in the osteoblast surface in the AP+Ovx rats. The resorptive activity was predominant since bone volume and trabecular number were decreased, and the trabecular separation was increased in both groups.
Estrogen
supplement (E2) fully reversed the effect of estrogen depletion in the Ovx but not in the AP+Ovx rats. In contrast to the typical Ovx rats, bone formation and resorption became uncoupled in the AP+Ovx rats. Therefore, hyperprolactinemia was likely to have some estrogen-independent and/or direct actions on bone turnover. Osteoblast-expressed PRL receptor transcripts and proteins shown in the present study confirmed our hypothesis. Furthermore, we demonstrated that the osteoblast-like cells, MG-63, directly exposed to PRL exhibited lower expression of
alkaline phosphatase
and osteocalcin mRNA, and a decrease in
alkaline phosphatase
activity. The ratios of receptor activator of nuclear factor kappaB ligand (RANKL) and osteoprotegerin (OPG) proteins were increased, indicating an increase in the osteoclastic bone resorption. The present data thus demonstrated that hyperprolactinemia could act directly on bone to stimulate bone turnover, with more influence on bone resorption than formation. PRL enhanced bone resorption in part by increasing RANKL and decreasing OPG expressions by osteoblasts.
...
PMID:Prolactin directly enhances bone turnover by raising osteoblast-expressed receptor activator of nuclear factor kappaB ligand/osteoprotegerin ratio. 1816 9
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