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)

Authors studied the effect of prolonged sex hormone deficiency on some parameters of bone metabolism in calcitonin sensitive young male rats. 30 rats were given aminoglutethimid (AG) for 36 days. Part of these animals received plus dehydroepiandrosterone (DEA) treatment. Corticoid deficiency was substituted by cortisone. In addition 22 rats were administered only cortisone, 11 animals cortisone and DEA, and 10 rats only DEA for 36 days. On day 37 the different parameters of treated rats were compared to findings in 31 control animals. It has been found that body weight, calcitonin hypocalcaemia, serum alkaline phosphatase, as well as bone ash weight pro unit body weight was significantly lower in AG treated rats as compared to controls and rats receiving DEA in addition to AG. Values of latter group did not differ from controls. It has also been established that neither cortisone substitution nor isolated DEA treatment did involve significant differences in the studied parameters of bone metabolism as compared to controls. The findings support the opinion that sex hormone deficiency, directly or indirectly results osteoporosis. The experimental model seems to be suitable for the study of androgen deficient osteopenia.
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PMID:Effects of prolonged aminoglutethimid and dehydroepiandrosterone treatment on rat bones. 613 17

This study was carried out in order to evaluate serum carboxy-terminal propeptide of human type I procollagen (PICP) in patients with primary hyperparathyroidism and to examine its changes following parathyroidectomy. Seventeen patients (four males and 13 famels, aged 53.8 +/- 3.1 SEM years) were studied in basal conditions; six patients also were investigated after successful parathyroid surgery. Mean serum PICP values of patients with primary hyperparathyroidism (194.5 +/- 27 SEM micrograms/l) were significantly higher (p < 0.001) with respect to those found in normal subjects. However, deviations from the norm (Z score values) were significantly less with respect to deviations of serum osteocalcin, alkaline phosphatase and urinary hydroxyproline/creatinine ratio. Following parathyroidectomy, it was possible to observe a discrepancy between markers of bone resorption and those of bone formation. The former tend to decrease, while the latter either do not show any significant change (serum alkaline phosphatase and serum osteocalcin) or increase (serum procollagen). The results of our investigation indicate that in basal conditions the assay of serum procollagen may be of clinical value but it would be better to use it in combination with other biomarkers of skeletal remodelling. The results obtained after parathyroidectomy are the opposite of those obtained following parathyroid hormone infusion and should be ascribed to the effect of acute hormone deficiency on collagen synthesis. The positive biochemical uncoupling following surgery might lend support to the rise of bone mineral density consistently reported in the first few months following parathyroidectomy.
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PMID:Serum carboxy-terminal propeptide of human type I procollagen in patients with primary hyperparathyroidism: studies in basal conditions and after parathyroid surgery. 820 59

To investigate the relationship of the hematopoietic system to the loss of bone due to ovarian hormone deficiency, we examined the effects of ovariectomy and estrogen administration on the thymus, spleen and the bone marrow, and on the proliferation of marrow progenitors of osteoclasts. We also assessed the effects of daily administration of interleukin-1 receptor antagonist (IL-1ra) on bone loss due to ovarian hormone deficiency. Ovariectomy resulted in decreased cancellous bone volume, increased trabecular osteoblast and osteoclast numbers, and increased serum alkaline phosphatase levels that were prevented by 17 beta-estradiol treatment. Thymus weight, spleen weight, thymus and spleen lymphocytes, and bone marrow monocytes and lymphocytes also increased significantly following ovariectomy, and the increases were suppressed by 17 beta-estradiol. Ovariectomy, in addition, caused a 4-fold increase in the number of tartrate resistant acid phosphatase (TRAP)-positive multinucleated cells formed in cultures of marrow cells and the increase was partially inhibited by 17 beta-estradiol. IL-1ra administration did not prevent the bone loss due to ovariectomy. Our findings indicate that ovariectomy-induced bone loss in the rat is accompanied by marked changes in the hematopoietic system, and that these changes are modulated by estrogen administration. In spite of the negative finding with IL-1ra, the nature of the involvement of the hematopoietic system in the pathogenesis of bone loss due to ovarian hormone deficiency merits continued exploration.
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PMID:Ovariectomy-induced bone loss and the hematopoietic system. 830 79

The purpose of this study was to examine whether soybean protein isolate prevents bone loss induced by ovarian hormone deficiency. Thirty-two 95-d-old Sprague-Dawley rats were randomly assigned to four treatment groups [sham-operated (sham); ovariectomized (ovx); ovx+soybean; ovx + 17 beta-estradiol (E2)] and killed after 30 d. Rats in the sham, ovx and ovx + 17 beta-estradiol groups were fed a casein-based diet, and the soybean group was fed soybean protein isolate instead of casein; the diets were otherwise comparable. Rats in the ovx group had significantly lower densities of the right femur (P < 0.001) and the fourth lumbar vertebra (P < 0.05) than rats in the sham group. These lower bone densities were not observed in animals receiving 17 beta-estradiol or fed soybean. The ovx group also had significantly (P < 0.01) greater serum concentrations of 1,25-dihydroxycholecalciferol than the other three groups. Our findings suggest that dietary soybean protein is effective in preventing bone loss due to ovarian hormone deficiency. Because serum activities of both alkaline phosphatase and tartrate-resistant acid phosphatase were significantly greater in the ovx group and in the ovx + soybean group but not in the group receiving 17 beta-estradiol, compared with sham animals, this confirms that ovariectomy enhances and 17 beta-estradiol suppresses the rate of bone turnover. Despite the higher rate of bone turnover in the soybean-fed animals, the vertebral and femoral bone densities of these rats were significantly greater than those of rats in the ovx group, suggesting that formation exceeded resorption. Further studies are needed to clarify whether this protective effect on bone is due to the protein itself or to the presence of isoflavones in soybean protein.
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PMID:Dietary soybean protein prevents bone loss in an ovariectomized rat model of osteoporosis. 855 97

The differential effects of sodium-induced renal hypercalciuria on the biochemical markers of bone metabolism and calcium homeostasis were studied in oophorectomized (Oophx) and sham-operated rats. The rats consuming a normal (0.4%) calcium semisynthetic diet were randomly allocated to either 0, 0.4, 0.6, 0.9, or 1.25% NaCl in their drinking water for 7 days. At that time fasting blood and urine specimens were collected and analyzed for bone-related biochemical variables. The urinary calcium/creatinine ratio was increased with increasing urinary sodium (p < 0.01) in both sham and Oophx animals. The hydroxyproline/creatinine ratio was elevated as a result of Oophx (p < 0.001) and was raised with increasing urinary sodium in both sham (p = 0.012) and Oophx animals (p = 0.007). Serum osteocalcin and alkaline phosphatase were elevated in Oophx rats (p < 0.02). While serum osteocalcin was raised with increasing urinary sodium in Oophx rats (p = 0.035), there was no effect on osteocalcin levels in sham-operated rats. This study demonstrates that sodium-induced renal hypercalciuria potentiates bone turnover in Oophx rats as compared with ovary-intact rats and indicates important implications for the effect of dietary salt on bone turnover with ovarian hormone deficiency.
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PMID:Increased urinary calcium excretion potentiates bone turnover in oophorectomized rats. 905 68

Conditions such as estrogen deficiency, skeletal unloading, and aging have all been demonstrated to have various effects on the proliferation and differentiation of bone marrow stroma-derived osteoprogenitor cells. Here we have sought to examine the effects of pituitary hormone deficiency on the proliferation and the differentiation of these osteoprogenitor cells using the hypophysectomized (HX) rat as a model. In the present study, we use an in vitro culture system to examine the effects of HX on the osteogenic potential of rat bone marrow stroma. With the intact animal as a control, we used [3H]thymidine incorporation and cell number as indexes of proliferation. We also measured alkaline phosphatase enzyme activity, relative levels of osteocalcin expression with RT-PCR, and osteopontin and bone sialoprotein steady-state levels by Northern blot to delineate the effect on differentiation. Our results indicate that osteoprogenitor cells exposed to a pituitary hormone-deficient environment in vivo demonstrate an enhanced proliferative capacity and also exhibit an augmented expression of differentiation markers when exposed to an optimal environment in vitro.
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PMID:Effect of hypophysectomy on the proliferation and differentiation of rat bone marrow stromal cells. 988 48

Ipriflavone (IP), a synthetic isoflavone has been reported to prevent bone loss in both postmenopausal women and ovariectomized (ovx) rats. The purpose of this study was to compare and contrast some of the bone protective mechanisms of IP to those of 17beta-estradiol (E(2)) in ovarian hormone deficiency. Forty-eight 95-day-old Sprague-Dawley rats were assigned to four groups: sham, ovx, ovx+IP, and ovx+E(2). The doses of IP and E(2) were 100 mg and 10 microg/kg body weight per day, respectively. Rats were fed a diet that contained 0.4% calcium, 0.3% phosphorus, and 0.195 nmol vitamin D(3)/g diet. After sacrifice, left femoral bone densities were measured and bone histomorphometry was performed on the proximal tibial metaphysis. Ipriflavone as well as E(2) treatment completely prevented the ovx-induced femoral bone density loss. However, in contrast to E(2), IP did not lower the ovx-induced rise in serum alkaline phosphatase (ALP) activity or insulin-like growth factor (IGF)-I and IGF binding protein (IGFBP)-3 concentrations. On histomorphometry analysis, the ovariectomy-induced increase (P < 0. 09) in bone formation rate (BFR) was significantly (P < 0.05) suppressed by E(2) treatment, whereas this higher BFR was maintained in IP-treated animals. These findings indicate that IP is effective in preventing the ovx-associated bone loss. The bone protective mechanisms of IP in ovarian hormone deficiency may be different from those of E(2) and may involve increased rates of bone formation.
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PMID:The synthetic phytoestrogen, ipriflavone, and estrogen prevent bone loss by different mechanisms. 1060 47

Thyroid hormone exerts its biological effect by binding to a TR. Both liganded and unliganded TRs regulate the transcription of T(3)-responsive genes. Cofactors with activating or repressing function modulate the transcriptional regulation by TRs. We showed that steroid receptor coactivator 1 (SRC-1)-deficient mice (SRC-1(-/-)) exhibit partial resistance to thyroid hormone at the level of the pituitary thyrotrophs. To determine whether SRC-1 deficiency affects globally T(3)-dependent transcriptional regulation, we studied the effects of thyroid hormone deprivation and replacement on the expression of several genes in different tissues of SRC-1(-/-) and wild-type mice (SRC-1(+/+)). Thyroid hormone deficiency was induced by a low iodine diet (LoI) supplemented with propylthiouracil (PTU) for 2 wk. L-T(3) was injected ip for the last 4 d in one group (PTU+T(3) group), and another group (PTU group) received only vehicle. Levels of mRNAs for T(3)-responsive genes were determined by Northern blotting: GH and TSH beta in pituitary; type 1 iodothyronine 5'-deiodinase, spot 14 (S14), and malic enzyme in liver; and sarcoplasmic reticulum calcium adenosine triphosphatase 2 and myosin heavy chain alpha and beta in heart. Serum parameters, TSH, total cholesterol, creatine kinase, and alkaline phosphatase (AP), were also measured. Hypothyroidism produced a comparable increase in TSH beta mRNA in both genotypes, but its suppression by L-T(3) was attenuated in SRC-1(-/-) mice. In contrast, hypothyroidism failed to reduce S14 mRNA levels in SRC-1(-/-) mice. As a consequence, the response to L-T(3) was not observed in these mice. SRC-1 deficiency had no effect on the expression of the rest of the T(3)-responsive genes examined. Of the four serum parameters, the T(3)-mediated decrease in TSH and changes in AP were attenuated in SRC-1(-/-) mice. We conclude that SRC-1 deficiency altered the expression of only some of the T(3)-responsive genes. SRC-1 appears to be involved not only in transcriptional activation by liganded TRs, but also in the suppression by liganded or unliganded TRs. Some of the effects of SRC-1 may be TR isoform specific.
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PMID:Steroid receptor coactivator-1 deficiency causes variable alterations in the modulation of T(3)-regulated transcription of genes in vivo. 1189 91

Growth hormone deficiency (GHD) is an important cause of decreased bone mass in childhood and adolescence. The role of other pituitary hormone deficiencies on bone mass is still a query in children. Thirty-nine children (28 with isolated GHD [IGHD] and 11 with multiple pituitary hormone deficiency [MPHD]) were investigated to show the effects of IGHD vs MPHD on bone status. Bone turnover markers (calcium, phosphate, alkaline phosphatase [ALP] Bone ALP [BALP], osteocalcin [OSC], carboxyterminal propeptide of type-1 collagen [CPP-I], parathyroid hormone [PTH]) were measured before and every four months during growth hormone (GH) therapy; bone mineral density (BMD) of the lumbar spine was measured before and every six months during therapy. All bone turnover markers except calcium and PTH increased significantly during 1 year of GH therapy. There were no differences in the levels of bone turnover markers between children with IGHD and MPHD at baseline, and after 4, 8 and 12 months of therapy. Lumbar spine BMD SDS of all patients increased significantly during 1 year of therapy (p = 0.035 after 6 months and p <0.001 after 12 months compared with baseline). BMD SDS of both IGHD and MPHD groups were similar at baseline and after 6 and 12 months of therapy (p = 0.235, p = 0.295 and p = 0.384). Height SDS (HtSDS) at baseline was the most important predictor of baseline BMD SDS in children with GHD (t = 4.166, p <0.001). DeltaHtSDS was also positively related to deltaBMD SDS after 1 year of GH therapy. In conclusion, there was no difference in bone status of the patients with IGHD and MPHD at baseline. GH therapy yielded similar increases in bone mass in both groups. Increase in height contributed to increase in BMD during 1 year of GH therapy.
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PMID:Responses of bone turnover markers and bone mineral density to growth hormone therapy in children with isolated growth hormone deficiency and multiple pituitary hormone deficiencies. 1209 91

The purpose of this study was to examine whether whole aqueous black tea extract (BTE) prevents bone loss induced by ovarian hormone deficiency. Eighteen 95-100 days old female albino rats were randomly assigned to three treatment groups [sham -operated control (sham); bilaterally ovariectomized (ovx) and ovx + aqueous black tea extract (BTE) ] and sacrificed after 28 days. All animals were fed a standard laboratory diet with free access to deionized water except on days of urinary parameter studies when animals were given only calcium free deionized water during the entire 24 h period of urine collection. Body weight study revealed that rats in the ovx group had significantly higher final body weight than rats in the sham group. This higher final body weight was not observed in animals receiving BTE. The ovx group also had significantly higher abdominal fat mass and liver weight and significantly lower uterus, right kidney and left kidney weights than in other two groups. All these organ weight changes in ovx group also were not observed in animals receiving BTE. Results of urinary studies revealed that rats in the ovx group had significantly higher urinary excretion of calcium (Ca), phosphate, creatinine (Cr), calcium to creatinine (Ca:Cr) ratio (P< 0.001) and hydroxyproline (HPr) (P< 0.01) than rats in the sham group. Significant recovery of all these parameters were observed in animals receiving BTE. The ovx group also had significantly higher (P< 0.001) serum alkaline phosphatase (AP) and tartrate-resistant acid phosphatase (TRAP) activity than rats in the other two groups. These changes could not be seen in animals receiving BTE. Also, identical changes were seen in bone density experiments. Rats in the ovx group had significantly lower densities of the right femur (P<0.001), eighth thoracic rib (P< 0.001), eighth thoracic vertebra (P< 0.05), and fourth lumbar vertebra (P< 0.01) than rats in the sham group; and significant improvement in densities of these bones were seen in animals supplemented with BTE. Animals of ovx group also showed significant decrease in calcium and phosphate level in all these bones which could be regained significantly when these animals were supplemented with BTE. Our findings suggest that aqueous BTE may be effective in preventing bone loss due to ovarian hormone deficiency. Because serum activity of AP, TRAP and urinary loss of bone minerals (Ca and Phosphate) and also the organic components of bone (Cr and HPr) were significantly greater in the ovx group, compared to sham animals and ovx + BTE group. This confirms that ovariectomy enhances and BTE suppresses the rate of bone turnover. The density results of ovx + BTE group are significantly greater than rats in the ovx group, suggesting further that formation exceeded resorption. Detailed studies are underway to clarify the mechanism of this protective effect of BTE on hypogonadal bone loss.
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PMID:Evidence for a prospective anti-osteoporosis effect of black tea (Camellia Sinensis) extract in a bilaterally ovariectomized rat model. 1522 90


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