Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the mechanism of action of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (AHPrBP, formerly APD) on bone metabolism, we have studied the influence of low doses of AHPrBP on bone resorption and formation in the mouse. Thirty-five-day-old mice were given daily injections of 0.16, 1.6, or 16 mumol/kg BW per day of AHPrBP for 10 days. At sacrifice biochemical parameters were measured in serum and bone ash, and histomorphometric parameters of bone formation and resorption were determined on undecalcified sections of caudal vertebrae after double 3H-proline and double tetracycline labelings. Serum calcium and 1,25-dihydroxyvitamin D levels remained normal at all dosage levels. Compared to controls, AHPrBP at doses of 1.6 and 16 mumol/kg per day increased the number of osteoclasts and the number of nuclei per osteoclast but markedly decreased the number of acid phosphatase-stained osteoclasts. Thus, AHPrBP appears to inhibit osteoclastic activity in vivo in part through reduction of acid phosphatase activity. At doses of 1.6 and 16 mumol/kg per day AHPrBP reduced serum alkaline phosphatase and the osteoblastic surface and decreased the endosteal osteoid surface and thickness. Both the matrix apposition rate and the mineral apposition rate were progressively reduced at the endosteal level, although they were not significantly changed at the periosteal level. Greater inhibition of bone resorption than bone formation resulted in increased endosteal bone density and bone mineral content. AHPrBP at a dose of 0.16 mumol/kg per day did not alter either the osteoclastic bone resorption or the mineral and matrix apposition rates.
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PMID:Inhibition of bone matrix apposition by (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (AHPrBP) in the mouse. 402 97

Low duodenal vitamin D-dependent calcium-binding protein has been reported in juvenile Hyp mice. Levels of this protein improved in adult Hyp mice. This led to the search for possible abnormal intestinal calcium absorption in juvenile Hyp mice and for evidence that calcium malabsorption, if present, would exacerbate the bone disease. A balance study was performed in 10 sets of normal and Hyp male mice at 5 and 12 weeks of age. Twelve-week-old Hyp mice had balances (24-h intake minus excretion) of Ca, P, Mg, Na, and K that were not significantly different from those of 12-week-old normal mice. However, 5-week-old Hyp mice had a significantly lower balance of Ca with higher fecal Ca and lower urinary Ca. No balance was also lower due to higher fecal Na. The balances of P, Mg, and K were not significantly affected in young Hyp mice. Growth and mineralization of the femur were compared in normal and heterozygous female Hyp mice from 3.5-46 weeks of age. The femora of Hyp mice gained ash weight at a rate comparable to that for normal mice, except for a lag between 3.5 and 7 weeks. There was life-long hypophosphatemia and elevated plasma alkaline phosphatase. It was concluded that the period of low levels of duodenal vitamin D-dependent calcium-binding protein was associated with low intestinal absorption and low skeletal mineralization. This dysfunction of the intestine in juvenile, rapidly growing Hyp mice may exacerbate the bone disease.
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PMID:A role for the intestine in the bone disease of juvenile X-linked hypophosphatemic mice: malabsorption of calcium and reduced skeletal mineralization. 609 Jan 1

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

Lactating female rats were fed diets containing 1.0, 0.1, or 0.04% Ca for 21 days. Fat-free dry weight, ash weight, calcium and phosphorus content of the humerus, plasma calcium levels, and bone acid and alkaline phosphatase activities were compared to those of nonlactating rats fed the same diets. Bone, plasma, and urinary cAMP levels were also studied. Dietary calcium deficiency and/or lactation caused significant loss of bone mass from experimental animals. Urinary cAMP levels reflecting increased parathyroid activity were elevated by the stresses of lactation and calcium deficiency over those of control animals. Plasma and bone levels of cAMP were not different. Bone alkaline and acid phosphatase activities were affected only by the most extreme stress. The results demonstrated that the calcium-deficient lactating rat is an excellent model for bone resorption studies.
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PMID:Metabolic aspects of bone resorption in calcium-deficient lactating rats. 625 31

In the four-week study the antirachitic action of vitamin D2 in different does (5000, 7500, 10 000 I. U. per kg food) and of vitamin D3 in a dose of 500 I. U. per kg food was investigated in chicks. The vitamin efficiency was measured with respect to the following seven parameters: weight gain, serum content of Ca and P, serum activity of alkaline phosphatase, bone ash content, content of Ca-binding protein in the duodenal mucosa, and weight of parathyroid glands. In regard to these parameters, vitamin D2 in a dose of 7500 I. U./kg and vitamin D3 in a dose of 500 I.U./kg produced a similar effect. Thus, the antirachitic effect of vitamin D3 was 15 times higher than that of vitamin D2. In the three-day study of the effect of vitamins D2 and D3 on the synthesis of Ca-binding protein it was found that they exerted a similar effect when the dose of vitamin D2 was 14.5 times higher than that of vitamin D3.
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PMID:[Comparative antirachitic activity of vitamins D2 and D3 in the body of chicks]. 627 66

Tibias of 6-day-old white Leghorn chick embryos treated with beta-aminopropionitrile (beta-APN; 0.1 mg/egg/day) for 4 days and injected with 3H-proline or 3H-tetracycline on the 11th day were analyzed for incorporation of 3H-proline and 3H-tetracycline. The incorporation of 3H-proline was comparable in the controls and beta-APN-treated embryos. However, the incorporation of 3H-tetracycline was significantly lower in beta-APN-treated embryos. The bone ash contents were also lower in the latter group. Alkaline phosphatase and Ca+2-ATPase were found to be significantly lower in beta-APN-treated embryonic bones. There was, however, no difference in the activity of Na+, K+-ATPase. The histochemical examination showed the alkaline phosphatase to be present on osteoblasts and matrix vesicle plasma membranes at the periosteal surface. The chick embryonic liver tissue showed no significant differences in the activities of any of the above enzymes. The results suggest that beta-APN-induced inhibition of the bone mineralization may be due to the bone-specific inhibition of alkaline phosphatase and Ca+2-ATPase.
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PMID:Investigations of alkaline phosphatase Ca+2-ATPase and Na+, K+-ATPase during beta-APN-induced initial bone mineralization inhibition. 628 59

Two experiments were conducted on dietary predisposition to rickets in poults. The first experiment compared fat type (corn oil or tallow), level of added fat (3.5 or 7%), vitamin D3 (900 or 2,400 IU/kg feed), and total calcium (.6, 1.2, or 3%) inclusion in the diet. Poults fed diets supplemented with corn oil had higher percentage tibia ash than poults fed tallow-supplemented diets. Vitamin D3 included at 2,400 IU/kg feed increased body weights significantly by 2 and 4 weeks of age and lowered plasma alkaline phosphatase (AP) at 2 and 4 weeks compared with diets containing 900 IU/kg feed. Tibia ash was significantly greater with the higher vitamin D3 supplementation at 2 weeks. At 2 weeks of age both low (.6%) and high (3%) levels of dietary calcium increased plasma AP, decreased tibia ash, and decreased body weight compared with diets containing 1.2% calcium. By 4 weeks of age, diets containing 1.2 and 3% calcium had no significant effects on body weight and plasma AP; however, tibia ash was significantly greater with these levels than with the .6% calcium diets. The second experiment compared level of dietary tallow inclusion (2.5 or 7%) and supplementary vitamin A (4,000, 16,000, or 44,000 IU/kg feed). The high tallow diets decreased tibia ash at 3 weeks, and the maximum supplementation of vitamin A significantly depressed body weight. Clinical rickets were first noted at 18 days of age. By 26 days of age the higher level of dietary fat and the highest level of vitamin A caused a significant increase in severity of rickets. The results suggested that rickets can be induced by high dietary levels of tallow and vitamin A.
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PMID:Dietary level of fat, calcium, and vitamins A and D3 as contributory factors to rickets in poults. 631 10

The effects of dietary phosphorus and sulphaguanidine levels, and sex differences on: (a) phytate digestibility, (b) calcium and P utilization, (c) the activities of alkaline phosphatase (EC 3.1.3.1), alkaline phytase (EC 3.1.3.8) and acid phosphatase (EC 3.1.3.2) in the intestinal mucosa of male and female rats were investigated. There was a linear increase in femur ash, Ca and P contents and the maximum force withstood by the fresh femurs as dietary P level was increased from 1.5 to 3.0 to 4.5 g/kg diet. The apparent digestibilities of Ca, P and phytate-P decreased as the level of P in the diet increased. Rats given the diets with 1.5 or 3.0 g P/kg were hypercalciuric and hypophosphaturic compared with rats receiving 4.5 g P/kg diet. The level of Ca retained was similar for all treatments. The level of P retained increased as the dietary P level increased. This suggests that P deprivation was a result of inadequate amounts of P retained and not due to the absorption of inositol phosphates formed during the enzymic hydrolysis of phytate. The addition of sulphaguanidine increased phytate digestibility without changing the activities of acid and alkaline phosphatase or alkaline phytase of the intestinal mucosa. This suggests that these enzymes did not play a role in the increase in phytate digestibility. However, dietary sulphaguanidine enhanced phytate digestibility, suggesting that alterations in the diet which modify either the composition or metabolism of the gastrointestinal microflora may be beneficial in enhancing the in vivo hydrolysis of phytate. Differences between males and females are reported and discussed.
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PMID:Influence of dietary phosphorus and sulphaguanidine levels on P utilization in rats. 632 99

The effects of maternal vitamin D3 carry-over to the poult and dietary vitamin D3 on kidney 25-hydroxyvitamin D3-1-hydroxylase (1-hydroxylase) (EC 1.14.13.13) activity were studied in poults from 6 days prehatching to 46 days of age. Large White female turkeys from day-old were fed diets with either 300, 900, or 2700 IU vitamin D3/kg feed. Progeny from each maternal group were fed diets with either 0, 300, 900, or 2700 IU vitamin D3/kg feed. Low maternal vitamin D3 carry-over increased kidney 1-hydroxylase activity in embryos and poults to at least 5 days of age. Low dietary vitamin D3 increased the enzyme activity over that of poults fed higher levels. Kidney 1-hydroxylase activity peaked at about 8 to 18 days to a level similar in all groups. This peak is coincident with the appearance of rickets often noted in the field. Maternal diet did not affect plasma calcium (Ca) but plasma inorganic phosphorus (Pi) decreased with decreasing maternal vitamin D3 up to 14 days of age. Plasma Ca increased at 14 days with higher dietary vitamin D3, as did plasma Pi from day 8. Plasma alkaline phosphatase increased with age to 18 days and then declined. Tibia ash increased with higher maternal vitamin D3 carry-over to 12 days and with higher dietary vitamin D3 after 12 days of age. Body weight was reduced with low maternal vitamin D3 carry-over until at least 2 weeks of age, after which the effect of progeny diet was highly significant; birds receiving 2700 IU vitamin D3/kg feed were almost twice as large as those receiving none. This study shows the importance of adequate maternal carry-over of vitamin D3 and its possible influence on the development of rickets in starting poults.
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PMID:Influence of maternal vitamin D3 carry-over on kidney 25-hydroxyvitamin D3-1-hydroxylase activity of poults. 632 70

Diabetes mellitus was induced in Lewis rats by streptozotocin, and these animals and control rats fed ad lib were studied after 7 weeks. At the time of sacrifice, nondecalcified histological sections of bone were prepared and subsequently quantitated by micromorphometric techniques. In addition, tibial alkaline phosphatase and mineral ash content were determined. The bones obtained from the diabetic animals are characterized by significant decrements in the quantities of osteoid and osteoclasts and by failure to acquire a tetracycline label. These histological features are attended by reduced quantities of urinary hydroxyproline and tibial alkaline phosphatase. As compared with control animals fed ad lib, diabetic rats are hyperphosphatemic and markedly hypercalciuric. Circulating alkaline phosphatase is also elevated and associated with a parallel increase in intestinal content of this enzyme. Although serum corticosterone levels are increased, diabetes is associated with decrements in both circulating immunoreactive parathyroid hormone and 1,25(OH)2D. We conclude that prolonged streptozotocin-induced diabetes mellitus in the rat results in reduced bone turnover. The relative roles that functional caloric deprivation, low circulating levels of 1,25(OH)2D, hypercalciuria, hypercortisolemia, and decreased blood parathyroid hormone levels play in the genesis of these skeletal abnormalities remain to be determined.
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PMID:The effect of streptozotocin-induced chronic diabetes mellitus on bone and mineral homeostasis in the rat. 645 Feb 54


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