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1.
Summary The purpose of this study was to evaluate whether the 1,25(OH) 2D 3-induced increased bone mineralization in the mouse occurs in response to stimulation of bone resorption. In order to inhibit
bone resorption, 35-day-old mice were given 16 μmol/kg/day of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (AHPrBP) for
10 days, the first injection occurring 3 days prior to the continuous infusion of 0.06, 0.13, or 0.20 μg/kg/day of 1,25(OH) 2D 3 for 7 days. Two groups of mice were treated with AHPrBP or 1,25(OH) 2D 3 alone. The skeletal changes were assessed by histomorphometric study of caudal vertebrae after double 3H-proline and double tetracycline labelings for evaluation of the matrix apposition rate (MaAR) and mineral apposition rate
(MiAR), respectively. Treatment with AHPrBP alone or combined to 1,25(OH) 2D 3 decreased the number of acid phosphatase-stained osteoclasts and reduced the endosteal MaAR and MiAR and the amount of osteoid.
When given alone, 1,25(OH) 2D 3 increased serum calcium above normal, enhanced the number of histochemically active osteoclasts, and stimulated the endosteal
MiAR. Pretreatment with AHPrBP blocked both the increase in serum calcium and the stimulation of the MiAR induced by 1,25(OH) 2D 3 infusion though serum 1,25(OH) 2D 3 levels rose according to the dose given. The results show that 1) the serum calcium and the bone resorbing responses to 1,25(OH) 2D 3 infusion are prevented by pretreatment with AHPrBP, and 2) the stimulatory effect of 1,25(OH) 2D 3 on the mineralization rate is blocked when bone resorption is inhibited. The data indicate that 1,25(OH) 2D 3 promotes bone mineralization in the mouse mainly in response to stimulation of bone resorption. 相似文献
2.
To determine the effect of consecutive oral administration of 1αOHD3 or 1,25(OH)2D3 on the metabolism of 1,25(OH)2D3, seven-month-old female rats were given 1αOHD3 (0.4 µg/kg/day) or 1,25(OH)2D3 (0.2 µg/kg/day) for 14 days. After the oral administration of 2 μCi of3H-1αOHD3 or3H-1,25(OH)2D3, the rats were sacrificed at 2,6 or 24 h, and the distribution of these tracers and their metabolites in the serum, intestines, liver, kidneys and bone were studied. The consecutive treatment with 1,25(OH)2D3 or 1αOHD3 did not basically alter the elution patterns of3H labeled metabolites on HPLC. The tissue levels of3H-1,25(OH)2D3, administered or converted from3H-1αOHD3, were lower in the treated rats than those in the controls at 24 h, indicating the accelerated disappearance of 3H-1,25 (OH)2D3 following the treatment with 1αOHD3 or 1,25(OH)2D3. The degree of acceleration, however, was less following the treatment with 1αOHD3 than that after treatment with 1,25(OH)2D3. The degree ofacceleration, however, was less following the treatment with 1αOHD3 than that after treatment with 1,25(OH)2D3. This finding might indicate that, when 1αOHD3 or 1,25(OH)2D3 is consecutively administered, the 1,25(OH)2D3 converted from 1αOHD3 by the liver remains longer in the tissues including bone than 1,25(OH)2D3 absorbed directly from the intestine. 相似文献
3.
Cells have been cultured from human bone that possess several characteristics of osteoblasts, including the capacity to produce osteocalcin (bone Gla protein). In these cultures the production of osteocalcin is dependent on 1,25(OH) 2D 3 but is not affected by 24,25(OH) 2D 3 either alone or in combination with 1,25(OH) 2D 3. Two glucocorticoids, prednisolone and deflazacort, reverse the stimulation of osteocalcin synthesis by 1,25(OH) 2D 3 in a dose-dependent manner (10 −9 − 10 −6M. Parathyroid hormone also inhibits osteocalcin production in a dose-dependent fashion (0.2–5 IU/ml). These results demonstrate that human bone cell cultures may be of considerable value in investigating the hormonal and pharmacologic regulation of the production of osteocalcin and other bone proteins in vitro. 相似文献
4.
Summary Vitamin D deficiency leads to disturbed calcification of growth cartilage and enlargement of growth plate, illustrating that
chondrocytes are a target for vitamin D. This observation prompted an investigation of 1,25(OH) 2D 3 receptor expression and action of vitamin D metabolites on chondrocyte proliferation. In primary cultures of tibial growth
cartilage of male SD rats (80 g), specific binding of [ 3H]-1,25(OH) 2D 3 is noted in both the logarithmic growth phase and at confluence (N max 12780 molecules/cell versus 4368 molecules/cell). Scatchard analysis revealed the presence of a single class of noninteracting
binding sites. K D was 10 −11 M irrespective of growth phase. The binding macromolecule had a sedimentation coefficient of 3.5 S. Interaction with DNA
was demonstrated by DNA cellulose affinity chromatography. In immunohistology, growth cartilage cells (rabbit tibia) expressed
nuclear 1,25(OH) 2D 3 receptors most prominently in the proliferative and hypertrophic zone. This corresponds to binding data which showed highest
N max in the proliferating cartilage. 1,25(OH) 2D 3 in the presence of delipidated fetal calf serum (FCS) had a biphasic effect on cell proliferation and density, i.e., stimulation
at 10 −12 M and dose-dependent inhibition at 10 −10 M and below. Inhibition was specific and not seen with 24,25(OH) 2D 3 or dexamethasone. Growth phase-dependent 1,25(OH) 2D 3 receptor expression and effects of 1,25(OH) 2D 3 on chondrocyte proliferation point to a role of vitamin D in the homeostasis of growth cartilage. 相似文献
5.
Summary Calvarial bones from hypophosphatemic (Hyp) mice and normal littermates were cultured in a chemically defined medium to determine:
(a) the effect of medium phosphate (Pi) concentration (1, 2, and 3 mM) on collagen synthesis; (b) the effect of 1,25-dihydroxycholecalciferol
[1,25(OH) 2D 3] (10 −12M–10 −7M) on collagen synthesis; and (c) whether bone responsiveness to 1,25(OH) 2D 3 was affected by changes in medium Pi concentration. Bone collagen synthesis was evaluated by measuring [ 3H]hydroxyproline formation. The distribution of labeled hydroxyproline between bone explant and culture medium (total and
dialyzable fraction) was studied. These experiments confirm that 1,25(OH) 2D 3 inhibits specifically bone collagen synthesis in vitro. We did not detect any effect of medium Pi concentration on basal
collagen synthesis but were able to demonstrate that lowering medium Pi concentration increased the 1,25(OH) 2D 3-induced inhibition of collagen synthesis. Bones from both genotypes responded to 1,25(OH) 2D 3, but modulation of this response by changes in Pi concentration was altered in Hyp bone as, in contrast to normal bone, its
response to 1,25(OH) 2D 3 was unaffected when medium Pi concentration was decreased from 3 to 2 mM. These findings support the hypothesis of an altered
response of bone to 1,25(OH) 2D 3 in the Hyp mouse. 相似文献
6.
Growth plate chondrocytes are affected by 1,25(OH) 2D 3 and androgens, which may critically interact to regulate proliferation and differentiation during the male pubertal growth spurt. We investigated possible interactions of 1,25(OH) 2D 3 and the non-aromatizable androgen dihydrotestosterone (DHT) in primary chondrocyte cultures from young male rats. DHT and 1,25(OH) 2D 3 independently stimulated DNA synthesis and cell proliferation in a dose-dependent manner with maximally effective doses of [10 -8 M] and [10 -12 M], respectively. Both DHT and 1,25(OH) 2D 3 stimulated the expression and release of IGF-I, and the proliferative effects of each hormone were prevented by an IGF-I antibody. DHT and 1,25(OH) 2D 3 increased messenger RNAs (mRNAs) of their cognate receptors and of IGF-I receptor mRNA (IGF-I-R). 1,25(OH) 2D 3 also stimulated mRNA of the androgen receptor (AR), whereas DHT did not affect mRNA of the vitamin-D receptor (VDR). Coincubation with both steroid hormones did not stimulate receptor mRNAs more than either hormone alone. The proliferative effects of DHT and 1,25(OH) 2D 3 were completely inhibited by simultaneous incubation with both hormones, despite potentiation of IGF-I synthesis. In contrast, both hormones synergistically stimulated cell differentiation as judged by alkaline phosphatase activity, collagen X mRNA, and matrix calcification in long-term experiments. We conclude that DHT and 1,25(OH) 2D 3 interact with respect to chondrocyte proliferation and cell differentiation. The proliferative effects of both hormones are mediated by local IGF-I synthesis. Simultaneous coincubation with both hormones blunts the proliferative effect exerted by either hormone alone, in favor of a more marked stimulation of cell differentiation. 相似文献
7.
Summary The effects of epidermal growth factor (EGF) on basal 1,25-dihydroxyvitamin D 3 (1,25-(OH) 2D 3) receptor level and on parathyroid hormone (PTH)-induced 1,25-(OH) 2D 3 (OH) 2D 3 receptor up-regulation were studied in the phenotypically osteoblastic cell line UMR 106. EGF in concentrations exceeding
0.1 ng/ml reduced the number of 1,25(OH) 2D 3 binding sites without changing the binding affinity. Maximal reduction was 30% at about 1 ng/ml. This reduction was independent
of a change in cAMP content. EGF dose-dependently attenuated both PTH-induced 1,25(OH) 2D 3 receptor up-regulation and PTH-stimulated cAMP production without and effect on the ED 50 of the PTH effects. For both PTH responses the IC 50 and the maximal effective dose were similar, 0.1 ng/ml an 1 ng/ml EGF, respectively. Reduction was first seen at 0.01 ng/ml
EGF. At this concentration. EGF reduced PTH-stimulated 1,25-(OH) 2D 3 receptor binding without an inhibition of the cAMP response. Time-course studies with 1 ng/ml EGF revealed that at 2 h preincubation
EGF reduced the heterologous up regulation by PTH, and maximal inhibition was seen after 4 h. In contrast, PTH-stimulated
cAMP production was just significantly inhibited only after 6 h, with 60% inhibition after 24 h preincubation. The effects
of prostaglandin E 2 and forskolin on both 1,25(OH) 2D 3 binding and cAMP production were inhibited in a similar fashion. On the other hand, dibutyryl cAMP- and 3-isobutyl-1-methylxanthinestimulated
1,25(OH) 2D 3 binding were not affected by EGF. Taken together, our results demonstrate that EGF reduces both the basal number of 1,25(OH) 2D 3 binding sites and the heterologous up-regulation of the 1,25(OH) 2D 3 receptor. The current data suggest that EGF reduces heterologous upregulation of the 1,25(OH) 2D 3 receptor independent of as well as dependent on the cAMP messenger system. The EGF effect is not primarily located at the
PTH receptor, at cAMP phosphodiesterase, or at protein kinase A level. 相似文献
8.
Macrophage colony stimulating factor (MCSF) is important for formation of osteoclasts. We investigated the ability of 1,25(OH) 2D 3 to regulate osteoblast production of MCSF. Mouse calvarial osteoblasts were cultured for 2 days ± 1,25(OH) 2D 3. Since 1,25(OH) 2D 3 decreased osteoblast proliferation by 17.6 ± 1% at 10 nM and 11 ± 4% at 1 nM, the effect of growth rate on MCSF secretion
was examined. Limiting cell proliferation by serum did not affect MCSF production. 1,25(OH) 2D 3 (1 nM) increased MCSF production (U/10 5 cells) maximally by 68 ± 33% (n = 3) with an ED 50 for 1,25(OH) 2D 3 of 5 × 10 −11 M. To investigate effects of 1,25(OH) 2D 3 on MCSF gene regulation, RT-PCR primers were designed to identify the mRNA coding for the membrane-bound isoform of MCSF.
Simultaneous RT-PCR of glyceraldehyde-phosphate dehydrogenase (GAP) allowed semiquantitative assessment of MCSF mRNA between
treatment groups expressed as the MCSF/GAP RT-PCR product ratio; both MCSF and GAP (+) primers were labeled with 32P-ATP for phosphorimage quantitation. The membrane-bound MCSF/GAP PCR product ratio was not affected by proliferative rate
when growth was limited by [serum]. The MCSF/GAP RT-PCR product ratio was dose dependently increased by 1,25(OH) 2D 3, maximally at 1 nM at 2.2 ± 0.2 = fold (n = 10). 1,25 (OH) 2D 3 also increased the expression of an RT-PCR MCSF/GAP product ratio which represented the secreted isoform of MCSF. The ability
of 1,25(OH) 2D 3 to pretranslationally regulate expression of membrane-bound osteoblast MCSF may be important in osteoblast:osteoclast interactions.
Received: 12 August 1995 / Accepted: 25 March 1996 相似文献
9.
Summary We investigated the effect of short-term, 1,25-dihydroxyvitamin D 3 therapy (4 μg/day for 4 days) on calcium metabolism in 27 postmenopausal women (11 cases with osteoporosis and 16 cases with
osteoarthritis). Bone mass at the axial and appendicular skeleton was higher in osteoarthritis than in osteoporosis. Initial
values of calcium metabolism were similar. Osteoporotic and osteoarthritic patients responded with a similar significant increase
in serum osteocalcin (+61% and +54%, respectively), fasting urinary calcium excretion (+178% and +124%, respectively) and
24 hour calcium excretion (+148% and +142%, respectively). Parathyroid hormone (PTH) levels decreased significantly in both
groups (−30% and −18%, respectively). Osteoclastic bone resorption, evaluated by urinary hydroxyproline excretion, was not
stimulated in either group. We conclude that in osteoporosis and also in osteoarthritis (1) 1,25-dihydroxyvitamin D 3 (1,25(OH) 2D 3) stimulation of osteoblast function is similar in production of osteocalcin; (2) the vitamin D target tissues react adequately
to 1,25(OH) 2D 3 stimulation; (3) short-term high dose of 1,25(OH) 2D 3 does not stimulate bone resorption; and (4) the differences in bone mass between osteoarthritis and osteoporosis are not
related to an alteration of the responsiveness to stimulation by 1,25 (OH) 2D 3. 相似文献
10.
Summary Vitamin D 3 metabolites have been shown to affect proliferation, differentiation, and maturation of cartilage cells. Previous studies
have shown that growth zone chondrocytes respond primarily to 1,25(OH) 2D 3 whereas resting zone chondrocytes respond primarily to 24,25(OH) 2D 3. To examine the role of calcium in the mechanism of hormone action, this study examined the effects of the Ca ionophore A23187,
1,25(OH) 2D 3, and 24,25(OH) 2D 3 on Ca influx and efflux in growth zone chondrocytes and resting zone chondrocytes derived from the costochondral junction
of 125 g rats. Influex was measured as incorporation of 45Ca. Efflux was measured as release of 45Ca from prelabeled cultures into fresh media. The pattern of 45Ca influx in unstimulated (control) cells over the incubation period was different in the two chondrocyte populations, whereas
the pattern of efflux was comparable. A23187 induced a rapid influx of 45Ca in both types of chondrocytes which peaked by 3 minutes and was over by 6 minutes. Influx was greatest in the growth zone
chondrocytes. Addition of 10 −8–10 −9 M 1,25(OH) 2D 3 to growth zone chondrocyte cultures results in a dose-dependent increase in 45Ca influx after 15 minutes. Efflux was stimulated by these concentrations of hormone throughout the incubation period. Addition
of 10 −6–10 −7 M 24,25(OH) 2D 3 to resting zone chondrocytes resulted in an inhibition in ion efflux between 1 and 6 minutes, with no effect on influx during
this period. Efflux returned to control values between 6 and 15 minutes. 45Ca influx was inhibited by these concentrations of hormone from 15 to 30 minutes. These studies demonstrate that changes in
Ca influx and efflux are metabolite specific and may be a mechanism by which vitamin D metabolites directly regulated chondrocytes
in culture. 相似文献
11.
Summary Mammalian cells increase net expression of 1,25(OH) 2D 3 receptors after exposure to physiological concentrations of 1,25(OH) 2D 3
in vitro. we examined specific binding of 1,25(OH) 2D 3 by human monocytes before and after daily administration of 1.5–2 ug 1,25(OH) 2D 3 p.o. for 3 days in 5 healthy normal D-replete probands. Median specific binding (N max) at baseline was 793 molecules/cell and 2052 or 2828 at 24h and 72h of 1,25(OH) 2D 3 treatment respectively. The results suggest (a) up-regulation of 1,25(OH) 2D 3 receptors occurs in man and (b) monocyte preparations can be used to assess receptor regulation in vivo. 相似文献
12.
Summary We have used cultured osteoblastlike rat osteogenic sarcoma cells (ROS 17/2) which have receptors for 1,25(OH) 2D 3 and for glucocorticoids, and have examined the modulation of the 1,25(OH) 2D 3 receptor by the potent glucocorticoid triamcinolone acetonide. We report that triamcinolone acetonide caused an increase
of the 1,25(OH) 2D 3 receptor concentration in these cells but it did not affect the affinity of the receptor to 1,25(OH) 2D 3; this phenomenon occurred in a dosedependent fashion for triamcinolone (10 −9 to 10 −7 M) with a maximum increase of 1,25(OH) 2D 3 receptor concentration of ⋍twofold. During the culture period, the 1,25(OH) 2D 3 receptor concentration was altered both in untreated as well as in triamcinolone-treated cells, being highest at the early
logarithmic phase and diminished progressively as cells approached confluence. However, throughout the culture period, the
1,25(OH) 2D 3 receptor concentration was higher in the triamcinolone-treated cells. 相似文献
13.
The secretion of phosphorylated matrix proteins is high in osteoblasts. Phosphorylation of these proteins may be catalyzed
by casein kinases (CK), and CK may play an important role in the site of bone mineralization. In this study, we examined the
effects of 1,25(OH) 2D 3 on CK activities in MC3T3-E1 osteoblast-like cells. Different concentrations (ranging from 10 −7 to 10 −11M) of 1,25(OH) 2D 3 were included in a culture medium. After incubation for various lengths of time, MC3T3-E1 cells were homogenized and segregated
into cytosolic (c) and microsomal (m) fractions. To measure CK activity, each fraction was used as an enzyme source to phosphorylate
casein. MC3T3-E1 cells showed the highest cCK activity after incubation for 21 days, and showed the highest mCK activity after
incubation for 14 days. 1,25(OH) 2D 3 inhibited mCK activity at the early stage of culture, but inhibited cCK activity at the late stage of culture. In contrast,
1,25(OH) 2D 3 had a slight stimulatory effect on CK activity in the culture medium of MC3T3-E1 cells. Our data suggest that cCK and mCK
may play different roles in the function of osteoblasts, and 1,25(OH) 2D 3 regulates intracellular and extracellular casein kinase activities related to the function of osteoblasts.
Received: 26 June 1997 / Accepted: 23 March 1998 相似文献
14.
Summary 1,25(OH) 2D 3, 25OHD 3, and intact parathyroid hormone, as well as various parameters of calcium-phosphorus metabolism were measured in 38 patients
with Graves' disease (GD) and in 24 patients with toxic nodular goiter (TNG). Plasma 1,25(OH) 2D 3 levels were lower in GD patients (82 ±29 pmol/liter) than in those with TNG (155±32 pmol/liter) ( P<0.0005). The mean value of 1,25(OH) 2D 3 in 45 controls was intermediate between the two groups of patients (140±41) and the difference was statistically significant.
GD patients before and after treatment had higher alkaline phosphatase ( P<0.05), lower intact parathyroid hormone (PTH) ( P<0.05), and lower 1,25(OH) 2D 3 levels ( P<0.0005 in the hyperthyroid and P<0.01 in the euthyroid state) than TNG patients. We conclude that increased skeletal calcium resorption is due to elevated
levels of T 3 causing suppression of 1,25(OH) 2D 3 production and of PTH levels in both groups of patients albeit of different degrees. Furthermore, we postulate that the profound
suppression of 1,25(OH) 2D 3 in GD is secondary to an immune-mediated phenomenon. 相似文献
15.
Summary Rachitic rats, maintained on diets with low or normal P contents, were given daily intraperitoneal doses of 1,25(OH) 2D 3 or 25OHD 3 at levels of 100 or 200 ng. Plasma chemistry was measured and the ash content and histological appearance of the bones investigated.
Using labeled material it was shown that the dosing levels of 1,25(OH) 2D 3 employed ensured a higher than normal plasma concentration of that metabolite over the period between doses. 1,25(OH) 2D 3 was not as effective as 25OHD 3 in raising bone ash or reducing the amount of osteoid. The difference between the effects of the metabolites was evident
at both dietary P levels, but more marked at the higher P level. In contrast, the metabolites reduced the width of the epiphyseal
plate to an approximately similar degree, and this is possibly the reason why there are discrepancies between previous reports
of the effectiveness of 1,25(OH) 2D 3 compared with 25OHD 3 or vitamin D 3. Dosing with 1,25(OH) 2D 3 failed to maintain a constant plasma P i value over the period between doses in animals fed the low P diet. 相似文献
16.
Summary Eighty-eight adult male Sprague-Dawley rats were given a diet with either (a) 0.5% Ca and 0.6% P or (b) 0.01% Ca and 0.6%
P. Osteopenia was created by adding prednisolone to the diet. The prophylactic effect of oral 1,25(OH) 2D 3 on the osteopenia was studied. It was found that prednisolone osteopenia in the rat was associated with defective Ca absorption.
By giving an oral dose of 1,25(OH) 2D 3, it was possible to maintain normal Ca absorption during prednisolone treatment and to prevent the bone loss. No significant
hypercalcemia or any kidney calcifications were seen. These results are in contrast to earlier findings, in which subcutaneous
administration of 1,25(OH) 2D 3 failed to prevent prednisolone osteopenia because of its tendency to increase bone resorption. 相似文献
17.
Summary We have previously shown that cyclosporin A (CsA) produces high bone remodeling with resorption exceeding formation and loss
of bone volume in the rat. This may have important clinical implications where CsA is widely used in organ transplantation.
1,25 dihydroxyvitamin D 3 (1,25(OH) 2D 3) is a bone mineralizing hormone which also has immune modifying properties. Consequently, we studied the effect of combined
CsA and 1,25(OH) 2D 3 administration over 28 days in four groups of rats. Group A received vehicle (n=10), group B CsA (15 mg/kg) (n=10) alone,
group C 1,25(OH) 2D 3 plus CsA (n=15), and group D 1,25(OH) 2D 3 alone (20 ng/100 g) (n=15). Rats were bled periodically at day 0, 7, 14, and 28 and Ca, parathyroid hormone (PTH), 1,25(OH) 2D, osteocalcin (bone Gla-protein, BGP), BUN, and creatinine were measured. Rats were sacrificed on day 28 and bones were examined
histomorphometrically. Compared to controls, CsA resulted in significant elevation of BGP and a transient increase in 1,25(OH) 2D with excess bone remodeling and loss of bone volume. 1,25(OH) 2D 3 administration produced hypercalcemia, a significant rise in BGP, with suppression of PTH and increased osteoid volume. Combined
therapy prevented the loss of bone volume probably due to increased osteoid tissue and enhanced osteoblast activity. Renal
dysfunction, a side-affect of CsA, was not a factor. In conclusion, 1,25(OH) 2D 3 combined with CsA restores bone volume which is accompanied by increases in serum calcium and BGP. 相似文献
18.
Summary This study presents measurements of serum vitamin D metabolites, calcium and phosphorus as well as measurements of the equilibrium
dissociation constant for duodenal 1,25(OH) 2D 3 receptor in 15-, 18-, 19-, and 20-day chick embryos in comparison to that in 1- and 118-day-old chicks and to vitamin D-deficient
chicks. The present results showed that: (a) serum 1,25(OH) 2D and 24,25(OH) 2D levels rise from 15 and 18 to days 19 and 20 of embryonic development while serum phosphate levels are stable; (b) serum
calcium levels rise at hatching to adult levels; (c) the duodenal 1,25(OH) 2D 3 receptor is detectable in 15-day-old embryo and has a Kd similar to that of 118-day-old vitamin D-replete chicks; and (d)
the activity of 1,25(OH) 2D 3 receptor in chick duodenal cytosol is maximal at hatching. 相似文献
20.
Summary We have reported recently that pharmacologic doses of 1,25 dihydroxyvitamin D 3 (1,25(OH) 2D 3) stimulated bone matrix formation but impaired mineralization. The objective of this study was to determine if parathyroid
hormone (hPTH 1-34) or calcitonin (sCT) would mineralize the osteoid induced by 1,25(OH) 2D 3 in rat long bones. In one experiment, male Sprague-Dawley rats were given daily subcutaneous injections of vehicle: 8 μg
hPTH(1-34); 125 ng 1,25(OH) 2D 3; or both 8 μg hPTH and 125 ng 1,25(OH) 2D 3 per 100 g body weight for 12 days. In a second experiment, rats received daily injections of vehicle: 2 U sCT; 125 ng 1,25(OH) 2D 3; or both 2 U sCT and 125 ng 1,25(OH) 2D 3 per 100 g body weight for 18 days. Calcium (Ca), hydroxyproline (Hyp), and dry weight (DW) of the distal femur and serum
calcium, phosphate, and serum bone Gla protein (BGP) were measured. In rats given both 1,25(OH) 2D 3 and hPTH, total bone DW and Hyp increased ( P<.01) without a corresponding increase in bone Ca so that Ca/Hyp decreased 47% ( P<.01) from control and remained comparable to values for rats treated with 1,25(OH) 2D 3 alone. In rats treated with both 1,25(OH) 2D 3 and sCT, total bone DW and Hyp increased while Ca decreased so that Ca/Hyp decreased 38% from control ( P<.05), and remained comparable to values for rats treated with 1,25(OH) 2D 3 alone. These results indicate that hPTH or sCT, given by intermittent injection to rats for 12 or 18 days respectively, failed
to mineralize the osteoid induced by high doses of 1,25(OH) 2D 3. 相似文献
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