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1.
Human parathyroid hormone (1–34) and salmon calcitonin do not reverse impaired mineralization produced by high doses of 1,25 dihydroxyvitamin D3 总被引:2,自引:0,他引:2
M. Gunness-Hey Dr. J. M. Hock I. Gera J. Fonseca J. Poser J. Bevan L. G. Raisz 《Calcified tissue international》1986,38(4):234-238
Summary We have reported recently that pharmacologic doses of 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) 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)2D3 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)2D3; or both 8 μg hPTH and 125 ng 1,25(OH)2D3 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)2D3; or both 2 U sCT and 125 ng 1,25(OH)2D3 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)2D3 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)2D3 alone. In rats treated with both 1,25(OH)2D3 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)2D3 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)2D3. 相似文献
2.
Socorro Vargas Roger Bouillon Hugo Van Baelen Dr. Lawrence G. Raisz 《Calcified tissue international》1990,47(3):164-168
Summary Vitamin D and its metabolites are tightly bound to the serum vitamin D-binding protein (DBP) and only the free hormone is
considered to be physiologically active. On the other hand, DBP could interact with cell membranes and even favor its intracellular
entry. The present study was undertaken to examine the effects of DBP on bone resorption stimulated by 1,25-dihydroxyvitamin
D3 [1,25(OH)2D3]. Forelimb bones from 19-day-old fetal rats were cultured for 5 days in the presence of purified human or rat serum albumin
(hSAP or rSAP) and 1,25(OH)2D3, with or without human or rat DBP (hDBP or rDBP). Bone resorption was assessed by measuring the release of previously incorporated45Ca. We found that the resorptive response to 1,25(OH)2D3 was minimally altered by hDBP (5 μM). The minimal effects of hDBP on 1,25(OH)2D3 activity on rat bones might be explained by a 6-fold lower affinity of hDBP (1.1×107 M−1) than rDBP (5.9×107 M−1) for 1,25(OH)2D3 or by species differences in cellular recognition of DBP. In a homologous rat system, however, rDBP at low (0.5 μM) or physiological
(5 μM) concentration significantly decreased 1,25(OH)2D3-induced bone resorption. These data therefore support the hypothesis that free rather than DBP-bound 1,25(OH)2D3 is physiologically important. 相似文献
3.
Sol Epstein M.D. Mark Schlosberg Michael Fallon Steven Thomas Colin Movsowitz Firhaad Ismail 《Calcified tissue international》1990,47(3):152-157
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 D3 (1,25(OH)2D3) is a bone mineralizing hormone which also has immune modifying properties. Consequently, we studied the effect of combined
CsA and 1,25(OH)2D3 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)2D3 plus CsA (n=15), and group D 1,25(OH)2D3 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)2D3 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)2D3 combined with CsA restores bone volume which is accompanied by increases in serum calcium and BGP. 相似文献
4.
Glenda L. Wong 《Calcified tissue international》1983,35(1):426-431
Summary The actions of PTH in OB bone cells appear to involve both calcium and cAMP. At present little information exists regarding
the relationship, if any, between these two putative second messengers of hormone action in bone cells. In this report the
molecular role of calcium in the actions of PTH and 1,25(OH)2D3 has been compared, since like PTH, the steroid 1,25(OH)2D3 is a potent bone resorbing hormone that exerts inhibition of citrate decarboxylation in OB cells, but unlike PTH does not
activate adenylate cyclase. It was found that 1,25(OH)2D3 could initiate near maximum inhibition of citrate decarboxylation at extracellular calcium levels as low as 0.05 mM, whereas
PTH effects began to be apparent only at 0.1 mM calcium, and maximum inhibition of citrate decarboxylation by PTH required
0.5 mM Ca. In addition, PTH-induced decrease in citrate decarboxylation was inhibited by low doses of TFP, an inhibitor of
calmodulin and calcium-dependent, phospholipid-sensitive protein kinases, in contrast to 1,25(OH)2D3, whose effects were not reduced by this agent. These results suggest that: (a) the actions of 1,25(OH)2D3 may not be directly dependent on calcium influx; (b) in OB cell response to PTH a relationship probably exists between cAMP
and calcium; and (c) this relationship may involve calmodulin, or calcium-dependent protein kinases that can be inhibited
by TFP. 相似文献
5.
Yuk-Luen Chan Charles McKay Evelyn Dye Eduardo Slatopolsky 《Calcified tissue international》1986,38(1):27-32
Summary Controversy exists over a direct effect of 1,25(OH)2D3 on PTH secretion. To investigate the possibility that the suppressive effect of 1,25(OH)2D3 on PTH secretion may be demonstrable in 1,25(OH)2D3-depleted tissue and/or after prolonged periods of exposure to 1,25(OH)2D3, primary monolayer cultures of bovine parathyroid cells were established in 1∶1 DMEM/Ham's F-12 media supplemented with 2%
calf serum but not 1,25(OH)2D3. Ionized calcium was maintained at 1.0 mM. Experiments were performed on 4-day-old culture cells. PTH concentration was measured
using both a mid-region/carboxyl and an amino-terminal PTH antisera. 1,25(OH)2D3 at a concentration of 0.1 ng/ml suppressed PTH secretion by 32±7% after 48 hours. High calcium concentration (2.0 mM) suppressed
PTH secretion by 37±10% and this effect was not additive over that of 1,25(OH)2D3. PTH secretion rate recovered fully 48 hours after normalization of the external calcium concentration but not after the
removal of 1,25(OH)2D3. It is concluded that 1,25(OH)2D3 directly suppresses PTH secretion by monolayer culture of bovine parathyroid cells. 相似文献
6.
I. Holt M. W. J. Davie I. P. Braidman M. J. Marshall 《Calcified tissue international》1994,55(2):114-119
The cytokine interleukin-6 (IL-6) was produced by neonatal mouse parietal bones during a 6- or 48-hour culture period in response to prostaglandin E2 (PGE2) and bovine parathyroid hormone (PTH) 1-34 fragment but not 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. At the same time there was an increase in tartrate-resistant, acid phosphatasepositive osteoclasts (TRAP+OC) with all three osteotropic effectors over 6 hours, and an increase in 45Ca release over 48 hours. TRAP+OC numbers on PGE2-stimulated bones were positively correlated with IL-6 concentration. Our aim was to determine if IL-6 mediated this response. Recombinant human IL-6 (rhIL-6) was added to parietal bones in culture at concentrations within the range that PGE2 or PTH would produce during incubation. However, over 6 or 48 hours, rhIL-6 did not stimulate TRAP+OC to increase in number nor did it cause an increase in calcium release over 48 hours. Adding an antibody against mouse IL-6 to bone cultures stimulated with PTH or PGE2 neutralized the resulting IL-6 bioactivity by up to 92% but did not inhibit TRAP+OC formation. We conclude that although IL-6 is produced in response to two important stimulators of bone resorption, it does not mediate osteoclast differentiation or bone resorption in this model.Part of this work has been presented as an abstract to the Bone and Tooth Society Winter Meeting on 6/12/93 at The Royal College of Obstetricians and Gynaecologists, London. 相似文献
7.
Summary The present investigation was undertaken to study the role of carbonic anhydrase in 1,25 dihydroxyvitamin D3-induced bone resorption. Calvaria were removed from 5- to 6-day-old mice and cultured for periods up to 96 h in Dulbecco's
Modified Eagle Medium (high glucose, 4,500 mg/dl) supplemented with antibiotics and either heat-inactivated horse and fetal
calf sera or bovine serum albumin. The experimental cultures contained 1×10−8 M 1,25 dihydroxyvitamin D3 (1,25(OH)2D3). All cultures were incubated at 37°C in 5% CO(in2)/95% air. Bone resorption was assessed by release of stable calcium into
the medium. Bone enzymes (acid and alkaline phosphatases and carbonic anhydrase) were determined following homogenization
in 0.25 M sucrose. The effects of 1,25(OH)2D3 were studied in the presence and absence of the carbonic anhydrase inhibitor acetazolamide and its analogue (CL 13,850),
which lacks inhibitory activity. Acetazolamide inhibited 1,25(OH)2D3-induced calcium release in a dose-dependent fashion from 10−5–10−4 M. When added to the cultures at a concentration of 1×10−4 M, acetazolamide completely blocked the 1,25(OH)2D3-induced calcium release, a phenomenon not seen with an equimolar concentration of CL 13,850. The most significant finding
was that 1,25(OH)2D3-induced calcium release was accompanied by a significant increase in the carbonic anhydrase activity of bone at both 48 (treated/control
ratio=2.05) and 96 (treated/control ratio=2.59) hours. Bone alkaline phosphatase activity decreased and acid phosphatase activity
increased in response to 1,25(OH)2D3. These findings support the concept that carbonic anhydrase is involved in bone resorption inducedin vitro by certain calcemic hormones and related compounds. 相似文献
8.
Summary The direct effect of 1,25(OH)2D3 upon osteoclast formation from precursor cells is still unknown. In the present experiments we have tested the effects of
1,25(OH)2D3 on the generation of osteoclastlike cells in cat bone marrow cultures. These cultures contain proliferating nonattached mononuclear
cells and precursor cells that subsequently attach to the culture flask surface and then fuse to form multinucleated osteoclastlike
cells. After 7 days of culture we separated the nonattached precursor cells from the attached cells and studied the effects
of 1,25(OH)2D3 (10−10 M–10−8 M) on multinucleated cell formation in these two cell populations. In cultures derived from the non-attached precursor cells,
7 days of treatment with 1,25(OH)2D3 (10−8 M) resulted in a 180% increase in the number of attached mononuclear cells and a 90% increase in the number of nuclei contained
within multinucleated cells. These effects were dose-dependent. 1,25(OH)2D3 did not have a consistent effect on the number of nonattached precursor cells. In cultures derived from attached cells, 7
days of treatment with 1,25(OH)2D3 (10−8 M) induced a 50% increase in the number of mononuclear attached cells and a 40% increase in the number of nuclei within polykaryons.
The most likely explanation for these results is that 1,25(OH)2D3 promotes the differentiation and subsequent adhesion of nonattached precursor cells, stimulates proliferation of attached
mononuclear precursor cells, and possibly stimulates fusion of these attached precursor cells. 相似文献
9.
J. M. Hock M. Gunness-Hey J. Poser H. Olson N. H. Bell L. G. Raisz 《Calcified tissue international》1986,38(2):79-86
Summary We previously reported that pharmacologic doses of 1,25 dihydroxyvitamin D3 (1,25-(OH)2D3) given for 2–3 days, inhibited osteoblastic collagen synthesis in young rats. In this study, we tested the effects of 5,
25, and 125 ng of 1,25(OH)2D3 injected subcutaneously into 6-week-old rats for 12 or 18 days. In rats given 125 ng, cortical bone of distal half femurs
exhibited decreased calcium (Ca) content but dry weight and hydroxyproline (Hyp) content were no different from control. Trabecular
bone Ca was not different from control but dry weight and Hyp were increased. When cortical and trabecular bone were combined,
there was a decrease in Ca, an increase in Hyp, and a 50% decrease in Ca:Hyp. Fluorescent labels given after 8 days of treatment
were either diffuse or absent in calcified sections from rats given 125 ng, indicating impaired mineralization. The 25 and
125 ng doses produced hypercalcemia with normal serum phosphate. There was a dose-related increase in serum immunoreactive
bone gla protein (BGP) and serum 1,25(OH)2D3 and a decrease in serum 25 (OH)D3. At the 5 ng dose, no adverse effects were seen on body growth. With 25 ng and 125 ng, growth was inhibited. Increased serum
urea nitrogen and histologic evidence of nephrocalcinosis occurred at the 125 ng dose. When 125 ng was given for 12 days and
then withdrawn for 6 days, systemic toxicity decreased and bone Hyp and Ca increased so that Ca:Hyp remained low and comparable
to that of rats treated with 1,25(OH)2D3 continuously We conclude that pharmacologic doses of 1,25(OH)2D3 stimulate trabecular bone matrix formation but produce impairment of mineralization, despite a high Ca×Pi product. 相似文献
10.
Summary Cultured mouse kidney cells grown in serum-free medium were used to assess the metabolism of 25-hydroxyvitamin D3 in the presence of simulated metabolic acidosis. Kidney epithelial cells isolated from 4–6 week old mice were grown to confluence
in a defined serum-free medium at pH 7.4. The confluent monolayers were incubated with tritiated 25-hydroxyvitamin D3 for 6 hours, the samples were extracted, and vitamin D metabolites were separated and quantitated by high pressure liquid
chromatography (HPLC). The pH of the incubation medium was set at 6.9, 7.1, 7.4, or 7.7 by adjusting the bicarbonate concentration,
using chloride as the balancing anion at constant Pco2. When pH was altered at the beginning of the 6 hour assay, production of 1,25-dihydroxyvitamin D3 was the same at each pH. More prolonged pH perturbation for a total of 30 hours likewise had no influence on 1,25-dihydroxyvitamin
D3 production. These results confirm that intact mammalian kidney cells in serum-free culture possess an active 25-hydroxyvitamin
D3-1-hydroxylase and that the activity of the enzyme is unaffected by pH over the range 6.8–7.7. In experiments where acidosis
has been shown to alter 1,25-dihydroxyvitamin D3 production, the mechanism was probably indirect. 相似文献
11.
Summary Vitamin D-deficient, second generation, rachitic rats showed significant decrease in bone Gla protein (BGP) levels in circulation
and in the skeleton. 1,25 dehydroxyvitamin D3 (1,25 (OH)2D3) exhibited the most potent influence on serum BGP levels in a dose-dependent manner. At a dose 25 ng/100 g body weight 1,25
(OH)2D3 showed a cumulative effect, i.e., the longer the treatment, the more circulating BGP was detected 24,25 dehydroxyvitamin
D3 (24,25(OH)2D3) at the same doses did not show similar effect on the serum BGP levels, regardless of the serum calcium levels. Bone BGP
levels assayed at various sites representing endochondral and intramenbranous ossification demonstrated an opposite pattern.
1,25(OH)2D3 administration was not sufficient to restore bone BGP levels to normalcy, whereas in animals treated with 24,25(OH)2D3 bone BGP and calcium levels were significantly higher than control (Vitamin D3-repleted) levels. The present results can be explained by the dual action of 1,25 (OH)2D3 on both synthesis and release of BGP by bone turnover, whereas 24,25 (OH)2D3 stimulates synthesis and accumulation of BGP in bone. These observations imply that caution is required in the interpretation
of clinical data based solely on serum BGP determination. 相似文献
12.
Summary 1,25 Dihydroxyvitamin D3 (1,25(OH)2D3) (2.0 μg) was given intramuscularly to 6 healthy adult males. Twenty-four circadian patterns of blood-ionized calcium (Ca2+), serum phosphate (Pi), and total calcium (CaT) were assessed pre- and posthormone administration. Correlations of mean mineral rhythms with normative models were significant
for each mineral pattern on both study days. Mean Ca2+ and CaT rhythms became weakly correlated after hormone treatment (r=.39). A small but statistically significant increment in the
24 h grand mean Ca2+ concentration was observed on the treatment day compared with the baseline day. However, this increment is less than the
year-to-year variability in the grand mean mineral concentrations derived from the same subjects studied under baseline conditions
previously. These data indicate that acute parenteral administration of near-physiological (2.0 μg) doses of 1,25(OH)2D3 appears to have no major effect on circadian mineral pattern shape or mean mineral concentrations. 相似文献
13.
Summary We measured mineral and acid balances, serum iPTH, urinary cAMP/creatinine, and plasma concentrations of 25OHD and 1,25(OH)2D in 7 healthy adults during control conditions and during increased fixed acid production achieved either by the administration
of NH4Cl (N=3) or by increased dietary protein intake (N=4). When acid production was increased, the subjects were in positive acid balance and negative Ca balance because of increased
urinary Ca excretion. Serum iPTH fell slightly but urinary cAMP and the plasma levels of vitamin D metabolites did not change.
We conclude that the accelerated skeletal and urinary losses of Ca that occur when fixed acid production is increased are
not contributed to nor compensated for by the parathyroid-vitamin D endocrine systems. 相似文献
14.
Anna Teti Gerhard Volleth Aldo Carano Alberta Zambonin Zallone 《Calcified tissue international》1988,42(5):302-308
Summary
3H-thymidine-labeled blood monocytes were cultured with osteoclasts in the presence or absence of parathyroid hormone or 1,25-dihydroxyvitamin
D3 (1,25(OH)2D3) in order to evaluate (1) the percentage of monocytes capable of fusing with osteoclasts, (2) if parathyroid hormone or 1,25(OH)2D3 influences the contribution of blood monocytes to osteoclast nuclear turnover. We found that within 24 hours of culture,
about 8% of blood monocytes fuse with osteoclasts regardless of the presence of parathyroid hormone (PTH) or 1,25(OH)2D3. On the other hand, formation of nonosteoclastic giant cells by fusion of monocytes is enhanced by 5×10−9 M 1,25(OH)2D3 but only in the presence of the bone resorptive cells. 相似文献
15.
Summary The effect of ovarian insufficiency on calcium metabolism has been thought to involve an increased bone resorptive effect
of parathyroid hormone and possible impaired synthesis of 1,25-dihydroxyvitamin D3. In the present study a rat model allowing for controlled serum levels of parathyroid hormone and 1,25-dihydroxyvitamin D3 was used. Oophorectomy in this species is associated with increased serum levels of 1,25-dihydroxyvitamin D3 and decreased bone mass. Although thyroparathyroidectomy increased bone mass, an increased sensitivity of bone to parathyroid
hormone in oophorectomized rats was not observed. Thus the development of the osteopenia did not seem to be related to increased
parathyroid hormone sensitivity or to reduced levels of 1,25-dihydroxyvitamin D3. Exogenous 1,25-dihydroxyvitamin D3 increased bone mass in oophorectomized as well as intact rats. Intestinal calcium transport was increased by moderate doses
of 1,25-dihydroxyvitamin D3. Intestinal calcium transport was also reduced by thyroparathyroidectomy and increased by the administration of parathyroid
extract. A tendency for increased accumulation of 1,25-dihydroxyvitamin D3 in blood in oophorectomized rats has been noted. It is suggested that the tendency to hypercalcemia in ovarian-insufficient
females given 1-hydroxylated vitamin D compounds may be related to a diminished metabolism of 1,25-dihydroxyvitamin D3. 相似文献
16.
Summary The effects of 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) administration on serum osteocalcin (Oc) concentrations were determined. 2.0 μg doses of 1,25(OH)2D3 were administered orally and intravenously to four healthy adult males. Blood was sampled hourly for 24 hours on four occasions:
once prior to the two treatment days (i.v. and p.o.), on each of the treatment days, and during a second nontreatment day
2 years later. Mean circadian Oc rythms of the four subjects on each study day were compared with each other and with a previously
derived mathematical representation of the normative Oc rhythm, the circadian Oc rhythm model. We found overall conservation
of the mean Oc pattern across time and 1,25(OH)2D3 treatment. However, 1,25(OH)2D3 administration resulted in a rapid rise (within 6 hours) in Oc concentrations that blunted or eliminated the morning fall
in Oc levels. The increased Oc levels were sustained for the remainder of the 24 hour period though pattern shapes converged
with those of the nontreatment days and the model. We conclude that serum Oc levels are rapidly responsive to near physiological
doses of 1,25(OH)2D3 in healthy adult males and that the effects are maintained for at least 24 hours. 相似文献
17.
Summary The responses of suckling rat pups of different ages to high doses of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) were determined. Four daily oral doses of 1,25(OH)2D3 (2 ng/g body wt) given to 9–13-day-old pups produced severe hypercalcemia 24 h after the last dose (15.52 ± 0.14 mg/dl vs.
10.94 ± 0.15 mg/dl in controls of the same age) and a 9-fold increase in kidney Ca content; the same doses given to 16–20-day-old
pups produced only modest hypercalcemia (12.34 ± 0.22 mg/dl vs. 10.57 ± 0.22 mg/dl in controls of the same age) and a 4-fold
increase in kidney Ca content. There was no change in serum phosphorus (P) at either age. Six-week-old weaned rats, given
the same doses of 1,25(OH)2D3, showed neither hypercalcemia nor kidney calcification and thus were protected against the toxic effects of the treatment.
The difference in responses of the twoages of suckling pups was also observed with lower doses. Removal of the solid food
from the diet of the 16–20-day pups showed that the consumption of solid food, in addition to milk, in this age group was
not the cause of the lower serum Ca response. The changes in both serum and kidney Ca after intraperitoneal (i.p.) injections
of 1,25(OH)2D3 at the same dose in each age group were similar to those observed with oral administration. The time course of the rise in
serum Ca following a single dose of 1,25(OH)2D3, given either orally or i.p., showed that the hypercalcemia was more pronounced and lasted longer in the 9–13-day pups than
in the 16–20-day pups. The results suggest that weaned rats are relatively well protected against hypervitaminosis D and that
younger pups gradually develop such protection during the suckling period. 相似文献
18.
Marcos Rothstein Klaus Olgaard Mario Arbelaez Delmar Finco Saulo Klahr Eduardo Slatopolsky M.D. 《Calcified tissue international》1983,35(1):449-454
Summary The role of 24,25(OH)2D3 on parathyroid gland function remains controversial. The present studies were performedin vitro using (a) dispersed normal bovine parathyroid cells (bPTC) and (b) dispersed canine PTC (cPTC) prepared from glands of normal
dogs, dogs with chronic renal failure (CRF), and dogs with CRF treated with 24,25(OH)2D3, 2.5 μg orally every day for more than 6 months. Bovine parathyroid cells were incubated for up to 180 min at 0.5, 1.0, and
3.0 mM external calcium in the presence or absence of 24,25(OH)2D3 (100 or 1000 nM). Similar experiments were conducted with cells incubated for 24 h in the presence of either the ethanol
vehicle or 24,25(OH)2D3 (1000 nM). Parathyroid hormone secretion, measured in the supernatant by both C-terminal and N-terminal assays, did not show
any differences between control and experimental groups at any time interval. Canine parathyroid cells obtained from uremic
animals showed an average threefold increase in the total amount of PTH secreted, on a per cell basis over 180 min at 0.5
mM Ca2+, when compared with normal controls. However, there was no significant difference in PTH secretion at any level of calcium
concentration between the cells obtained from parathyroid glands of CRF dogs and 24,25(OH)2D3-treated CRF dogs. Acute exposure to 24,25(OH)2D3 (1000 nM)in vitro of the cells obtained from the glands of CRF dogs also had no effect on PTH secretion. We conclude that 24,25(OH)2D3 has no direct effect on PTH secretion from dispersed parathyroid cells of either normal or uremic animals. 相似文献
19.
Norman H. Bell Judith Shary Sheryl Shaw Russell T. Turner 《Calcified tissue international》1985,37(6):588-591
Summary Studies are described in a 53-year-old man with far-advanced pulmonary tuberculosis who developed transient increases in circulating
1,25 dihydroxyvitamin D (1,25(OH)2D) and hypercalcemia while on antituberculous treatment. Serial dilution of an extract of the patient's serum obtained while
he was hypercalcemic displaced [3H]-1,25(OH)2D3 from chick intestinal receptor in a manner identical to authentic 1,25(OH)2D3. Serum 25-hydroxyvitamin D (25OHD) was suppressed during the abnormal elevation of serum 1,25(OH)2D. It is concluded that tuberculosis is another chronic granulomatous disease in which hypercalcemia may result from abnormal
metabolism of vitamin D. 相似文献
20.
Dr. Michael Silbermann Klaus von der Mark Nitza Mirsky Marion van Menxel Dina Lewinson 《Calcified tissue international》1987,41(2):95-104
Summary Thein vivo effects of high doses of 1,25(OH)2D3 were studied in condylar cartilage of suckling mice. Seven-day-old animals were treated with 20 ng of the hormone for 7 consecutive
days. Biochemical assays on collagen content and synthesis were complemented by structural studies using light and electron
microscopy. Indirect immunofluorescent methods were used for the localization of type I and II collagens and for fibronectin.
This study revealed that the protein content of the condyle decreased substantially following the administration of the hormone.
Protein synthesis increased in hormone-treated animals during the first 4 days but was significantly inhibited theeafter.
Collagen synthesis, however, was inhibited instantaneously, followed by a decrease in the percentage of cold hydroxyproline
of the total protein. Hormone-treated condyles showed a marked decrease in the distribution of type I collagen, no apparent
change in the distribution of type II collagen, but an enhanced reactivity for fibronectin especially around hypertrophic
chondrocytes. SDS-gel electrophoresis of collagen chains suggested that the hormone did not induce a significant change in
the ratios of type I and II collagen chains, yet additional peaks became evident in 1,25(OH)2D3-treated specimens. The decrease in collagen synthesis was accompanied by ultrastructural changes in the appearance of the
extracellular collagen bundles. They later appeared as a dense meshwork of collagen fibrils, a feature that was lacking in
control tissues. The changes in collagen fibrillogenesis could be explained by ourin vitro studies indicating a marked depression of35S-sulfate incorporation secondary to treatment with 1,25(OH)2D3. The hormone was also found to suppress the incorporation of3H-thymidine, hence it may be concluded that 1,25(OH)2D3, when used in high concentrations, possesses an inhibitory effect upon both the proliferative activity of the cartilage progenitor
cells as well as upon the metabolic activity of the condylar cells as related to collagen and glycosaminoglycans synthesis. 相似文献