Interaction of 24,25-Dihydroxyvitamin D3 and parathyroid hormone on bone enzymes in vitro

Lieberherr, Michèle; Garabédian, M; Guillozo, H.; Bois, M. Bailly du; Balsan, S

doi:10.1007/bf02441160

Cited by 40 publications

(21 citation statements)

References 13 publications

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“…The latter results are in contrast to those obtained by Lieberherr et al [11] using the isolated calvaria.…”

Section: Discussioncontrasting

confidence: 82%

“…More recently, there has been increased interest in 24R,25(OH)2D3, mainly because it may exhibit biological activities that are qualitatively different from those of 1,25(OH)2D3, and there are speculations that it may have an important physiological function of its own [5,11].…”

mentioning

confidence: 98%

“…There has been only one study dealing with the interaction of 24,25(OH)zDa and parathyroid hormone on 4~Ca release from rat calvaria in vitro [11]. …”

mentioning

confidence: 99%

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Interaction between 24R,25-dihydroxycholecalciferol and 1,25-dihydroxycholecalciferol on45Ca release from bone in vitro

Mahgoub

1981

Calcif Tissue Int

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Interaction among vitamin D3 metabolites on bone receptor sites is not known. Therefore, interaction between the most potent vitamin D3 metabolite, 1,25(OH)2D3, and the most abundant dihydroxymetabolite, 24R,25(OH)2D3, was studied on isolated rat fetal bone by measuring 45Ca release from prelabeled bones. 24R,25(OH)2D3 at concentrations of 10-50 ng/ml caused marked inhibition of the bone-resorbing activity of 1,25(OH)2D3 at concentrations of 10-50 pg/ml. 24S,25(OH)2 (unnatural enantiometer), on the other hand, at a concentration of 100 ng/ml did not inhibit the bone-resorbing effect of 10 pg/ml 1,25(OH)2D3. 24R,25(OH)2D3 at a concentration of 20 ng/ml did not inhibit the 45Ca-releasing effect of a submaximal concentration of PTH (500 ng/ml). Therefore, the inhibitory effect of 24R,25(OH)2D3 on the bone response to 1,25(OH)2D3 appeared to be specific and probably due to a competitive inhibitory effect. In addition, the inhibitory effect of 24R,25(OH)2D3 was weak, since it could be partially overcome by increasing the concentration of 1,25(OH)2D3.

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“…The latter results are in contrast to those obtained by Lieberherr et al [11] using the isolated calvaria.…”

Section: Discussioncontrasting

confidence: 82%

mentioning

confidence: 98%

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Interaction between 24R,25-dihydroxycholecalciferol and 1,25-dihydroxycholecalciferol on45Ca release from bone in vitro

Mahgoub

1981

Calcif Tissue Int

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“…Recent (11)(12)(13). In vitro studies from our laboratory produced evidence that 24,25-(OH)2D3 at very low concentrations stimulates the synthesis of specific proteoglycans by chondrocytes (14) and suppresses the action of agents known to stimulate bone resorption, such as parathyroid hormone, vitamin D, and heparin (15,16). A few clinical trials have led to the assumption that 24,25-(OH)2D3 may be the metabolite that principally promotes bone formation (17).…”

Section: Introductionmentioning

confidence: 99%

“…The biochemical and histological changes observed were partly parathyroid hormone and calcitonin independent, as they also occurred in parathyroidectomized hypocalcemic rats. Pretreatment with 650 pmol of 24,25-dihydroxycholecalciferol 16 h before nephrectomy prevented bone calcium mobilization and diminished the rise in serum total calcium and citrate both in parathyroidintact and in parathyroidectomized animals. In parathyroid-intact rats, serum immunoreactive parathyroid hormone and calcitonin remained normal in spite of the fall in serum-ionized calcium, and the number of osteoclasts did not increase.…”

mentioning

confidence: 99%

Suppressive Effects of 24,25-Dihydroxycholecalciferol on Bone Resorption Induced by Acute Bilateral Nephrectomy in Rats

Pavlovitch¹,

Cournot-Witmer²,

Bourdeau³

et al. 1981

J. Clin. Invest.

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A B S T R A C T The possible suppressive effects of 24,25-dihydroxycholecalciferol on secondary hyperparathyroidism and increased bone resorption were investigated in adult rats raised on a diet normal in calcium, phosphorus, and vitamin D, and subjected to acute bilateral nephrectomy. The animals had received subcutaneous radiocalcium 4 wk before the experiment. 5 h after nephrectomy an increase in serum total calcium, 45Ca-specific activity, citrate, phosphorus, and magnesium concentrations were observed. Serum immunoreactive parathyroid hormone increased, while serum calcitonin decreased. The osteoclast count in the tibial metaphyses was augmented. The biochemical and histological changes observed were partly parathyroid hormone and calcitonin independent, as they also occurred in parathyroidectomized hypocalcemic rats. Pretreatment with 650 pmol of 24,25-dihydroxycholecalciferol 16 h before nephrectomy prevented bone calcium mobilization and diminished the rise in serum total calcium and citrate both in parathyroidintact and in parathyroidectomized animals. In parathyroid-intact rats, serum immunoreactive parathyroid hormone and calcitonin remained normal in spite of the fall in serum-ionized calcium, and the number of osteoclasts did not increase. In parathyroidectomized rats, 24,25-dihydroxycholecalciferol did not prevent the postnephrectomy rise in the osteoclast count. This latter observation suggests that this metabolite exerts its effect on bone either by acting on cells other than osteoclasts, i.e., the osteocytes, or by inhibiting cell activity. At equimolar dosage 1,25-dihydroxycholecalciferol had a potent stimulatory effect on bone resorption. This effect of 1,25-dihydroxycholecalciferol was partly blocked by the simultaneous administration of 24,25-dihydroxycholecalciferol. The potential clinical significance of these observations remains to be determined.

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Oscillations in inositol 1,4,5-trisphosphate and diacyglycerol induced by vitamin D3 metabolites in confluent mouse osteoblasts

Grosse

Bourdeau

Lieberherr

1993

Journal of Bone and Mineral Research

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For the last 5 years, attention has focused on the nongenomic effects of 1,25-(OH)2D3, but considerably less is known about the mechanisms of the nonnuclear actions of 24,25-(OH)2D3. The present study examines and compares the rapid (5-90 s) effects of 100 pM to 10 nM 24,25-(OH)2D3, 10 pM to 1 nM 1,25-(OH)2D3, and 1-100 nM 25-OHD3 on the formation of inositol phosphates and lipids in confluent mouse osteoblasts. 24,25-(OH)2D3 and 25-OHD3 effects were dose dependent; those of 1,25-(OH)2D3 were dose dependent in a bell-shaped manner. The two dihydroxylated metabolites induced a multiphasic response in inositol 1,4,5-trisphosphate (IP3) formation with three stimulation peaks; the IP3 response to 25-OHD3 was monophasic. The amplitude of the IP3 response to 24,25-(OH)2D3 was greater and its oscillation period was slower than that induced by 1,25-(OH)2D3. The diacylglycerol (DAG) responses to secosteroids showed two stimulation peaks that appeared at different times depending on the secosteroid used. Pretreatment with neomycin totally inhibited the first DAG response; neomycin had no effect on the second peak of DAG induced by 25-OHD3, whereas it partially blocked the second response of DAG to 24,25-(OH)2D3 and 1,25-(OH)2D3. These data show for the first time that 24,25-(OH)2D3 can modulate phospholipid metabolism in confluent mouse osteoblasts as early as 5-10 s. The first pathway used by all three secosteroids is that of the hydrolysis of phosphatidylinositol 4,5-bisphosphate via phospholipase C activation, leading to the formation of the two second messengers, IP3 and DAG, since neomycin totally blocked the response. Thus, the action of these secosteroids on the osteoblast membrane may also implicate several steps of the phosphatidylcholine cycle, according to the metabolite tested. Finally, these data point to a direct interaction of vitamin D metabolites with specific membrane recognition moieties.

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Interaction of 24,25-Dihydroxyvitamin D3 and parathyroid hormone on bone enzymes in vitro

Cited by 40 publications

References 13 publications

Interaction between 24R,25-dihydroxycholecalciferol and 1,25-dihydroxycholecalciferol on45Ca release from bone in vitro

Interaction between 24R,25-dihydroxycholecalciferol and 1,25-dihydroxycholecalciferol on45Ca release from bone in vitro

Suppressive Effects of 24,25-Dihydroxycholecalciferol on Bone Resorption Induced by Acute Bilateral Nephrectomy in Rats

Oscillations in inositol 1,4,5-trisphosphate and diacyglycerol induced by vitamin D3 metabolites in confluent mouse osteoblasts

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