Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Osteocalcin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1993

Osteocalcin levels in maternal and cord blood.

OBJECTIVE: To measure osteocalcin levels in fetal and maternal blood. METHODS: Osteocalcin was measured by radioimmunoassay in paired maternal and umbilical venous and arterial blood obtained at term deliveries. RESULTS: Umbilical venous osteocalcin levels (mean +/- standard deviation) were significantly higher than arterial levels (10.28 +/- 4.99 versus 3.85 +/- 2.27 micrograms/L). Umbilical venous but not arterial levels of osteocalcin were significantly higher than maternal values (2.54 +/- 1.19 micrograms/L). CONCLUSION: Higher osteocalcin levels in umbilical venous blood than in umbilical arterial blood suggest that the placenta may be the main source of osteocalcin in late fetal life.

Female↗
PubMed1995

[Study of variations of osteocalcin concentrations in function of collection, assay method and its nyctohemeral rhythm].

Osteocalcin or bone GLA protein (BGP) can be used as well as a peripheral marker of the action of hormones on osteoblast. In the present study, we report our clinical and biological results in three different conditions: the kits used for determination, the time and the hour of withdrawal. We used 4 different radioimmunoassay kits: two kits (Elsa-os-nat (cis), Osca-test (Henning)) detect intact osteocalcin molecules only and the two others (Elsa-osteo(cis), Ostk-PR(cis)) detect intact osteocalcin molecules and osteocalcin fragments. Time between collection and assay is important: we observed a diminution of osteocalcin level which can be due to the degradation of intact molecules, of 25% to 49% (depending on the kit used). The clinical profile was studied with circadian rhythm. We observed a variation of osteocalcin level in 30% of circadian rhythm according to the hour of collection sample. In conclusion, we have seen two differents situations at risk of wrong interpretation due to low level BGP: inadequate serum collection or single blood collection instead of circadian cycle.

Adult↗
PubMed1996

Identification of an osteocalcin gene promoter sequence that binds AP1.

Osteoblasts are differentiated cells that produce bone matrix components including the bone-specific protein osteocalcin. The osteocalcin gene promoter has become a model for understanding how genes are regulated, specifically in osteoblasts. One model for cell-specific regulation suggests that osteoblast-expressed genes are regulated through common promoter sequences which bind osteoblast-specific transcriptional activators. The phenotype suppression model suggests osteoblast-specific promoters are switched off through the action of the common transcriptional activator AP1. We previously demonstrated that a short sequence element (OSCARE-2) in the osteocalcin promoter was homologous to a repressive element in the collagen type 1 (alpha 1) promoters. In this paper we use electrophoretic mobility shift (EMS) assays to examine DNA-protein interactions in the OSCARE-2 sequence. In EMS assays, OSCARE-2 binds a complex of proteins, including AP1. This supports the role of AP1 sites in contributing to the regulation of the osteocalcin promoter. Exogenous c-JUN protein bound to OSCARE-2 and increasing c-JUN incubated with nuclear extract amounts caused a progressive increase in a higher-molecular-weight complex, consistent with c-JUN involvement in protein-protein as well as DNA-protein interactions. Anti-c-FOS antibody was capable of supershifting OSCARE-2 DNA-protein complexes produced using osteoblast-like cell nuclear extracts. In addition, EMS assays of nuclear proteins from osteoblast-like cells indicated that 1,25 (OH)2D3-inducible proteins are bound to OSCARE-2. Osteocalcin promoter constructs showed that OSCARE-2 contributed to the 1,25 (OH)2D3 response, albeit in a minor way. These data support the role of AP1 protein as a regulator of osteoblast-specific gene expression during osteoblast development.

Base Sequence↗
PubMed1997

Juvenile rheumatoid arthritis. Effects of disease activity and recombinant human growth hormone on insulin-like growth factor 1, insulin-like growth factor binding proteins 1 and 3, and osteocalcin.

OBJECTIVE: To investigate possible mechanisms of growth impairment in children with juvenile rheumatoid arthritis (JRA). METHODS: Eighteen prepubertal children with JRA and growth retardation received recombinant human growth hormone (rHuGH) for 1 year. Growth hormone profiles over 24 hours were obtained before treatment in 12 patients; the levels did not differ from those in "short normal" children. Levels of insulin-like growth factor 1 (IGF-1), IGF binding proteins (IGFBPs) 1 and 3, insulin, osteocalcin, and C-reactive protein (CRP), as well as the erythrocyte sedimentation rate were measured serially. Pretreatment levels were compared with control levels. RESULTS: In JRA patients, IGF-1, IGFBP-3, and osteocalcin levels were significantly lower and insulin levels significantly higher than those in controls, but there was no significant difference in the level of IGFBP-1. With rHuGH treatment, height velocity and mean levels of IGF-1, osteocalcin, and insulin increased significantly, while mean levels of IGFBP-1 fell significantly. Levels of IGFBP-3 correlated with those of IGF-1. The height velocity correlated positively with IGF-1 and osteocalcin, and negatively with IGFBP-1. Levels of IGFBP-1 were inversely related to those of insulin and IGF-1. There was a significant negative correlation between the CRP and height velocity, IGF-1 level, and osteocalcin level. CONCLUSION: IGF-1 production is impaired in children with active JRA. Treatment with a therapeutic dose of rHuGH can rectify the IGF-1 deficiency within 4 days, but its effect is adversely influenced by the acute-phase response, as reflected by an elevated CRP level.

Analysis of Variance↗
PubMed1994

Transcriptional activation of the human osteocalcin gene by basic fibroblast growth factor.

Basic fibroblast growth factor (bFGF) has been detected in bone cells and stimulates osteoblast proliferation; however, its role in the regulation of bone metabolism remains speculative. We demonstrated that the human osteocalcin promoter is activated by bFGF when transfected into rat osteoblastic (ROS 17/2.8) cells. This effect is concentration dependent, with a twofold induction at 10 ng/ml detected after 20 h. The bFGF response is independent of both the 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and retinoic acid activation of the osteocalcin promoter. To identify the promoter sequences through which bFGF exerts its effect, we tested a series of promoter deletion constructs for their response to bFGF. Deletion of the upstream region between -673 and -588 bp results in a significant loss of induction. Gel-shift analysis demonstrates that proteins present in ROS 17/2.8 nuclear extracts bind specifically to these sequences. This region alone was unable to confer the bFGF response on a minimal osteocalcin or an heterologous promoter. However, sequences between -678 and -476 bp, which also includes the vitamin D response element (VDRE), were able to confer bFGF inducibility on both a minimal osteocalcin and a heterologous promoter. These data suggest that induction of the human osteocalcin promoter by bFGF requires the interaction of more than one sequence element.

Animals↗
PubMed1996

Expression of osteocalcin in the patella of experimentally immobilized and remobilized rats.

The exact mechanisms by which mechanical loading-unloading affects bone tissue are mostly unknown. Recently, osteocalcin, a direct product of osteoblasts, has been shown to reflect the activity of the mineralization phase of the newly formed bone matrix, and therefore, the in situ detection of osteocalcin could be used for studying the effects of physical activity-inactivity on the osteoblast function or bone formation in the target bone. In this study, the effect of various loading states (immobilization and three forms of subsequent remobilization) on the in situ expression of osteocalcin in the rat patellas and their osteotendinous junctions was studied immunohistochemically using a polyclonal rat antiosteocalcin as the primary antibody. Following immobilization for 3 weeks, the immunoreactivity of osteocalcin was markedly decreased or was completely absent in all the patellar areas which normally show intense reaction as a sign of mineralization of the newly formed bone, that is, in the subperiosteal and subchondral regions, in the osteoid tissue that lies on the surface of the trabecular bone, and around the cortical lacunae. The same was true in the mineralized fibrocartilage zone of the osteotendinous junction of the quadriceps tendon. Free remobilization for 8 weeks (free cage activity) could not improve the situation, but after intensified remobilization of the same duration (low and especially high intensity treadmill running) high osteocalcin expression was observed in the above-mentioned anatomic sites. These findings indicate that formation of new bone tissue is rapidly regulated by the loading states of the bone. Higher than normal activity seems to be needed to restore the bone formation from the disuseinduced depression to normal.

Animals↗
PubMed1991

A role for osteocalcin in osteoclast differentiation.

Specific cellular interactions with components of the extracellular matrix can influence cellular differentiation and development of many tissues. The extracellular matrix of bone is composed of organic constituents and a solid phase of calcium and inorganic phosphate (apatite). When implanted subcutaneously in rats, particles of bone matrix (BPs) recruit progenitors that differentiate into multinucleated cells with osteoclastic features. Because BPs deficient in osteocalcin, a bone matrix protein, were less efficient at promoting osteoclast formation than were normal BPs, we directly examined the influence of osteocalcin on osteoclast differentiation. We evaluated tissue responses to particles of synthetic crystalline apatite alone (Ap), having many of the features of native apatite of mature bone, or to apatite prepared with osteocalcin (Ap/OC), bovine serum albumin (Ap/BSA) or rat bone collagen (Ap/Col). Twelve days after subcutaneous implantation in normal rats, Ap, Ap/BSA, and Ap/Col particles generated a mild foreign body reaction with multinucleated cells in direct contact with the particles; these cells were negative for tartrate-resistant acid phosphatase (TRAP) activity and lacked ruffled borders. In contrast, Ap particles containing approximately 0.1% osteocalcin were partially resorbed and they generated more multinucleated cells that were TRAP-positive, were immunoreactive with an antibody against tartrate-resistant purple acid phosphatase, and displayed ultrastructural features of active osteoclasts including ruffled borders and clear zones. These data support the hypothesis that osteocalcin may function as a matrix signal in the recruitment and differentiation of bone-resorbing cells.

Acid Phosphatase↗
PubMed1995

Proximal promoter binding protein contributes to developmental, tissue-restricted expression of the rat osteocalcin gene.

Osteocalcin is a 6 kD tissue-specific calcium binding protein associated with the bone extracellular matrix. The osteocalcin gene is developmentally expressed in postoproliferative rat osteoblasts with regulation at least in part at the transcriptional level. Multiple, basal promoter and enhancer elements which control transcriptional activity in response to physiological mediators, including steroid hormones, have been identified in the modularly organized osteocalcin gene promoter. The osteocalcin box (OC box) is a highly conserved basal regulatory element residing between nucleotides -99 and -76 of the proximal promoter. We recently established by in vivo competition analysis that protein interactions at the CCAAT motif, which is the central core of the rat OC box, are required for support of basal transcription [Heinrichs et al. J Cell Biochem 53:240-250, 1993]. In this study, by the combined utilization of electrophoretic mobility shift analysis, UV cross linking, and DNA affinity chromatography, we have identified a protein that binds to the rat OC box. Results are presented that support involvement of the OC box-binding protein in regulating selective expression of the osteocalcin gene during differentiation of the rat osteoblast phenotype and suggest that this protein is tissue restricted.

Animals↗
PubMed1995

G/C element contributes to the cell line-specific expression of the proximal osteocalcin promoter.

Sequential activation of cell type-specific genes occurs during osteoblast development. The promoter of one such gene, osteocalcin, has been widely studied, but the DNA sequences that govern osteoblast-specific expression have not been defined. The proximal osteocalcin promoter linked to pTKCAT directs strong promoter activity in osteoblast-like ROS17/2.8 cells and comparatively weak promoter activity in nonosteoblastic NIH3T3 cells. To identify sequences important in conferring cell-specific expression of the osteocalcin gene, a deletion series of the human proximal promoter was constructed and the activities assessed in ROS17/2.8 and NIH3T3 cells. These studies identified a 30 bp sequence within the proximal promoter (osteocalcin repressor element-1 [ORE-1]) which is responsible for repressing the transcriptional activity in NIH3T3 cells. In electrophoretic mobility shift assays from both NIH3T3 and ROS17/2.8 cells, a protein complex bound to the ORE-1 that was related to a complex which binds the G/C-rich repressor element in the collagen type I (alpha 1) promoter. In addition, there was a second complex from NIH3T3 cells but not ROS17/2.8 cells that bound the ORE-1 fragment. The presence of this additional factor in NIH3T3 cells parallels the observation that constructs carrying the ORE-1 sequence have repressed promoter activity relative to the analogous constructs lacking the ORE-1 when transfected into NIH3T3 and suggests that the NIH3T3-specific factor is a repressor. These data indicate that the G/C element in the ORE-1 contributes to the repression of osteocalcin gene transcription in a nonosteoblast cell line. The high homology between the ORE-1 sequence and a related sequence in the collagen type I (alpha 2) proximal promoter suggests that homologous regions in other osteoblast-expressed genes may function similarly.

3T3 Cells↗
PubMed2001

Relation of polymorphism in the promotor region for the human osteocalcin gene to bone mineral density and occurrence of osteoporosis in postmenopausal Chinese women in Taiwan.

Osteoporosis is a common disorder with a strong genetic component. Our aim was to evaluate the correlation of the HindIII osteocalcin gene polymorphism to bone mineral density (BMD) and their relationship to osteoporosis. We determined the HindIII osteocalcin gene polymorphism using polymerase chain reaction (PCR)-based restriction analysis in postmenopausal Chinese women in Taiwan. The osteocalcin gene polymorphism was detected by the restriction enzyme HindIII, where the H allele indicated the absence of the cuttable site and the h allele indicated its presence. We then related the genotypes to BMD and occurrence of osteoporosis in these women. The allelic frequencies for postmenopausal Chinese women in Taiwan were 64% for h and 36% for H in HindIII restriction fragment length polymorphisms. The prevalence of each genotype in the study population was 37.7% hh, 52.6% Hh, and 9.7% HH. The subjects with genotype hh had the greatest BMD at the lumbar spine and the femoral neck, and those with HH had the smallest BMD at the femoral neck, but these differences did not reach statistical significance. The HindIII osteocalcin genotype showed a significant effect on the prevalence of osteoporosis in the subjects at the femoral neck, that is, women with genotype HH had a 6.4 times greater risk for osteoporosis (P < 0.05), and those with genotype Hh had a 1.2 times greater risk than women with genotype hh. In conclusion, the HindIII osteocalcin gene polymorphism is associated with reduced BMD and predisposes women to osteoporosis at the femoral neck.

Aged↗
PubMed1993

Ovariectomy decreases the mRNA levels of transforming growth factor-beta 1 and increases the mRNA levels of osteocalcin in rat bone in vivo.

Estrogen depletion causes postmenopausal osteoporosis. Here we report that steady state mRNA levels of transforming growth factor-beta 1 (TGF-beta 1) and osteocalcin in bone persistently decreased and increased, respectively, in vivo in estrogen-depleted rats after ovariectomy (OVX). 21 female Wistar rats (7-month-old) were randomized and underwent OVX or sham-operation, total RNA was extracted from tibiae and assessed by Northern blot analysis. OVX induced 70-80% decrease in TGF-beta 1 mRNA levels and 2- to 3-fold increase in mRNA levels of osteocalcin compared with controls three weeks after surgery. These changes persisted up to twelve weeks post-operation. OVX caused 15% reduction in femoral bone mineral density and 2-fold elevation in serum osteocalcin levels as early as two weeks post-operation. Moreover, estrogen depletion resulted in marked decrease and increase, respectively, in steady state mRNA levels of TGF-beta 1 and osteocalcin in vitro in osteoblastic rat osteosarcoma cells, ROS 17/2.8. Our results provide the first in vivo evidence that expression of TGF-beta and osteocalcin in bone is reciprocally regulated at the transcriptional level in estrogen deficient OVX rats and suggests that TGF-beta 1 may play a role in estrogen-dependent maintenance of normal bone density.

Amino Acid Isomerases↗
PubMed1998

24R,25-dihydroxyvitamin D3 increases cyclic GMP contents, leading to an enhancement of osteocalcin synthesis by 1,25-dihydroxyvitamin D3 in cultured human osteoblastic cells.

The effect of the physiological vitamin D metabolite 24R, 25-dihydroxyvitamin D3 [24R,25(OH)2D3] on human osteoblastic cells was assessed. Physiological concentrations (10(-9)-10(-8) M) of 24R, 25(OH)2D3 significantly increased the cyclic guanosine 5'-monophosphate (cGMP) content in the human osteoblastic cells by approximately 200% in 5 to 15 min. In contrast, 24S, 25-dihydroxyvitamin D3 had only a weak effect on the cGMP content, and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] did not affect the content. The production of osteocalcin was not induced by 10(-9)-10(-8) M of 24R,25(OH)2D3 in the absence of 1,25(OH)2D3. However, the same concentration of 24R,25(OH)2D3 showed stimulatory effects on osteocalcin synthesis in the presence of 10(-9) M 1, 25(OH)2D3. Rp-8Br-cyclic GMP, a specific inhibitor of cyclic GMP-dependent protein kinase, significantly inhibited the cooperative effect of 24R,25(OH)2D3 with 1,25(OH)2D3 on the osteocalcin synthesis, although Rp-8Br-cyclic AMP, a specific inhibitor of cyclic AMP-dependent protein kinase, did not affect the cooperative effect. In addition, okadaic acid enhanced the osteocalcin synthesis induced by 1,25(OH)2D3. These observations suggest that 24R,25(OH)2D3 has a unique activity of increasing cGMP contents in osteoblastic cells, and that the increase in cGMP contents may lead to the cooperative effect of 24R,25(OH)2D3 with 1, 25(OH)2D3 on osteocalcin synthesis. These data support the hypothesis that 24R,25(OH)2D3 has a physiological role in human bone and mineral metabolism.

24,25-Dihydroxyvitamin D 3↗
PubMed1996

Plasma osteocalcin in healthy Nigerian children and in children with calcium-deficiency rickets.

Osteocalcin is an osteoblast-specific protein believed to be associated with events occurring during bone mineralization, which has been widely used clinically as an indicator of osteoblast function. Plasma osteocalcin concentrations (pOC) were studied in 94 (59 male, 35 female) healthy and 44 (21 male, 23 female) rachitic Nigerian children, all one to five years of age. The study was aimed at establishing a reference range for healthy Nigerian children determining any changes in plasma osteocalcin levels occurring in children with calcium-deficiency rickets. In the controls, pOC levels ranged from 3-89 ng/ml, with a mean value of 23 +/- 19 ng/ml. The values were higher in girls (29 +/- 21 ng/ml) than in boys (21 +/- 18 ng/ml), though not significantly. The controls had values consistent with other published pediatric ranges from Europe and North America. In the younger rachitic children (under 3 years) the mean pOC was lower than in the controls (P = 0.04) despite the much elevated plasma levels of 1,25(OH)2D. In the controls, pOC correlated with 1,25(OH)2D (r = 0.59, P = 0.003), alkaline phosphatase (r = 0. 22, P = 0.03), and inorganic phosphate (r = 0.27, P = 0.01). These correlations were lost in the rickets group. The findings in the controls confirm the known association between plasma 1,25(OH)2D and circulating osteocalcin levels, whereas the findings in the rickets group suggest that the stimulatory effects of 1,25(OH)2D on osteocalcin may depend on other permissive factors, such as normal circulating levels of calcium and phosphate.

Alkaline Phosphatase↗
PubMed1987

[Osteocalcin and bone histology in osteoporosis].

The decoupling of bone formation and bone resorption causes an insidious bone loss that is responsible for the negative skeletal balance in the frequent form of low turnover osteoporosis. The reduction of bone formation can hardly be verified by clinical methods. Osteocalcin, a non-collagenous bone protein, has proved to be a useful new indicator of bone formation. To establish its predictable value, plasma levels of osteocalcin were compared to conventional serological data of bone turnover and to histomorphometric parameters of iliac crest trabecular bone. In cases of osteoporosis with normal bone turnover activity (as confirmed by histomorphometry) no differences were observed in any of our laboratory data including osteocalcin. However, there was a significant lower mean serum level of osteocalcin in a group of patients with histomorphometrically proven low turnover osteoporosis in comparison to those with normal bone turnover. Serum levels of osteocalcin below 2.0 ng/ml seem to indicate a low turnover in the individual case of osteoporosis while this is unlikely when serum levels above 6.0 ng/ml are measured (according to our RIA).

Adult↗
PubMed1991

Reversion of the steroid-induced decrease of serum osteocalcin with sodium fluoride.

Osteopenia observed in corticotherapy is due, among other causes, to a decrease in bone formation as can be shown by a steroid-induced osteocalcin decrease. Although various treatments have been proposed there is no agreement as to which one is the best. Two such treatments, sodium fluoride and vitamin D administration increase osteocalcin levels. We treated a group of 12 patients under corticoid therapy (mean dose 16 mg per day) with 50 mg/day p.o. sodium fluoride, and determined osteocalcin levels before and two weeks after sodium fluoride treatment. Similarly, another group of 9 patients with a similar mean steroid dose was treated with 0.5 micrograms/day of 1 alpha (OH)2D3 in order to assess the effect of this vitamin on osteocalcin and to determine which was the best treatment. Both groups were compared with respective control groups. A significant osteocalcin increase was observed in the control groups (p less than 0.001); similar significance was observed in the sodium fluoride group, whereas a lower significance (p less than 0.01) was observed in the vitamin D group. These results suggest that sodium fluoride could be more effective than vitamin D in the treatment of steroid-induced osteopenia.

Adrenal Cortex Hormones↗
PubMed1986

Metabolism of osteocalcin.

After intravenous injection, labeled bovine osteocalcin was rapidly removed from rat plasma and taken up mainly by kidney, liver, and bone. The rate of disappearance was slowed by nephrectomy but not as much by ureteric ligation, suggesting renal destruction of osteocalcin rather than renal excretion. Both liver and kidney tissue rapidly degraded osteocalcin, both in vivo and in vitro. The enzyme activity was found in microsomal, mitochondrial, and supernatant fractions. EDTA was the most potent inhibitor, suggesting that metalloenzymes are involved. Comparison of three methods of analysis--trichloroacetic acid precipitation, gel filtration on Sephadex G-50, and SDS polyacrylamide gel electrophoresis--showed that the last gave a much faster rate of degradation of osteocalcin and suggests that osteocalcin and/or fragments bind to larger proteins in the tissue homogenates.

Animals↗
PubMed1991

Serum osteocalcin and bone isoenzyme alkaline phosphatase in growth hormone-deficient patients: dose-response studies with biosynthetic human GH.

Serum osteocalcin and bone alkaline phosphatase (BAP) were measured in samples drawn at 8 a.m. in 7 patients with GH deficiency treated with recombinant human growth hormone (rhGH) (2 IU/day subcutaneously at 8 p.m.), and 7 normal controls. Patients treated with 2 IU/day had lower BAP than controls (P less than 0.05). Further, increasing doses of rhGH were given subcutaneously to each of the 7 patients for 3 consecutive 14-day periods (2, 4, and 6 IU/day at 8 p.m.) followed by 14 days off treatment. At the end of each period, the patient was hospitalized for frequent blood sampling from 8 p.m. to 11 a.m. the following day. A dose-dependent increase in area under the curve (AUC) was seen for osteocalcin (P less than 0.05), whereas the increase in AUC for BAP just failed to reach significance (P less than 0.10). The nocturnal pattern of serum osteocalcin in patients on 4 and 6 IU/day were statistically indistinguishable from those in controls. During treatment with 2 IU/day and the off-treatment period, the pattern was significantly different from controls (P less than 0.05). In conclusion, rhGH has a dose-dependent effect on basal osteoblastic activity and the nocturnal pattern of osteocalcin. Serum osteocalcin increases within hours following rhGH administration. However, 2 IU/day is inadequate to maintain normal levels and nocturnal variation in markers of osteoblastic activity.

Adolescent↗
PubMed1991

Evaluation of the usefulness of serum phosphatases and osteocalcin as serum markers in a calcium depletion-repletion rat model.

The present study examined the usefulness of the serum alkaline phosphatase (ALP) activity, osteocalcin, and tartrate-resistant acid phosphatase (TrACP) activity as bone turnover markers in a calcium depletion/repletion rat model. Weanling rats were fed calcium-deficient diet for 4 weeks, followed by 2 weeks of dietary calcium repletion. Serum phosphatases and osteocalcin were determined and compared with those of corresponding age-matched, pair-weighted controls. Rats were sacrificed at the end of each phase of the study, and bone phosphatase activities in tibiae and vertebrae were measured. During calcium depletion, rats developed hypocalcemia and lost significant bone calcium, which were reversed with dietary calcium repletion. During depletion when previously published histologic studies indicated a suppressed bone formation and stimulated bone resorption, serum ALP activity and osteocalcin levels were significantly elevated and serum TrACP activity reduced; at the same time, the bone ALP and TrACP activities were increased. Because the serum level of 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) which has been shown to stimulate the synthesis of skeletal ALP and of osteocalcin, was also significantly increased during depletion, the increased serum ALP and osteocalcin level could be indirect consequences of the hypocalcemia-mediated elevation in 1,25(OH)2D3 level. These effects were reversed upon calcium repletion, during which previously published histologic studies demonstrated a stimulated bone formation and a suppressed resorption in these rats. In conclusion, although there is increasing evidence for the usefulness of these serum proteins as markers of bone metabolism in humans, a great deal more work is required before we can understand the significance of these assays. Until such is accomplished, these assays should not be assumed to be validated.

Acid Phosphatase↗