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PubMed2005

Level of undercarboxylated osteocalcin in reproductive Thai females.

Osteocalcin is a vitamin K dependent protein requiring vitamin K as a cofactor for the enzyme gamma glutamyl carboxylase which converts the glutamate residues at 17, 21, 24 position of the molecule into gamma carboxyglutamate or Gla residues. The carboxylation makes immature osteocalcin or undercarboxylated osteocalcin (ucOC) into mature osteocalcin which enhances calcium binding in bone. The level of undercarboxylated osteocalcin is recognized as a marker of vitamin K2 bone. The level of undercarboxylated osteocalcin is recognized as a marker of vitamin K2 in blood necessary for this process. Mature osteocalcin has a higher affinity for hydroxyapatite than undercarboxylated osteocalcin. Foreign studies have shown that ucOC level is increased in elderly women and postmenopausal women in comparison with young, healthy, reproductive women and level of ucOC is also the marker to predict the risk of hip fracture. The standard value of undercarboxylated osteocalcin in Thai women is not available. The aim of the present study was to find the level of ucOC in reproductive Thai females. 357 healthy female volunteers who had regular menstruation, 20-50 years of age, average age 38.5 years old. The volunteers had no intake of any kind of medicine affecting bone metabolism before blood examination. The mean value of undercarboxylated osteocalcin is 2.69 ng/ml, median is 2.10_ng/ml standard deviation = 2.02,_standard error = 0.107 with 95% confident interval = 2.485 to 2.906 ng/ml. In the authors previous pilot study in elderly and postmenopausal women, the authors found that the mean of ucOC in Thai elderly and postmenopausal women was higher than that of reproductive women.

Adult↗

PubMed1997

Developmental regulation of osteocalcin expression in MC3T3-E1 osteoblasts: minimal role of the proximal E-box cis-acting promoter elements.

Osteoblasts undergo a temporal sequence of development characterized by transcriptional upregulation of osteoblast-specific genes. Basic helix-loop-helix (bHLH) transcription factors may control this developmental process through binding to E-box cis-acting elements in developmentally regulated genes. To investigate the role of bHLH proteins in MC3T3-E1 osteoblasts, which undergo a developmental sequence in vitro, we analyzed the transcriptional control of osteocalcin gene expression by stable transfection of an osteocalcin promoter-luciferase chimeric gene (p637OC-luc) and assessed the role of E-box cis-acting elements in osteocalcin promoter by DNA binding assays. We compared our findings in MC3T3-E1 osteoblasts with transient DNA transfections and DNA binding experiments in Ros 17/2.8 osteoblasts. We found that the activity of 637-OC luciferase promoter was low in undifferentiated 5-day-old cultures but increased in parallel with endogenous osteocalcin message expression in mature MC3T3-E1 osteoblasts, consistent with developmental stage-specific transcriptional upregulation of the osteocalcin gene. We identified two putative E-box elements in the proximal osteocalcin promoter, E-box 1 (CACATG) at -102 and E-box 2 (CAGCTG) at position -149. In gel mobility shift assays, factors present in nuclear extracts derived from differentiated osteoblast bound to oligonucleotide probes containing the E-box 1 and E-box 2 elements. Binding to the E-box 2 probe was not specific for the core CAGCTG element, whereas the CACATG site in E-box 1 oligonucleotide was required for specific binding of these nuclear factors. Stable transfection of p637OC-luc containing a mutant E1 site (p637OC-luc E1m), however, did not alter the developmental upregulation of osteocalcin promoter activity in MC3T3-E1 osteoblasts. Moreover, the E-box 1 mutation had no effect on either basal or vitamin D-stimulated activity of the osteocalcin promoter in Ros 17/2.8 osteoblasts in transient transfection experiments. These data suggest that osteoblasts contain underfined factors that bind to the E-box 1 CACATG site in the proximal osteocalcin promoter; however, this E-box element does not play a significant role in the developmental stage-specific regulation of the osteocalcin gene in MC3T3-E1 osteoblasts.

3T3 Cells↗

PubMed2001

Correlations between osteocalcin content, degree of mineralization, and mechanical properties of C. carpio rib bone.

Osteocalcin is one of the most abundant noncollagenous proteins in bone. It is strongly associated with the mineral phase of bone, and has long been associated as a marker of bone turnover. However, its relationship to bone composition, strength, and structure is unclear. Carp rib bone is an excellent model for the study, because osteocalcin represents almost 60% of the total extractable noncollagenous proteins found in it. Because of the abundance of osteocalcin relative to other extractable proteins, any changes in the properties of carp rib bone would be more likely influenced by the osteocalcin concentration. To test the hypotheses that the concentration of osteocalcin is reflected in other properties of bone, the correlations between the osteocalcin concentration and the mineral content, microstructural properties, and physical characteristics of the bone mineral crystals were determined utilizing radioimmunoassay (RIA), spectrophotometry, nanoindentation, and small-angle X-ray scattering (SAXS) techniques, respectively. Osteocalcin concentration was found to be correlated to the molar Ca/P ratio and inversely correlated to the elastic modulus and hardness in the longitudinal plane. This study provides evidence for a putative relationship between the concentration of osteocalcin and the microstructural mechanical properties of bone. Correlations were also found between the mechanical properties in the longitudinal plane and both the phosphate content and the molar Ca/P ratio. However, no relationships could be identified between osteocalcin concentration and several parameters of bone crystals, as determined by SAXS.

Animals↗

PubMed1993

Gallium nitrate regulates rat osteoblast expression of osteocalcin protein and mRNA levels.

Gallium nitrate, a group IIIa metal salt, has been found to be clinically effective for the treatment of accelerated bone resorption in cancer-related hypercalcemia and Paget's disease. Here we report the effects of gallium nitrate on osteocalcin mRNA and protein levels on the rat osteoblast-like cell line ROS 17/2.8. Gallium nitrate reduced both constitutive and vitamin D3-stimulated osteocalcin protein levels in culture medium by one-half and osteocalcin mRNA levels to one-third to one-tenth of control. Gallium nitrate also inhibited vitamin D3 stimulation of osteocalcin and osteopontin mRNA levels but did not affect constitutive osteopontin mRNA levels. Among several different metals examined, gallium was unique in its ability to reduce osteocalcin mRNA levels without decreasing levels of other mRNAs synthesized by ROS 17/2.8 cells. The effects of gallium nitrate on osteocalcin mRNA and protein synthesis mimic those seen when ROS 17/2.8 cells are exposed to transforming growth factor beta 1 (TGF beta 1); however, TGF-beta 1 was not detected in gallium nitrate-treated ROS 17/2.8 cell media. Use of the RNA polymerase II inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole demonstrated that gallium nitrate did not alter the stability of osteocalcin mRNA. Transient transfection assays using the rat osteocalcin promoter linked to the bacterial reporter gene chloramphenicol acetyltransferase indicated that gallium nitrate blocked reporter gene expression stimulated by the osteocalcin promoter. This is the first reported effect of gallium nitrate on isolated osteoblast cells.

Animals↗

PubMed1993

Induction of bone-related proteins, osteocalcin and osteopontin, and their matrix ultrastructural localization with development of chondrocyte hypertrophy in vitro.

Endochondral bone formation occurs by a series of developmentally regulated cellular events from initial formation of cartilage tissue to stages of calcified cartilage, resorption, and replacement by bone tissue. Several studies have raised the question of the possibility that the hypertrophic chondrocytes associated with the calcifying cartilage matrix can acquire properties similar to osteoblasts. We have addressed this possibility by measuring synthesis within hypertrophic chondrocytes in vitro of two bone-related proteins, osteopontin and osteocalcin. Chondrocytes derived from chick embryo ventral vertebral tissue were cultured under conditions that promoted extracellular matrix mineralization and differentiation towards the hypertrophic phenotype as indicated by the induction of Type X collagen, alkaline phosphatase, and diminished expression of Type II collagen and the core protein of large proteoglycan. In these cultures, osteopontin synthesis was detected in early cultures in the absence of a calcified matrix; in contrast, an absence of the bone-specific protein osteocalcin was observed. However, with onset of development of the hypertrophic phenotype an induction of protein expression for osteocalcin was observed with a significant (twofold) increase in osteopontin. Maximal levels of osteocalcin synthesis occurred with the peak of alkaline phosphatase activity and Type X collagen mRNA levels. The levels of osteocalcin synthesis were induced fiftyfold from the earliest level of detection but this level was only one one-hundredth of that observed for mature chick osteoblast cultures. Osteocalcin and osteopontin were characterized by several criteria (electrophoresis, immunoblotting, chromatographic characteristics, and response to 1,25(OH)2D3) which confirmed their molecular properties as being identical to osteoblast synthesized proteins. The coordinate change in the cellular phenotype to the hypertrophic chondrocyte was shown to be concurrent with ultrastructural maturation of the cells and the accumulation of osteocalcin and osteopontin in the extracellular matrix associated with hydroxyapatite at sites of mineralization. Since the ultrastructural features of the cells in vitro and the extracellular matrix surrounding the lacunae have features of the hypertrophic chondrocyte and associated matrix in vivo, the induction of the bone-specific protein osteocalcin suggests that at least a population of these cells may develop osteoblastic phenotypic markers in association with mineralizing matrix. The detection of osteocalcin and the high level of synthesis of osteopontin may represent an advanced stage of chondrocyte hypertrophy or the possibility of a trans-differentiation of the chondrocytes to an osteoblastic-like cell.

Animals↗

PubMed1988

The metabolic clearance rate of osteocalcin in sheep.

Plasma osteocalcin has been proposed as a useful and convenient biochemical marker of bone formation. However, the effect on plasma osteocalcin due to variations in the rate of its removal from the circulation has been little investigated. We have measured the metabolic clearance rate of plasma osteocalcin in adult oophorectomized sheep. Two methods were used: intravenous bolus injection (six animals) and 6 hour constant intravenous infusion (four animals) of 125I-ovine osteocalcin. Using the bolus injection method, the plasma clearance of osteocalcin was found to be 3.3 liters/h. With the constant infusion method, the calculated value was 2.8 liters/h; based on this value and the mean ovine plasma osteocalcin concentration of 26.9 ng/ml (N = 29), a plasma production rate of 1.8 mg/day was derived. Osteocalcin clearance was relatively constant among animals in a basal state. Hence, the present approach should permit us to evaluate the relative contributions to changes in circulating osteocalcin levels from altered osteocalcin plasma clearance and production under various physiological and pathological conditions.

Animals↗

PubMed2000

Development and application of a serum C-telopeptide and osteocalcin assay to measure bone turnover in an ovariectomized rat model.

Biochemical markers applicable to the ovariectomized rat model can provide important tools for studying the bone remodeling process in this animal model of postmenopausal osteoporosis. We describe the development and application of two biochemical markers, a C-telopeptide (of type-I collagen) enzyme-linked immunosorbent assay (ELISA) for measuring bone resorption and an osteocalcin radioimmunoassay (RIA) for measuring bone formation in rat serum. The C-telopeptide ELISA is based on an affinity purified polyclonal antibody generated against human sequence DFSFLPQPPQEKAHDGGR. The antibody epitope involves amino acid sequence, which is similar in rat and human carboxyl terminal peptide of type-I (alpha 1) collagen. Sensitivity of the ELISA was 0.3 ng/ml. The averaged intra- and interassay variation was CV <7%. Averaged dilution and spiked recoveries were 91% and 105%, respectively. The second marker developed is a synthetic peptide-based osteocalcin RIA, which does not require isolation and purification of intact osteocalcin from rat bone. Osteocalcin antiserum used in the RIA was generated in rabbits against a synthetic peptide comprising amino acids 33-49 of the rat osteocalcin sequence. The sensitivity of the RIA was 0.15 ng/ml of peptide. The averaged intra (n = 10) and interassay variations for two controls were CV <9% and 12%, respectively. The averaged dilution and spiked recoveries were 99.6%. In vivo validation of the C-telopeptide ELISA and osteocalcin RIA was performed in an ovariectomized (OVX) rat model. In 12-week-old OVX Sprague Dawley rats, the C-telopeptide and osteocalcin concentrations were approximately 65% and 40%, respectively, higher than the sham group. Estradiol repletion significantly lowered the C-telopeptide and osteocalcin concentration to the levels of the sham group. In addition, changes in serum C-telopeptide concentration correlated negatively with trabecular BMD measured by pQCT (r = -0.51, P < 0.001). In conclusion, the C-telopeptide ELISA and osteocalcin RIA exhibited required sensitivity, accuracy, and adequate discriminatory power to be used for measuring bone resorption and bone formation in the ovariectomized rat model.

Amino Acid Sequence↗

PubMed1999

Simple, rapid enzyme-linked immunosorbent assay (ELISA) for the determination of rat osteocalcin.

Determination of the concentration of osteocalcin in rat serum is frequently performed using a commercially available radioimmunoassay (RIA). However, this assay takes 3 days to complete, uses radioactive material, and has a narrow linear range. The limited range of the RIA makes it necessary to test multiple dilutions of the sample which frequently results in values that differ, depending on the dilution. In order to overcome these limitations, we have developed an ELISA that utilizes the same standards and anti-rat osteocalcin antiserum, as is used in the RIA. The principle of the ELISA is that the osteocalcin in the sample competes with osteocalcin previously immobilized on a microtiter plate to bind to the available anti-rat osteocalcin antibodies. The amount of antibody bound to the immobilized osteocalcin is determined colorimetrically using a secondary antibody coupled to alkaline phosphatase. This ELISA has a three-log linear response with a sensitivity of 0.1-0.15 ng/ml and intra- and interassay coefficient of variance (CV) values of less than 10%. Most importantly, the assay is rapid and only requires a 2-hour incubation of the sample with the antiserum. The incubation time is important since we and others have observed a significant decrease in the osteocalcin level from serum samples incubated for long periods of time with the antiserum, presumably due to degradation of the osteocalcin. In general, the commercially available RIA gives osteocalcin values that are one-half to one-fourth that of the ELISA because the RIA requires a 48-hour incubation time.

Aging↗

PubMed2005

Expression of osteocalcin and Jun D in the early period during reactionary dentin formation after tooth preparation in rat molars.

We examined, in rats, the expression of osteocalcin and Jun D in the early stage of reactionary dentin formation after tooth preparation and the accompanying morphological changes. Reverse transcription/polymerase chain reaction analysis revealed strong expression of osteocalcin mRNA in pulp tissue at 2 and 3 days post-preparation compared with that in control teeth. Light microscopy demonstrated that, at the dentin-pulp interface, damaged odontoblasts were detached from the dentin matrix immediately after preparation, with neutrophils lining the dental surface after 1 day. After 2-3 days, differentiated odontoblasts appeared at the interface. Reactionary dentin with tubular structures was formed under the cavity after 10 days. Immunoelectron microscopy showed that trace amounts of osteocalcin were expressed in odontoblasts at 2 days post-preparation, and abundant osteocalcin was found in the highly developed Golgi apparatus and granules at 3 days post-preparation. Osteocalcin was also found on type I collagen fibrils in newly formed predentin. The existing dentinal tubules were filled with osteocalcin-coated type I collagen fibrils. We observed, by immunohistochemistry, that Jun D was temporally expressed in the nuclei of the odontoblasts at 1 and 2 days post-preparation. However, no Jun D was found in the dental pulp cells at any other time or in control teeth. Thus, osteocalcin expression is correlated with reactionary dentin formation, and Jun D is associated with osteocalcin expression in odontoblasts. Osteocalcin may also serve as an obturator of the dentinal tubules to protect dental pulp vitality against external irritants after preparation.

Animals↗

PubMed2001

Expression of mouse osteocalcin transcripts, OG1 and OG2, is differently regulated in bone tissues and osteoblast cultures.

Osteocalcin is a noncollagenous protein that is abundant in mineralized bone matrix. Mice have a gene cluster of osteocalcin that consists of OG1, OG2, and ORG. We established a new method to directly analyze the expression levels of OG1, OG2, and ORG mRNAs relative to total osteocalcin mRNA. They were amplified as 371-bp fragments by reverse transcription-polymerase chain reaction (RT-PCR) at the same time using common primers, digested with ApaLI, and separated in a polyacrylamide gel. ApaLI digestion did not affect the mobility of the OG1-derived 371-bp fragment, whereas both 371-bp fragments, derived from OG2 and ORG, were digested into 350 bp. Total RNA prepared from mouse bone was then subjected to RT-PCR followed by ApaLI digestion. OG1 and OG2 mRNAs were found to be expressed at ratios of 80%-86% and 14%-20%, respectively, to the total osteocalcin mRNA in mouse bone. The ratios were almost constant in various bones in vivo, independent of the animal's genetic background, age, or gender, or different parts of bone. RT-PCR using specific primers revealed that mouse bone tissues strongly expressed osteocalcin mRNA derived from OG1 and OG2, but not ORG. In contrast, cells cultured in vitro showed different expression ratios of osteocalcin mRNA: 53%-65% for OG1 and 35%-47% for OG2 to the total osteocalcin mRNA in the osteoblast cell line and primary osteoblasts in culture even though they formed many mineralized bone nodules. Similar results were obtained in both KS483 osteoblasts and C2C12 myoblasts, when they were cultured with bone morphogenetic protein-2 (BMP-2) to induce osteocalcin mRNA. Taken together, these findings indicate that OG1 is the predominant transcript among the three osteocalcin genes in mouse bone in vivo. It is also suggested that the expression of OG1 and OG2 is regulated differently in bone tissues and osteoblast cultures.

Animals↗

PubMed1992

The effect of active vitamin D3 analogs and dexamethasone on the expression of osteocalcin gene in rat tibiae in vivo.

We tested the effects of 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3), 2 beta-(3-hydroxypropoxy)-1 alpha,25-dihydroxyvitamin D3 (ED-71) and dexamethasone on osteocalcin mRNA levels in rat tibiae in vivo. Northern blot analysis showed that both 1,25-(OH)2D3 and ED-71 caused an increase in osteocalcin mRNA levels in bone: 1,25-(OH)2D3 induced a transient increase in the mRNA levels followed by a decrease in the control level by 12 h post administration. In contrast, ED-71 caused a persistent increase in osteocalcin mRNA level for seven days post administration. Serum osteocalcin levels paralleled the osteocalcin mRNA level in bone in both groups. Dexamethasone caused a marked reduction in both osteocalcin mRNA and serum osteocalcin levels. Suppressive effect of dexamethasone on osteocalcin expression was persistent for seven days at higher dose. Our results represent the first demonstration of the effect of active vitamin D and corticosteroid on the expression of osteocalcin mRNA in bone in vivo.

Amino Acid Isomerases↗

PubMed1990

Lead impairs the production of osteocalcin by rat osteosarcoma (ROS 17/2.8) cells.

The serum level of osteocalcin, a bone-specific protein produced by osteoblasts and an index of bone formation, is decreased in lead-intoxicated children. To elucidate the effect of lead on the hormonal regulation of osteocalcin production, ROS 17/2.8 cells were treated with 0, 5, 10, or 25 microM lead acetate for 24 hr, followed by an additional 24-hr lead treatment with or without 100 pg 1,25-dihydroxyvitamin D3/ml medium. At the end of this period a radioimmunoassay was conducted to determine the amount of osteocalcin present in the cells and secreted into the medium. 1,25-Dihydroxyvitamin D3 increased osteocalcin secretion in control cultures, but this increase was prevented by lead in a concentration-dependent manner. Osteocalcin secretion by cultures treated with 10 or 25 microM lead was even lower than in cultures not stimulated with 1,25-dihydroxyvitamin D3. Intracellular levels of osteocalcin were slightly elevated with 1,25-dihydroxyvitamin D3, and there was no lead effect on cellular levels. These data indicate that lead attenuates basal and 1,25-dihydroxyvitamin D3-stimulated production of osteocalcin in ROS 17/2.8 cells. Because osteocalcin appears to play a central role in bone mineralization, altered osteocalcin production may be a key event in the skeletal toxicity of lead.

Animals↗

PubMed1988

The acute effect of high dose corticosteroid treatment on serum osteocalcin.

Osteocalcin is a vitamin K-dependent protein that is synthesized by osteoblasts and present in circulation. We measured serum osteocalcin concentrations in nine asthmatics before and during treatment with high IV dosages of glucocorticoids, betamethasone 0.65 mg/h. This treatment induced within 13 +/- 1.5 (SEM) hours a reduction of serum osteocalcin form 2.6 +/- 0.3 (SEM) to 1.2 +/- 0.3 microgram/L (P less than .001). During the following 24-hour period the osteocalcin levels further declined and reached a level about 30% of the pretreatment level. Continued treatment did not induce a further reduction of serum osteocalcin. A positive correlation was seen between the pretreatment osteocalcin concentration and the steady-state osteocalcin value during steroid therapy. The corticosteroids did not influence the serum calcium and phosphate concentrations but induced a minor, significant (P less than .001) decrease of serum alkaline phosphatase. After completion of steroid therapy, the osteocalcin values remained depressed for another 24 hours but had reached the pretreatment levels after another three days. Our data suggest osteocalcin as a sensitive marker of the corticosteroid induced depression of osteoblast activity.

Adrenal Cortex Hormones↗

PubMed1994

DNase I hypersensitive sites in promoter elements associated with basal and vitamin D dependent transcription of the bone-specific osteocalcin gene.

Nuclease hypersensitive sites were mapped in the proximal promoter of the osteocalcin gene, which is expressed only in bone cells exhibiting the mature osteoblast phenotype. Nuclei from proliferating and confluent rat osteosarcoma (ROS) 17/2.8 cells were subjected to DNase I digestion, and hypersensitivity was assayed by the indirect end-labeling method, using osteocalcin gene probes. Hypersensitive sites were detected in two promoter domains: -590 to -390, which spans the vitamin D responsive element, and -170 to -70, which spans the TATA box and the CCAAT-containing OC box domain. Together, these elements regulate basal and vitamin D enhanced osteocalcin gene transcription. We observed a parallel relationship between the intensity of bands representing the hypersensitive sites and the extent to which the osteocalcin gene is transcribed. Both in confluent cultures and in response to vitamin D, when osteocalcin transcription was upregulated, the hypersensitive bands were significantly intensified. Additionally, the bands were decreased under conditions that downregulate osteocalcin gene transcription. A functional relationship between the presence of hypersensitive sites and osteocalcin gene transcription is further supported by the absence of hypersensitivity in nonosseous cells that do not express osteocalcin, although these proliferating cells exhibited hypersensitivity in a cell cycle regulated histone gene promoter. Our results suggest the involvement of chromatin structure in transcriptional responsiveness of the osteocalcin gene to physiologic modulation.

Animals↗

PubMed2024

Osteocalcin of maternal and embryonic origins synergize to establish homeostasis in offspring.

Many physiological osteocalcin-regulated functions are affected in adult offspring of mothers experiencing unhealthy pregnancy. Furthermore, osteocalcin signaling during gestation influences cognition and adrenal steroidogenesis in adult mice. Together these observations suggest that osteocalcin may broadly function during pregnancy to determine organismal homeostasis in adult mammals. To test this hypothesis, we analyzed in unchallenged wildtype and Osteocalcin-deficient, newborn and adult mice of various genotypes and origin maintained on different genetic backgrounds, the functions of osteocalcin in the pancreas, liver and testes and their molecular underpinnings. This analysis revealed that providing mothers are Osteocalcin-deficient, Osteocalcin haploinsufficiency in embryos hampers insulin secretion, liver gluconeogenesis, glucose homeostasis, testes steroidogenesis in adult offspring; inhibits cell proliferation in developing pancreatic islets and testes; and disrupts distinct programs of gene expression in these organs and in the brain. This study indicates that osteocalcin exerts dominant functions in most organs it influences. Furthermore, through their synergistic regulation of multiple physiological functions, osteocalcin of maternal and embryonic origins contributes to the establishment and maintenance of organismal homeostasis in newborn and adult offspring.

Animals↗

PubMed1991

Osteocalcin levels in uremic patients: influence of calcitriol treatment through two different routes and type of dialysis.

Osteocalcin, the most abundant non-collagen protein of bone, is synthesized by the osteoblast. Serum osteocalcin concentration depends primarily on new cellular synthesis, and is a sensitive marker of bone turnover reflecting osteoblastic function. In uremic and hemodialysis (HD) patients, a direct relationship between serum osteocalcin and histological parameters of bone formation has been observed. The modality of dialysis may influence serum osteocalcin levels though the available data are controversial. The aim of this study is to assess the acute and chronic effects of calcitriol and the influence of modality of dialysis on serum osteocalcin levels. Twelve patients on continuous ambulatory peritoneal dialysis (CAPD) were treated with calcitriol. For control purposes, 24 patients, 12 on CAPD and 12 on HD, not treated with calcitriol serum osteocalcin levels were included. In CAPD patients previously treated with calcitriol, serum osteocalcin levels were higher than in nontreated patients. The higher levels occur independent of serum levels of parathyroid hormone (PTH), Ca and P. Hemodialysis patients had osteocalcin levels similar to those of CAPD patients under calcitriol treatment. However, the levels of HD patients were higher than CAPD nontreated patients. Serum ionized Ca was similar in CAPD and HD nontreated patients; however, total Ca was significantly higher in HD than in CAPD patients, both with and without calcitriol. After the intravenous administration of calcitriol, serum osteocalcin levels increased from 9.2 + 2.5 to 13.5 + 5.4 ng/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1995

Umbilical cord osteocalcin in normal pregnancies and pregnancies complicated by fetal growth retardation or diabetes mellitus.

A homologous radioimmunoassay for human osteocalcin was used to measure cord serum osteocalcin concentrations in normal pregnancies and in pregnancies complicated by intrauterine growth retardation (IUGR) and diabetes. The mean osteocalcin concentrations in term newborns (100-110 micrograms/l) were comparable with levels that we previously measured in pubertal children. There was a small increase in mean osteocalcin concentrations during the third trimester of fetal life, with the maximum at 35 weeks; between weeks 36 and 41, the osteocalcin levels dropped by 13%. Osteocalcin was 20% lower in IUGR neonates than in age- or weight-matched newborns. The newborns of diabetic mothers had markedly lower osteocalcin concentrations than the weight-matched neonates, and 16 of the 19 samples were more than 1 SD below the mean of the gestational-age osteocalcin regression curve. Cord serum osteocalcin appears to be a useful parameter in studying normal and abnormal fetal mineralization.

Female↗

PubMed1987

Bone and serum concentrations of osteocalcin as a function of 1,25-dihydroxyvitamin D3 circulating levels in bone disorders in rats.

Osteocalcin, the vitamin K-dependent protein in bone containing gamma-carboxyglutamic acid, has been found to be significantly decreased in the osteomalacic bone of chicks made vitamin D deficient for 6 weeks. To evaluate whether this decrease in bone osteocalcin was due directly to the decrease or absence of vitamin D and its metabolites or to the secondary hypocalcemia and osteomalacia or other changes accompanying the deficiency of vitamin D, three experimental groups of Holtzman rats were studied. One group was made rachitic by a diet deficient in vitamin D, and the other groups were made rachitic by diets deficient in inorganic orthophosphate or calcium. The changes in bone and serum osteocalcin, serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], and bone mineral content were evaluated, and morphological evaluation of bone was made. In the vitamin D-deficient animals, osteomalacia was evident histologically by 7 weeks, at which time serum 1,25-(OH)2D3 was not detectable, bone osteocalcin was decreased by 50%, and serum osteocalcin was decreased by 20%. In the animals fed a diet deficient in either calcium or inorganic orthophosphate but which were not depleted of vitamin D, the osteocalcin content of osteomalcic bone was normal, and an increase in the concentration of serum osteocalcin accompanied an increase in serum 1,25-(OH)2D3. These data are consistent with the conclusion that the metabolism of osteocalcin is affected by serum 1,25-(OH)2D3 and that the diminished level of osteocalcin in the bone of vitamin D-deficient animals is the result of a direct action of the metabolites and is not secondary to a decrease in the mineralization of bone tissue.

Animals↗