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Brief introduction on osteocalcin (OCN) Bone, at earlier times, had mostly been regarded as a static and isolated organ believed to provide only structural support to the body ( Elefteriou et al. 2014 ). However, more interesting discoveries
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homoeostasis. The revelation that bone itself regulates energy metabolism in a reciprocal manner via a secreted hormone osteocalcin (OC) was finally uncovered several years ago ( Lee et al . 2007 ). Thus, in the last few years, an explosion of avant
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Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, Fukuoka, Japan
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Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, Fukuoka, Japan
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. 2018 ), interventions to reverse this disease and its related disorders are of particular clinical importance. Many recent studies have revealed that the osteoblast-derived hormone osteocalcin in its uncarboxylated form (GluOC) is able to reverse the
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Department of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, Texas, USA
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Department of Cell and Microbiology, Weill Cornell Medical College, New York, New York, USA
Department of Genetics, The University of Texas Anderson Cancer Center, Houston, Texas, USA
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Department of Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, Texas, USA
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Department of Cell and Microbiology, Weill Cornell Medical College, New York, New York, USA
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( Seferovic et al. 2018 ). The bone-derived hormone osteocalcin (OC) acts uniquely in a feed-forward loop and binds to pancreatic β-cells ( Pi et al. 2011 ); OC −/− mice are both hyperglycemic and hypoinsulinemic, demonstrating poor insulin sensitivity
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osteocalcin (a marker of bone formation) did not change ( Labib et al. 1989 , Sripanyakorn et al. 2009 ). In addition, serum CTX and osteocalcin levels increased in postmenopausal women following 2 weeks of abstinence from ethanol, and these levels
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in the regulation of energy metabolism. Indeed, in mice, osteocalcin (OC), a molecule produced by osteoblasts has been found to increase both the secretion and sensitivity of insulin, in addition to increasing the number of insulin-producing cells and
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ABSTRACT
Indirect evidence has suggested that the kidney is a major organ of clearance for osteocalcin, a circulating marker of osteoblast function. The objectives of the present study were (1) to confirm the role of the kidney in osteocalcin clearance (2) to quantify the contribution of extrarenal sites and (3) to investigate the renal mechanism(s) of osteocalcin clearance. Plasma osteocalcin levels, osteocalcin plasma clearance rate (PCR) and plasma production rate (PPR) were determined in oophorectomized (OX) and uninephrectomized oophorectomized (UOX) sheep. The osteocalcin renal extraction efficiency (REE) and the effective renal plasma flow (ERPF) were measured, and the osteocalcin renal clearance rate (RCR) was calculated.
The osteocalcin PCR was reduced significantly in UOX compared with OX sheep (2·0±0·1 (n = 9) vs 2·5±0·1 litres/h (n = 44); P < 0·0005). In UOX sheep with plasma creatinine levels ≤ 130 μmol/l, the osteocalcin REE was 9±1·3% and the osteocalcin RCR was 50–91% of osteocalcin PCR (n = 4). In UOX sheep with plasma creatinine levels in the range 100–440 μmol/l, there was a linear relationship between osteocalcin PCR and ERPF; the osteocalcin RCR was related to the osteocalcin PCR (RCR = 0·9 × PCR −0·50). Intravenous infusion of the synthetic glucocorticoid triamcinolone acetonide (TA) in UOX sheep led to marked decrements in plasma osteocalcin levels and the osteocalcin PPR, and a significant increase in the osteocalcin PCR. These changes were accompanied by a 44% increase in ERPF. During i.v. infusion of 125I-labelled osteocalcin in three UOX sheep, the urinary excretion of trichloroacetic acid-precipitable radioactivity represented 27% (range 22–31%) of the amount cleared by the kidney. Bio-Gel P6 chromatography of urine suggested the presence of intact 125I-labelled osteocalcin and at least one radiolabelled osteocalcin fragment.
These findings confirm that the kidney is the major site of osteocalcin clearance and show that extrarenal sites also make an appreciable contribution. ERPF is an important determinant of the osteocalcin PCR. Augmentation of the ERPF by TA may mediate the induction of osteocalcin clearance by this glucocorticoid. In the UOX sheep, urinary excretion of intact osteocalcin may account for up to 30% of renal osteocalcin clearance.
Journal of Endocrinology (1991) 130, 213-221
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ABSTRACT
Concentrations of osteocalcin were measured in plasma and bone of normal and diabetic rats during the reproductive cycle and compared with plasma 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) concentrations. The age-dependence of osteocalcin was also examined. Plasma concentrations of osteocalcin levels were low but detectable in 21-day-old fetuses (3·7 ± 0·3 nmol/l); osteocalcin concentrations were highest in weaning rats (104 ± 9 nmol/l) and decreased thereafter. In adult rats, plasma concentrations of both osteocalcin and 1,25-(OH)2D3 increased during the last days of normal pregnancy, and even more so in rats fed a diet low in calcium and phosphate. After an early post-partum decline, osteocalcin concentrations in plasma remained at non-pregnant levels in lactating rats fed a high calcium/phosphate diet while their 1,25-(OH)2D3 concentrations were higher than in non-pregnant rats; however, lactating rats fed a low calcium/phosphate diet showed increasing osteocalcin concentrations.
In spontaneously diabetic BB rats, plasma osteocalcin concentrations were severely decreased compared with those in non-diabetic rats, more than would have been expected from their decreased 1,25-(OH)2D3 concentrations. Moreover, plasma osteocalcin did not increase during pregnancy or lactation in diabetic rats, even when fed a low calcium/phosphate diet. Fetuses of diabetic rats also had lower plasma osteocalcin levels than fetuses from non-diabetic rats or than weight-matched fetuses from semistarved rats. In contrast to plasma osteocalcin concentrations, bone osteocalcin concentrations and content were not altered by pregnancy, lactation, low calcium/phosphate diet or diabetes.
These data show that plasma osteocalcin concentrations change during the reproductive period in normal rats but not in diabetic rats, and that osteocalcin levels do not seem to be regulated solely by 1,25-(OH)2D3.
Journal of Endocrinology (1989) 120, 143–151
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ABSTRACT
The effects of six natural vitamin D metabolites of potential biological and therapeutic interest, 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), 25-hydroxyvitamin D3 (25-OH-D3), 24R,25-dihydroxyvitamin D3 (24R,25-(OH)2D3), 1,24R,25-trihydroxyvitamin D3 (1,24R,25-(OH)3D3), 25S,26-dihydroxyvitamin D3 (25S,26-(OH)2D3) and 1,25S,26-trihydroxyvitamin D3 (1,25S,26-(OH)3D3) on cell replication and expression of the osteoblastic phenotype in terms of osteocalcin production were examined in cultured human bone cells. At a dose of 5 × 10−12 mol/l, 1,25-(OH)2D3 stimulated cell proliferation, whereas at higher doses (5 × 10−9−5 × 10 −6 mol/l) cell growth was inhibited in a dose-dependent manner. The same pattern of effects was seen for the other metabolites in a rank order of potency: 1,25-(OH)2D3> 1,25S,26-(OH)3D3 = 1,24R,25-(OH)3D3>25S,26-(OH)2D3 = 24R,25-(OH)2D3 = 25-OH-D3. Synthesis of osteocalcin was induced by 1,25-(OH)2D3 in doses similar to those required to inhibit cell proliferation. Biphasic responses were observed for some of the metabolites in terms of osteocalcin synthesis, inhibitory effects becoming apparent at 5 × 10−6 mol/l. The cells did not secrete osteocalcin spontaneously. These results indicate that vitamin D metabolites may regulate growth and expression of differentiated functions of normal human osteoblasts.
J. Endocr. (1985) 105, 391–396
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Serum osteocalcin is a sensitive marker of suppressive effects of exogenous glucocorticoids on bone turnover. It has been suggested, however, that the degree of suppression detected by different assays may vary. Whether discrepancies between various assays influence conclusions from group studies of exogenous glucocorticoids has not been evaluated. The aim of the present study was to compare the CAP fluoroimmunoassay (FEIA), OSTK-PR and ELSA-OSTEO assays for assessment of prednisolone-induced effects on serum osteocalcin. Twelve men and eight premenopausal women aged 19-45 (mean 31) years were studied. All subjects were healthy. The design was a randomised double-blind, placebo-controlled parallel- group study with 2 days run-in, 3 days treatment and 4 days run-out. During run-in and run-out no medication was given. During the treatment period the subjects took either 20 mg prednisolone twice daily or placebo. Blood was collected on the last day of each period. Intra- and intergroup comparisons showed prednisolone treatment to be associated with a statistically significant suppression of osteocalcin which was detected by all assays (ANOVA;P<0.0001). In the individual subjects the response to prednisolone was the same for each assay. The CAP FEIA, OSTK-PR and ELSA-OSTEO assays seem equally sensitive for evaluation of osteocalcin in group studies of oral glucocorticoids.
