Relationship of body composition and circulatory adiponectin to bone mineral density in young premenopausal women.
Suwannee ChanprasertyothinSunee SaetungPenpan PayattikulRajata RajatanavinBoonsong Ongphiphadhanakul
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Adiponectin is a recently discovered hormone secreted by adipocytes. Adiponectin plays an important role in the regulation of insulin sensitivity as well as the propensity to inflammation and atherosclerosis. In the present study, the authors explore the relationship between adiponectin and bone mass in premenopausal women. The relationship of fat mass compared to lean body mass to bone mass was also investigatedTwo hundred premenopausal women aged between 20 and 40 years were studied. Bone mineral density (BMD) was measured at L2-4 and femoral neck by dual-energy X-ray absorptiometry (DEXA). Serum adiponectin concentrations were measured by radioimmunoassay.At the lumbar spines, factors associated with BMD were age (p < 0.01) and lean body mass (p < 0.001). No independent association with fat mass was demonstrated Likewise, at the femoral neck, only lean body mass was related to BMD (p < 0. 01). In terms of the relation of serum adiponectin to BMD, no association of serum adiponectin to BMD at the lumbar spines or femoral neck was foundAltogether, the present findings do not suggest the independent role of adiponectin in the accrual of bone mass in females, although such a role still cannot be excluded in men or postmenopausal women.Cite
Abstract Our study indicates that recombinant adiponectin induced RANKL and inhibited OPG expression in human osteoblasts through the AdipoR1/p38 MAPK pathway, and these responses contributed to the adiponectin-induced osteoclasts formation in the co-culture of osteoblast and peripheral blood monocytes systems. These findings showed that adiponectin increased osteoclast formation indirectly through stimulating RANKL and inhibiting OPG production in osteoblasts. It also suggests the pharmacological nature of recombinant adiponectin that indirectly induces osteoclasts formation. Introduction: Recently, adiponectin has emerged as an element in the regulation of bone metabolism, but the mechanism remains. This study was undertaken to investigate the action of adiponectin on osteoclastogenesis through revealing RANKL and osteoprotegerin (OPG) expression in osteoblasts and osteoclast formation. Materials and Methods: Real-time quantitative PCR and ELISA were used to detect RANKL and OPG mRNA and protein expression in cultured human osteoblasts. The involved signal pathway was studied using mitogen-activated protein kinase (MAPK) inhibitor and adiponectin receptor 1 (AdipoR1) siRNA. The effects of recombinant adiponectin on osteoclasts formation also were examined in the co-culture systems of osteoblast and peripheral blood monocytes (PBMCs) systems or purified CD14 + PBMCs cultures. Results: Our study showed that recombinant adiponectin induced RANKL and inhibited OPG mRNA expression in human osteoblasts in a dose- and time-dependent manner. Adiponectin also increased soluble RANKL and decreased OPG secretion in osteoblasts conditioned media. Suppression of AdipoR1 with siRNA abolished the adiponectin-regulated RANKL and OPG mRNA expression in osteoblasts. Furthermore, pretreatment of osteoblasts with the MAPK inhibitor SB203580 abolished adiponectin-regulated RANKL and OPG mRNA expression. Adiponectin induced osteoclast formation in the co-culture systems of osteoblast and PBMCs systems, and OPG entirely blocked this response. However, adiponectin had no direct effect on the differentiation of osteoclast precursor purified CD14 + PBMCs. Conclusions: These data indicate that recombinant adiponectin induced RANKL and inhibited OPG expression in human osteoblasts through the AdipoR1/p38 MAPK pathway, and these responses contributed to the adiponectin-induced osteoclast formation in the co-culture of osteoblast and PBMCs systems. These findings showed that adiponectin increased osteoclast formation indirectly through stimulating RANKL and inhibiting OPG production in osteoblasts. It suggests the pharmacological nature of recombinant adiponectin that indirectly induces osteoclasts formation.
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Fat mass is a predictor of BMD; however, the mechanisms involved remain uncertain. Two adipokines, leptin and adiponectin, were examined as potential mediators of this relation in 80 perimenopausal women. Adiponectin did not exert any effect on BMD, whereas leptin exerted a negative one, with insulin acting as a confounder to this relation.Fat mass is an important determinant of bone density, but the mechanism involved in this relation is uncertain. Leptin and adiponectin, as circulating peptides of adipocyte origin, are potential contributors to this relation. We investigated the role of leptin and adiponectin in mediating fat mass effects on the skeleton of perimenopausal women.Twenty-five premenopausal and 55 postmenopausal, healthy women (42-68 years old) participated in our study. Lumbar spine BMD (BMD(L2-L4)) and total body BMC (TBBMC) were measured with DXA, leptin levels with ELISA, and adiponectin levels with radioimmunoassay (RIA). Additionally, body composition analysis was performed, as well as measurements of several hormones.It was shown that serum leptin levels were negatively correlated with BMD (beta = -0.005, p = 0.027) and TBBMC (beta = -14.32, p = 0.013). The above correlation was observed only when serum insulin levels were included, as an independent variable, in the regression analysis model. Adiponectin was not significantly correlated with BMD(L2-L4) nor with TBBMC, either in the presence or absence of insulin.Circulating adiponectin does not seem to exert any effect on bone mass. In contrast, circulating leptin showed a negative correlation with bone mass, dependent on serum insulin levels.
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Recent evidence suggests that adiponectin may play a role in bone metabolism. Previous studies demonstrated that the adiponectin levels had a negative correlation with bone mineral density (BMD) in women. However, little is known about the relationship between adiponectin and BMD in men. The aim of this study was to determinate the relationship between the adiponectin levels and BMD in elderly men.Cross-sectional study including 92 healthy men aged 60-80 years.Main outcome measures were the adiponectin levels estimated by RIA and BMD at lumbar spine and femoral neck using dual energy X-ray absorptiometry. Results The negative correlation between adiponectin and BMD at the spine was r=-0.209, (P<0.05) and at the femoral neck was r=-0.237, (P<0.001). These correlations disappeared after adjustment for body mass index (BMI). When stratified by BMI, the relationship between BMD and adiponectin remained significant in the subgroup of participants with BMI >27 kg/m(2), but disappeared in men with BMI 27.BMD is negatively associated with the adiponectin levels in men older than 60 years and this relationship is greater in those men with BMI >27, which suggests a plausible connection between bone and fat tissue.
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The aim of the current investigation was to determine the possible relationships of fasting adiponectin level with body composition, bone mineral, insulin sensitivity, leptin, and cardiorespiratory fitness parameters in 153 women. Subjects were classified as premenopausal ( n = 42; 40.8 ± 5.7 yr) if they had regular menstrual periods, early postmenopausal ( n = 49; 56.7 ± 3.6 yr) if they had been postmenopausal for more than >1 yr but <7 yr (5.5 ± 1.3 yr), and postmenopausal ( n = 62; 72.2 ± 4.5 yr) if they had been postmenopausal for >7 yr. All women studied had a body mass index (BMI) <30 kg/m 2 . Adiponectin values were higher ( P < 0.05) in middle-aged (12.0 ± 5.1 μg/ml) and older (15.3 ± 7.3 μg/ml) postmenopausal women compared with middle-aged premenopausal women (8.4 ± 3.2 μg/ml). Mean plasma adiponectin concentration in the total group of women ( n = 153) was 12.2 ± 6.3 μg/ml and was positively related ( P < 0.05) to age, indexes of overall obesity (BMI, body fat mass), and cardiorespiratory fitness (PWC) values. In addition, a negative association ( P < 0.05) between adiponectin with central obesity (waist-to-hip and waist-to-thigh ratio), fat-free mass, bone mineral (bone mineral content, total and lumbar spine bone mineral density), and leptin and insulin resistance (insulin, fasting insulin resistance index) values was observed. However, multivariate regression analysis revealed that only age, fasting insulin resistance index, and leptin were independent predictors of adiponectin concentration. In conclusion, circulating adiponectin concentrations increase with age in normal-weight middle-aged and older women. It appears that adiponectin is independently related to age, leptin, and insulin resistance values in women across the age span and menstrual status.
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Recent evidence suggests that adiponectin may play a role in bone metabolism, but studies of the correlation between serum adiponectin and bone mineral density (BMD) have given conflicting results, and the impact on fracture risk is unknown.Our objective was to investigate the association between serum adiponectin levels and BMD and fracture risk. DESIGN, SETTING, PARTICIPANTS, MAIN OUTCOME MEASURES: We used regression analyses to estimate the relationship between adiponectin and BMD in the Prospective Investigation of the Vasculature in Uppsala Seniors cohort of 441 men and 457 women aged 70 yr. The association was thereafter analyzed in the Uppsala Longitudinal Study of Adult Men (ULSAM), in which adiponectin was analyzed at age 70 yr and BMD at 82 yr in 507 men. Fractures in the ULSAM were documented in 314 men during 15 yr follow-up. Cox regression analysis was used to determine the risk of fracture according to serum adiponectin levels.In multivariable analysis a negative association between adiponectin and BMD was found in both cohorts. When individuals in the highest quintile of adiponectin were compared with those in the lowest quintile, adjusted BMD was 9.7% lower at the lumbar spine, 7.1% lower at the proximal femur, and 5.2% lower for total body in the Prospective Investigation of the Vasculature in Uppsala Seniors (P < 0.001 for all three), and 8.1, 5.1, and 4.1% (P < 0.003 for all three), respectively, in the ULSAM. However, the hazard ratio for fracture per 1 sd of serum adiponectin was 0.99 (95% confidence interval 0.89-1.11).Although adiponectin was a negative determinant of BMD in two independent cohorts, it was not associated with fracture risk in men.
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Bone mineral density (BMD) is positively associated with body weight. This association persists even at non-load bearing sites, suggesting that a nonmechanical factor such as an adipocyte-derived hormone may modulate BMD.The objective of the study was to evaluate the relationship between adiponectin, an adipocyte-derived hormone, and BMD.A total of 1735 nondiabetic women were recruited from a large, population-based cohort (mean age, 50.0 yr). We employed linear regression methods to estimate the relationship between adiponectin and BMD.Percentage change in BMD (as measured at total hip, spine, femoral neck, and forearm) and markers of bone turnover associated with a doubling of fasting serum adiponectin levels were measured.Employing age-adjusted analysis, each doubling of serum adiponectin was associated with a mean 2.7% decrease in BMD [total hip, -3.2% (95% confidence interval, -4.1, -2.3); femoral neck, -3.1% (-4.0, -2.1); forearm, -2.0 (-2.6, -1.4); spine, -2.6 (-3.5, -1.7)]. After adjustment for potential confounding factors, including BMI, serum leptin, central fat mass, hormone replacement therapy, smoking, and exercise, this relationship persisted, although decreased in magnitude. When stratified by menopausal status, the relationship between serum adiponectin and BMD strengthened in postmenopausal women but disappeared in premenopausal women. Serum adiponectin was positively associated with serum osteocalcin but not with urine deoxypyridinoline.After adjustment of measures of body fat, increasing levels of adiponectin were associated with a decrease in BMD, even at non-load bearing sites. These data suggest that adiponectin, an adipocyte-derived hormone, may play a role in bone metabolism through nonmechanical mechanisms and that this effect may be mediated by menopausal status.
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