Serum Adiponectin and Bone Mineral Density in Women (original) (raw)

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1Twin Research and Genetic Epidemiology Unit (J.B.R., A.M.V., U.C.P., T.D.S.), St. Thomas’ Hospital, London SE1 7EH, United Kingdom

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1Twin Research and Genetic Epidemiology Unit (J.B.R., A.M.V., U.C.P., T.D.S.), St. Thomas’ Hospital, London SE1 7EH, United Kingdom

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2Addenbrookes Hospital (K.B.), University of Cambridge, Cambridge CB2 0QQ, United Kingdom

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1Twin Research and Genetic Epidemiology Unit (J.B.R., A.M.V., U.C.P., T.D.S.), St. Thomas’ Hospital, London SE1 7EH, United Kingdom

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1Twin Research and Genetic Epidemiology Unit (J.B.R., A.M.V., U.C.P., T.D.S.), St. Thomas’ Hospital, London SE1 7EH, United Kingdom

*Address all correspondence and requests for reprints to: Dr. T. D. Spector, M.D., Twin Research and Genetic Epidemiology Unit, St. Thomas’ Hospital, London SE1 7EH, United Kingdom.

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Received:

25 September 2006

Accepted:

19 January 2007

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J. B. Richards, A. M. Valdes, K. Burling, U. C. Perks, T. D. Spector, Serum Adiponectin and Bone Mineral Density in Women, The Journal of Clinical Endocrinology & Metabolism, Volume 92, Issue 4, 1 April 2007, Pages 1517–1523, https://doi.org/10.1210/jc.2006-2097
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Abstract

Context: 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.

Objective: The objective of the study was to evaluate the relationship between adiponectin, an adipocyte-derived hormone, and BMD.

Design, Setting, Participants: 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.

Main Outcome Measures: 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.

Results: 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.

Conclusions: 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.

Copyright © 2007 by The Endocrine Society

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