Leptin Is a Negative Independent Predictor of Areal BMD and Cortical Bone Size in Young Adult Swedish Men

Authors

  • Mattias Lorentzon MD, PhD,

    Corresponding author
    1. Center for Bone Research at the Sahlgrenska Academy (CBS), Department of Internal Medicine, Gothenburg University, Gothenburg, Sweden
    • Division of Endocrinology, Department of Internal Medicine, Gröna Sträket 8, Sahlgrenska University Hospital, 413 45 Gothenburg, Sweden
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  • Kerstin Landin,

    1. Center for Bone Research at the Sahlgrenska Academy (CBS), Department of Internal Medicine, Gothenburg University, Gothenburg, Sweden
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  • Dan Mellström,

    1. Center for Bone Research at the Sahlgrenska Academy (CBS), Department of Internal Medicine, Gothenburg University, Gothenburg, Sweden
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  • Claes Ohlsson

    1. Center for Bone Research at the Sahlgrenska Academy (CBS), Department of Internal Medicine, Gothenburg University, Gothenburg, Sweden
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  • The authors state that they have no conflicts of interest.

Abstract

The association between leptin and areal BMD has been controversial, and the predictive role of leptin on cortical volumetric BMD and bone size has not previously been studied. We show that leptin is a negative independent predictor of aBMD (DXA), at several measured sites, and of cortical bone size (pQCT) in a large population of young men.

Introduction: Recent findings suggest that both adipose tissue (AT) and bone mass are regulated by leptin. Previous reports studying the association between leptin and areal BMD (aBMD) have yielded conflicting results. The role of leptin on volumetric BMD (vBMD) and bone size of the cortical and trabecular bone compartments has not previously been studied.

Materials and Methods: The Gothenburg Osteoporosis and Obesity Determinants (GOOD) study is a population-based study of 1068 men (age, 18.9 ± 0.6 [SD] years). aBMD of the total body, lumbar spine, femoral neck, both radii, and trochanter, as well as total body AT and lean mass (LM) were measured using DXA, whereas cortical and trabecular vBMD and bone size were measured by pQCT.

Results: Total body LM could explain a larger magnitude of the difference in the variation in aBMD and cortical bone size than what total body AT could (total body aBMD: LM 37.4% versus AT 8.7%; tibia cross-sectional area [CSA]: LM 46.8% versus AT 5.6%). The independent role of leptin on bone parameters was studied using a multiple linear regression model, including age, total body LM and AT, height, present physical activity, calcium intake, and smoking as covariates. Leptin was found to be a negative independent predictor of aBMD (total body: β =−0.08, p =0.01; lumbar spine: β =−0.13, p < 0.01; trochanter: β =−0.09, p =0.01), as well as of the cortical bone size (CSA and thickness) of both the radius (CSA: β =−0.12, p < 0.001) and tibia (CSA: β =−0.08, p < 0.01), but not of the cortical or trabecular vBMD of these bones.

Conclusion: Our results indicate that LM has a greater impact on bone mass than AT. Our findings further show that leptin is a negative independent predictor of aBMD at several measured sites and of bone parameters reflecting cortical bone size, but not vBMD, in a large population of young Swedish men.

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