Abstract

Lean body mass (LBM) is a determinant of areal bone mineral density (aBMD) through its mechanical actions and quite possibly through its endocrine functions. The threefold aims of this study are: to determine the effects of obesity (OB) on aBMD and myokines; to examine the potential link between myokines and bone parameters; and to determine whether the effects of LBM on aBMD are mediated by myokines. aBMD and myokine levels were evaluated in relation to the body mass index (BMI) in 179 women. Compared with normal-weight controls (CON; n = 40), women with OB (n = 139) presented higher aBMD, myostatin and follistatin levels and lower irisin levels. Except for irisin levels, all differences between the OB and CON groups were accentuated with increasing BMI. For the whole population (n = 179), weight, BMI, fat mass (FM) and LBM were positively correlated with aBMD at all bone sites, while log irisin were negatively correlated. The proportion of the LBM effect on aBMD was partially mediated (from 14.8% to 29.8%), by log irisin, but not by follistatin or myosin. This study showed that myokine levels were greatly influenced by obesity. However, irisin excepted, myokines do not seem to mediate the effect of LBM on bone tissue.

Highlights

  • Several studies have demonstrated that subjects with obesity present higher areal bone mineral density than normal-weight subjects [1,2,3,4,5]

  • In a large group of subjects with obesity, we confirmed [6] that areal bone mineral density (aBMD) correlates better with a dynamic load resulting from lean body mass (LBM) than a static load allocated to fat mass (FM) and that LBM is independently linked to aBMD [4,16,17,18]

  • This study confirmed that obesity is associated with an increase in aBMD and reduced bone turnover

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Summary

Introduction

Several studies have demonstrated that subjects with obesity present higher areal bone mineral density (aBMD) than normal-weight subjects [1,2,3,4,5]. More surprisingly, a gain in aBMD and microarchitecture adaptations were reported at the radius [3,4,6,9,10], a less mechanically solicited bone site, and these changes cannot be induced only by the gravitational forces associated with increased body weight These results suggest that systemic biologically active molecules, related to obesity, may interact with bone metabolism. In a large group of subjects with obesity, we confirmed [6] that aBMD correlates better with a dynamic load resulting from lean body mass (LBM) than a static load allocated to fat mass (FM) and that LBM is independently linked to aBMD [4,16,17,18] These findings suggest that LBM, rather than FM, has a protective effect on bone tissue in this population. This, in turn, might have repercussions on bone formation and resorption

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