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      Association between Body Fat and Bone Mineral Density in Normal-Weight Middle-Aged Koreans

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          Abstract

          Background

          Osteoporosis and osteopenia are characterized by reduced bone mineral density (BMD) and increased fracture risk. Although the risk of fractures is higher in underweight people than in overweight people, the accumulation of body fat (especially abdominal fat) can increase the risk of bone loss. This study aimed to evaluate the association between body fat percentage and BMD in normal-weight middle-aged Koreans.

          Methods

          This study included 1,992 adults (mean age, 48.7 years; 52.9% women). BMD and body fat were measured using dual-energy X-ray absorptiometry. Multiple linear regression analyses and analysis of covariance were used to assess the association between BMD and body fat. Body fat percentage was grouped by cut-off values. The cut-off values were 20.6% and 25.7% for men with a body mass index of 18.5–22.9 kg/m 2, while the cut-off values were 33.4% and 36% for women.

          Results

          Body fat percentage tended to be negatively associated with BMD. Increased body fat percentage was associated with reduced BMD in normal-weight middle-aged adults. The effects of body fat percentage on BMD in normal-weight individuals were more pronounced in men than in women.

          Conclusion

          There was a negative correlation between BMD and body fat percentage in middle-aged Korean men and women with normal body weight. This association was stronger in men than in women.

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          Most cited references10

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          Pathways for bone loss in inflammatory disease.

          Chronic inflammation including autoimmune disease is an important risk factor for the development of osteoporosis. Receptor activator of nuclear factor-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) play a central role in osteoclast differentiation and function, and the molecular pathways by which M-CSF and RANKL induce osteoclast differentiation have been analyzed in detail. Proinflammatory cytokines directly or indirectly regulate osteoclastogenesis and bone resorption providing a link between inflammation and osteoporosis. Tumor necrosis factor-α, interleukin (IL)-1, IL-6, and IL-17 are the most important proinflammatory cytokines triggering inflammatory bone loss. Inhibition of these cytokines has provided potent therapeutic effects in the treatment of diseases such as rheumatoid arthritis. Further investigation is needed to understand the pathophysiology and to develop new strategies to treat inflammatory bone loss. This review summarizes new data on inflammatory bone loss obtained in 2011.
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            Postmenopausal osteoporosis as a failure of bone's adaptation to functional loading: a hypothesis.

            There is substantial evidence that bones' ability to withstand functional loading without damage depends on the processes of bone modeling and remodeling, which are responsible for establishing and maintaining bone architecture, being influenced by a feedback mechanism related to the control of functional strains. It is probably useful to consider the diminished ability to maintain bone strength in postmenopausal osteoporosis as a failure of this mechanism. Acceptance of this approach would not only increase understanding of the etiology of postmenopausal osteoporosis but also significantly influence the ways in which it is investigated and treated. This would not mean that the many other factors affecting bone mass and bone cell activity will be ignored, but rather these factors will be put in perspective. Research to prevent or treat osteoporosis could be directed usefully to understanding how osteoblasts, lining cells, and osteocytes respond to mechanically derived information and how these responses are converted into stimuli controlling structurally appropriate modeling and remodeling. Evidence suggesting that early strain-related responses of bone cells in males and females involve the estrogen receptor (ER) could explain decreased effectiveness of this pathway when ER levels are low.
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              Structural adaptation to changing skeletal load in the progression toward hip fragility: the study of osteoporotic fractures.

              Longitudinal, dual-energy X-ray absorptiometry (DXA) hip data from 4187 mostly white, elderly women from the Study of Osteoporotic Fractures were studied with a structural analysis program. Cross-sectional geometry and bone mineral density (BMD) were measured in narrow regions across the femoral neck and proximal shaft We hypothesized that altered skeletal load should stimulate adaptive increases or decreases in the section modulus (bending strength index) and that dimensional details would provide insight into hip fragility. Weight change in the approximately 35 years between scan time points was used as the primary indicator of altered skeletal load. "Static" weight was defined as within 5% of baseline weight, whereas "gain" and 'loss" were those who gained or lost >5%, respectively. In addition, we used a frailty index to better identify those subjects undergoing changing in skeletal loading. Subjects were classified as frail if unable to rise from a chair five times without using arm support. Subjects who were both frail and lost weight (reduced loading) were compared with those who were not frail and either maintained weight (unchanged loading) or gained weight (increased loading). Sixty percent of subjects (n = 2,559) with unchanged loads lost BMD at the neck but not at the shaft, while section moduli increased slightly at both regions. Subjects with increasing load (n = 580) lost neck BMD but gained shaft BMD; section moduli increased markedly at both locations. Those with declining skeletal loads (n = 105) showed the greatest loss of BMD at both neck and shaft; loss at the neck was caused by both increased loss of bone mass and greater subperiosteal expansion; loss in shaft BMD decline was only caused by greater loss of bone mass. This group also showed significant declines in section modulus at both sites. These results support the contention that mechanical homeostasis in the hip is evident in section moduli but not in bone mass or density. The adaptive response to declining skeletal loads, with greater rates of subperiosteal expansion and cortical thinning, may increase fragility beyond that expected from the reduction in section modulus or bone mass alone.
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                Author and article information

                Journal
                Korean J Fam Med
                Korean J Fam Med
                KJFM
                Korean Journal of Family Medicine
                Korean Academy of Family Medicine
                2005-6443
                2092-6715
                March 2019
                16 November 2018
                : 40
                : 2
                : 100-105
                Affiliations
                Department of Family Medicine, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea
                Author notes
                [* ]Corresponding Author: Min-Kyu Choi https://orcid.org/0000-0001-7987-0209 Tel: +82-2-829-5270, Fax: +82-2-829-5365, E-mail: abbi21c@ 123456hallym.or.kr
                Author information
                http://orcid.org/0000-0001-7987-0209
                Article
                kjfm-17-0082
                10.4082/kjfm.17.0082
                6444091
                30441887
                82f4bc8a-eeaa-4c66-988b-8cfbb6a75d5d
                Copyright © 2019 The Korean Academy of Family Medicine

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 4 July 2017
                : 29 August 2017
                : 12 October 2017
                Categories
                Original Article

                Medicine
                abdominal fat,body mass index,osteoporosis
                Medicine
                abdominal fat, body mass index, osteoporosis

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