Influence of lean and fat mass on bone mineral density (BMD) in postmenopausal women with osteoporosis

Dytfeld, Joanna; Ignaszak-Szczepaniak, Magdalena; Gowin, Ewelina; Michalak, Michał; Horst‐Sikorska, Wanda

doi:10.1016/j.archger.2011.01.002

Cited by 39 publications

(24 citation statements)

References 33 publications

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“…The multiple regression analyses, revealed that these constitutive and body composition factors make the strongest contribution to explained the dependents variables, when the variance explained by all other variables in the model was controlled for. Specifically, age, TLTM and TFM for FNBMD in both genders and TFM in men and TFM and age in women for LSBMD and FSI, Other studies have shown that age (Hannan et al, 2000), BM (Dargent-Molina et al, 2000;Felson et al, 1993), TLTM (Dytfeld et al, 2011;Ho-Pham et al, 2010;Travison, Araujo, Esche, Beck, & McKinlay 2008) and TFM (Ho-Pham et al, 2010) are important predictors of BMD in older adults males and females, corroborating our findings. Results from multiple regression analysis in our study, showed that age, TLTM and TFM entered as the primary and most significant contributors for FNBMD in our study, accounting for between 13-21.1% and 16.2-36.9% of the explained variation in these measures in males and females, respectively.…”

Section: Predictorssupporting

confidence: 81%

Multivariate analysis of lifestyle, constitutive and body composition factors influencing bone health in community-dwelling older adults from Madeira, Portugal

Gouveia

Blimkie

Maia

et al. 2014

Archives of Gerontology and Geriatrics

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Section: Predictorssupporting

confidence: 81%

Multivariate analysis of lifestyle, constitutive and body composition factors influencing bone health in community-dwelling older adults from Madeira, Portugal

Gouveia

Blimkie

Maia

et al. 2014

Archives of Gerontology and Geriatrics

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“…By contrast, a number of previous studies have observed that increased BMI is a positive factor on femur cortical bone mass due to its effect on leptin signaling (12). However, an increasing number of studies have indicated that obesity in female mice is accompanied by bone loss (8,(13)(14)(15). This may be due to the role of adipose tissue as an endocrine organ, secreting pro-inflammatory cytokines, whose effects damage the trabecular bone (16).…”

Section: Discussionmentioning

confidence: 52%

Adipocytes regulate the bone marrow microenvironment in a mouse model of obesity

Hang

et al. 2013

Molecular Medicine Reports

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Abstract. Obesity is markedly associated with abnormal bone density indicating the importance of adipocytes in bone metabolism. However, the specific function of adipocytes remains unclear, with marked discrepancies in observations of previous studies. In the present study, the effect of adipocytes on osteoblasts/osteoclasts was analyzed. A mouse model of obesity was established and an in vitro co-culture system was utilized containing adipocyte and MC3T3/RAW 264.7 cells in a Transwell plate. Compared with control mice, obese mice exhibited low body weight and bone mineral density of the tibia and fat cells were observed to accumulate in bone marrow. MC3T3/RAW 264.7 cells were co-cultured with adipocytes and the mRNA and protein expression of alkaline phosphatase and osteocalcin was found to be decreased in MC3T3-E1 cells and mRNA and protein expression of tartrate-resistant acid phosphatase and cathepsin K was significantly increased in RAW 264.7 cells. In addition, the effect of adipocytes on the osteoprotegerin (OPG)/receptor activator of nuclear factor κB ligand (RANKL)/RANK system indicated that the RANKL/OPG ratio secreted by osteoblasts increased and RANK expression by osteoclasts increased, leading to increased osteoclastogenesis. These results indicate that bone metabolism is impaired in obese mice leading to decreased osteoblastogenesis and marked increases in osteoclastogenesis and low bone mass. IntroductionObesity is becoming increasingly prevalent, leading to reduced life expectancy and increased health problems (1). High body mass index (BMI) is associated with various diseases, including cardiovascular, obstructive sleep apnea, diabetes mellitus type 2, specific types of cancer and osteoarthritis (2). Bone metabolism is also abnormal in obesity (3) and positive and negative factors have been identified to be associated with bone health status (4-6). A number of previous studies have revealed that obesity stimulates bone formation by inhibiting apoptosis. A recent study demonstrated that high BMI prevents normal bone fracture and osteoporotic fracture in various age groups and genders (7). By contrast, it has also been reported that osteoporosis occurs in obese individuals (8). These inconsistencies may be due to the use of different animal models in each study.Adipose tissue, a large endocrine organ, secretes a number of hormones that affect bone metabolism. Adipocytes in the bone marrow microenvironment differentiate from bone marrow mesenchymal cells and secrete cytokines which affect osteoblast and osteoclast levels in bone marrow. The effect of adipocytes on osteoblasts/osteoclasts remains controversial.The aim of the present study was to identify the function of adipocytes in the bone marrow microenvironment. To analyze the biological foundations of bone metastasis in obesity, a high-fat diet was selected to establish a mouse model of obesity (9). The results indicate that adipocytes accumulate in the bone marrow environment and affect bone turnover and osteoblast/osteoclast differentiation....

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“…Body weight is made up of two components, fat mass and lean mass. The relative contribution of these two components to the variation in BMD has been controversial, although in postmenopausal women fat mass has been often shown to be important (Reid et al 1992, Dytfeld et al 2011. The intimate association between fat and bone has been extensively described.…”

Section: Introductionmentioning

confidence: 99%

AMP-activated protein kinase pathway and bone metabolism

Jeyabalan

Shah²,

Viollet³

et al. 2011

Journal of Endocrinology

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There is increasing evidence that osteoporosis, similarly to obesity and diabetes, could be another disorder of energy metabolism. AMP-activated protein kinase (AMPK) has emerged over the last decade as a key sensing mechanism in the regulation of cellular energy homeostasis and is an essential mediator of the central and peripheral effects of many hormones on the metabolism of appetite, fat and glucose. Novel work demonstrates that the AMPK signaling pathway also plays a role in bone physiology. Activation of AMPK promotes bone formation in vitro and the deletion of a or b subunit of AMPK decreases bone mass in mice. Furthermore, AMPK activity in bone cells is regulated by the same hormones that regulate food intake and energy expenditure through AMPK activation in the brain and peripheral tissues. AMPK is also activated by antidiabetic drugs such as metformin and thiazolidinediones (TZDs), which also impact on skeletal metabolism. Interestingly, TZDs have detrimental skeletal side effects, causing bone loss and increasing the risk of fractures, although the role of AMPK mediation is still unclear. These data are presented in this review that also discusses the potential roles of AMPK in bone as well as the possibility for AMPK to be a future therapeutic target for intervention in osteoporosis.

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Influence of lean and fat mass on bone mineral density (BMD) in postmenopausal women with osteoporosis

Cited by 39 publications

References 33 publications

Multivariate analysis of lifestyle, constitutive and body composition factors influencing bone health in community-dwelling older adults from Madeira, Portugal

Multivariate analysis of lifestyle, constitutive and body composition factors influencing bone health in community-dwelling older adults from Madeira, Portugal

Adipocytes regulate the bone marrow microenvironment in a mouse model of obesity

AMP-activated protein kinase pathway and bone metabolism

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