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Review
. 2008 Jan;23(1):17-29.
doi: 10.1359/jbmr.070813.

Correlation of obesity and osteoporosis: effect of fat mass on the determination of osteoporosis

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Review

Correlation of obesity and osteoporosis: effect of fat mass on the determination of osteoporosis

Lan-Juan Zhao et al. J Bone Miner Res. 2008 Jan.

Abstract

It was previously believed that obesity and osteoporosis were two unrelated diseases, but recent studies have shown that both diseases share several common genetic and environmental factors. Body fat mass, a component of body weight, is one of the most important indices of obesity, and a substantial body of evidence indicates that fat mass may have beneficial effects on bone. Contrasting studies, however, suggest that excessive fat mass may not protect against osteoporosis or osteoporotic fracture. Differences in experimental design, sample structure, and even the selection of covariates may account for some of these inconsistent or contradictory results. Despite the lack of a clear consensus regarding the impact of effects of fat on bone, a number of mechanistic explanations have been proposed to support the observed epidemiologic and physiologic associations between fat and bone. The common precursor stem cell that leads to the differentiation of both adipocytes and osteoblasts, as well the secretion of adipocyte-derived hormones that affect bone development, may partially explain these associations. Based on our current state of knowledge, it is unclear whether fat has beneficial effects on bone. We anticipate that this will be an active and fruitful focus of research in the coming years.

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Figures

FIG. 1
FIG. 1
Least-squares mean (±SE) of the TB BMC stratified by percentage fat mass in normal weight (18.5 < BMI ≤ 25.0 kg/m2), overweight (25.0 < BMI ≤ 30.0 kg/m2), and obese (BMI > 30.0 kg/m2) white men and women. Each bar in each BMI stratum represents quartiles (Q) 1, 2, 3, and 4 (from left to right) of percentage fat mass. A linear mixed model was used with age, weight, exercise, and menopause status as covariates to adjust TB BMC. Familial relationships were treated as random effects in the model. *p < 0.0001.
FIG. 2
FIG. 2
Common factors shared in osteoblast and adipocyte differentiation. Osteoblasts and adipocytes originate from common progenitor-mesenchymal stem cells. The balance of their differentiation is determined by several common factors, such as PPAR-γ, Wnt, TGF-β, leptin, and estrogen. Adipocytes express and secrete a variety of bioactive peptides, such as estrogen, resistin, leptin, adiponectin, and inflammatory cytokines. Some of these peptides affect human energy homeostasis and may be involved in bone metabolism. Adapted from Reference 15.

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