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      BMI and BMD: The Potential Interplay between Obesity and Bone Fragility

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          Abstract

          Recent evidence demonstrating an increased fracture risk among obese individuals suggests that adipose tissue may negatively impact bone health, challenging the traditional paradigm of fat mass playing a protective role towards bone health. White adipose tissue, far from being a mere energy depot, is a dynamic tissue actively implicated in metabolic reactions, and in fact secretes several hormones called adipokines and inflammatory factors that may in turn promote bone resorption. More specifically, Visceral Adipose Tissue (VAT) may potentially prove detrimental. It is widely acknowledged that obesity is positively associated to many chronic disorders such as metabolic syndrome, dyslipidemia and type 2 diabetes, conditions that could themselves affect bone health. Although aging is largely known to decrease bone strength, little is yet known on the mechanisms via which obesity and its comorbidities may contribute to such damage. Given the exponentially growing obesity rate in recent years and the increased life expectancy of western countries it appears of utmost importance to timely focus on this topic.

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          Most cited references204

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          Annual medical spending attributable to obesity: payer-and service-specific estimates.

          In 1998 the medical costs of obesity were estimated to be as high as $78.5 billion, with roughly half financed by Medicare and Medicaid. This analysis presents updated estimates of the costs of obesity for the United States across payers (Medicare, Medicaid, and private insurers), in separate categories for inpatient, non-inpatient, and prescription drug spending. We found that the increased prevalence of obesity is responsible for almost $40 billion of increased medical spending through 2006, including $7 billion in Medicare prescription drug costs. We estimate that the medical costs of obesity could have risen to $147 billion per year by 2008.
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            Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia.

            Plasma concentrations of adiponectin, a novel adipose-specific protein with putative antiatherogenic and antiinflammatory effects, were found to be decreased in Japanese individuals with obesity, type 2 diabetes, and cardiovascular disease, conditions commonly associated with insulin resistance and hyperinsulinemia. To further characterize the relationship between adiponectinemia and adiposity, insulin sensitivity, insulinemia, and glucose tolerance, we measured plasma adiponectin concentrations, body composition (dual-energy x-ray absorptiometry), insulin sensitivity (M, hyperinsulinemic clamp), and glucose tolerance (75-g oral glucose tolerance test) in 23 Caucasians and 121 Pima Indians, a population with a high propensity for obesity and type 2 diabetes. Plasma adiponectin concentration was negatively correlated with percent body fat (r = -0.43), waist-to-thigh ratio (r = -0.46), fasting plasma insulin concentration (r = -0.63), and 2-h glucose concentration (r = -0.38), and positively correlated with M (r = 0.59) (all P < 0.001); all relations were evident in both ethnic groups. In a multivariate analysis, fasting plasma insulin concentration, M, and waist-to-thigh ratio, but not percent body fat or 2-h glucose concentration, were significant independent determinates of adiponectinemia, explaining 47% of the variance (r(2) = 0.47). Differences in adiponectinemia between Pima Indians and Caucasians (7.2 +/- 2.6 vs. 10.2 +/- 4.3 microg/ml, P < 0.0001) and between Pima Indians with normal, impaired, and diabetic glucose tolerance (7.5 +/- 2.7, 6.1 +/- 2.0, 5.5 +/- 1.6 microg/ml, P < 0.0001) remained significant after adjustment for adiposity, but not after additional adjustment for M or fasting insulin concentration. These results confirm that obesity and type 2 diabetes are associated with low plasma adiponectin concentrations in different ethnic groups and indicate that the degree of hypoadiponectinemia is more closely related to the degree of insulin resistance and hyperinsulinemia than to the degree of adiposity and glucose intolerance.
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              The medical care costs of obesity: an instrumental variables approach.

              This paper is the first to use the method of instrumental variables (IV) to estimate the impact of obesity on medical costs in order to address the endogeneity of weight and to reduce the bias from reporting error in weight. Models are estimated using restricted-use data from the Medical Expenditure Panel Survey for 2000-2005. The IV model, which exploits genetic variation in weight as a natural experiment, yields estimates of the impact of obesity on medical costs that are considerably higher than the estimates reported in the previous literature. For example, obesity is associated with $656 higher annual medical care costs, but the IV results indicate that obesity raises annual medical costs by $2741 (in 2005 dollars). These results imply that the previous literature has underestimated the medical costs of obesity, resulting in underestimates of the economic rationale for government intervention to reduce obesity-related externalities. Copyright © 2011 Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                28 May 2016
                June 2016
                : 13
                : 6
                : 544
                Affiliations
                [1 ]Department of Endocrinology and Diabetes, University Campus Bio-Medico, Via Alvaro del Portillo, 21, Rome 00128, Italy; d.tuccinardi@ 123456unicampus.it (D.T.); g.defeudis@ 123456unicampus.it (G.D.); a.pantano@ 123456unicampus.it (A.L.P.); n.napoli@ 123456unicampus.it (N.N.); p.pozzilli@ 123456unicampus.it (P.P.); s.manfrini@ 123456unicampus.it (S.M.)
                [2 ]Department of Experimental Medicine, Sapienza University of Rome, Rome 00185, Italy; mikiko.watanabe@ 123456gmail.com
                [3 ]Department of Experimental Medicine, Polo Pontino, Sapienza University of Rome, Rome 00185, Italy; luca.donofrio@ 123456live.com
                [4 ]Centre of Diabetes, Barts & the London School of Medicine, London E1 2AT, UK
                Author notes
                [* ]Correspondence: a.palermo@ 123456unicampus.it ; Tel.: +39-062-254-1696
                [†]

                These authors contributed equally to this work.

                Article
                ijerph-13-00544
                10.3390/ijerph13060544
                4924001
                27240395
                097d27d2-2028-4426-9788-5e1b92d5ed5b
                © 2016 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 27 March 2016
                : 19 May 2016
                Categories
                Review

                Public health
                osteoporosis,obesity,inflammation,fracture,body composition
                Public health
                osteoporosis, obesity, inflammation, fracture, body composition

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