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      Local Body Composition Is Associated with Gender Differences of Bone Development at the Forearm in Puberty

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          Background/Aims: The present analyses intend to clarify if gender and puberty modify the relationship between bone development (modeling and remodeling) and fat mass at the forearm. Methods: Data were collected from participants (139 males, 157 females, age = 5–19 years) of the Dortmund Nutritional and Anthropometric Longitudinally Designed study in a cross-sectional investigation. The main outcome measures were total and trabecular bone mineral density (BMDtot and BMDtrab), strength strain index (SSI) and parameters associated with modeling (cortical area, CA; periosteal circumference, CP) and remodeling (cortical bone mineral density, BMDcort, endosteal circumference, CE) were analyzed in their relationship to cross-sectional fat (FA) and muscle area (MA) at the forearm. Results: BMDtot was correlated with FA in pubertal males (r = –0.25). BMDtrab was contrarily predicted by FA in pubertal males and females (r = –0.28 vs. 0.31). FA was correlated with BMDcort (r = –0.32) and CE (r = 0.26) in pubertal females. MA was positively correlated with CA, CP and SSI. Conclusions: Modeling and bone strength were primarily predicted by MA. Markers of remodeling were positively correlated with FA in pubertal females, but not in prepubertal individuals and pubertal males. Therefore, gender and puberty modify the relationship between FA and bone development.

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          Leptin Inhibits Bone Formation through a Hypothalamic Relay

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            Serum leptin level is a regulator of bone mass.

            Leptin is a powerful inhibitor of bone formation in vivo. This antiosteogenic function involves leptin binding to its receptors on ventromedial hypothalamic neurons, the autonomous nervous system and beta-adrenergic receptors on osteoblasts. However, the mechanisms whereby leptin controls the function of ventromedial hypothalamic antiosteogenic neurons remain unclear. In this study, we compared the ability of leptin to regulate body weight and bone mass and show that leptin antiosteogenic and anorexigenic functions are affected by similar amounts of leptin. Using a knock-in of LacZ in the leptin locus, we failed to detect any leptin synthesis in the central nervous system. However, increasing serum leptin level, even dramatically, reduced bone mass. Conversely, reducing serum-free leptin level by overexpressing a soluble receptor for leptin increased bone mass. Congruent with these results, the high bone mass of lipodystrophic mice could be corrected by restoring serum leptin level, suggesting that leptin is an adipocyte product both necessary and sufficient to control bone mass. Consistent with the high bone mass phenotype of lipodystrophic mice, we observed an advanced bone age, an indirect reflection of premature bone formation, in lipodystrophic patients. Taken together, these results indicate that adipocyte-derived circulating leptin is a determinant of bone formation and suggests that leptin antiosteogenic function is conserved in vertebrates.
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              Accurate assessment of precision errors: How to measure the reproducibility of bone densitometry techniques


                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                August 2008
                12 June 2008
                : 70
                : 2
                : 105-111
                aChildren’s Hospital, University of Cologne, Cologne, and bResearch Institute of Child Nutrition, Dortmund, Germany; cDepartment of Pediatrics, Second Medical Faculty, Charles University Prague, Prague, Czech Republic
                139153 Horm Res 2008;70:105–111
                © 2008 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 4, References: 29, Pages: 7
                Original Paper


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