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      Puberty and Body Composition

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          Abstract

          Body composition during puberty is a marker of metabolic changes that occur during this period of growth and maturation, and, thus, holds key information regarding current and future health. During puberty, the main components of body composition (total body fat, lean body mass, bone mineral content) all increase, but considerable sexual dimorphism exists. Methods for measuring body composition (e.g. densitometry and dual-energy X-ray absorptiometry) and degree of maturity will be discussed in this review. Components of body composition show age-to-age correlations (i.e. ‘tracking’), especially from adolescence onwards. Furthermore, adipose tissue is endocrinologically active and is centrally involved in the interaction between adipocytokines, insulin and sex-steroid hormones, and thus influences cardiovascular and metabolic disease processes. In conclusion, pubertal body composition is important, not only for the assessment of contemporaneous nutritional status, but also for being linked directly to the possible onset of chronic disease later in life and is, therefore, useful for disease risk assessment and intervention early in life.

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          Most cited references 13

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          Body composition estimates from NHANES III bioelectrical impedance data.

          Body composition estimates for the US population are important in order to analyze trends in obesity, sarcopenia and other weight-related health conditions. National body composition estimates have not previously been available. To use transformed bioelectrical impedance analysis (BIA) data in sex-specific, multicomponent model-derived prediction formulae, to estimate total body water (TBW), fat-free mass (FFM), total body fat (TBF), and percentage body fat (%BF) using a nationally representative sample of the US population. Anthropometric and BIA data were from the third National Health and Nutrition Examination Survey (NHANES III; 1988-1994). Sex-specific BIA prediction equations developed for this study were applied to the NHANES data, and mean values for TBW, FFM, TBF and %BF were estimated for selected age, sex and racial-ethnic groups. Among the non-Hispanic white, non-Hispanic black, and Mexican-American participants aged 12-80 y examined in NHANES III, 15 912 had data available for weight, stature and BIA resistance measures. Males had higher mean TBW and FFM than did females, regardless of age or racial-ethnic status. Mean TBW and FFM increased from the adolescent years to mid-adulthood and declined in older adult age groups. Females had higher mean TBF and %BF estimates than males at each age group. Mean TBF also increased with older age groups to approximately 60 y of age after which it decreased. These mean body composition estimates for TBW, FFM, TBF and %BF based upon NHANES III BIA data provide a descriptive reference for non-Hispanic whites, non-Hispanic blacks and Mexican Americans in the US population.
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            Age- and maturity-related changes in body composition during adolescence into adulthood: the Fels Longitudinal Study.

            To examine patterns of change in total body fat (TBF), percent body fat (%BF), and fat-free mass (FFM), from 8-20 y of age and the effect of rate of skeletal maturation. To determine the degree of tracking of body composition for individuals from childhood into adulthood. Annual serial data for TBF, %BF and FFM from underwater weighing using a multicomponent body composition model were collected from 130 Caucasian males and 114 Caucasian females between 1976 and 1996. Rate of maturation was defined as FELS skeletal age (SA) less chronological age (CA). Random effects models were used to evaluate general patterns of change and tracking of individual serial data over the 12 y age range. Changes in TBF followed a quadratic model for males and for females with declining rates of change. Changes for %BF followed a cubic model for males and females. General patterns of change for FFM followed a cubic model for males and a quadratic model for females. TBF for males and females increased with age, but the rates of change declined with age. %BF for females increased from age 8-20 y. For males, %BF increased with age, but the positive rates of change declined and became a negative when aged about 13 y and reached a minimum at about the age of 15 y. The rate of change for %BF increased thereafter. FFM for males and females increased with age, but the rates of change decreased with age. The extent of tracking is inversely related to the length of the time interval. At the same age, rapidly-maturing children have significantly larger amounts of TBF, %BF and FFM then slow-maturing children. Tracking in body composition for individuals persisted from childhood to adulthood. (1) There are gender-associated differences in these patterns of change for %BF and FFM but not for TBF; (2) TBF, %BF and FFM increased with increased rates of maturation; (3) significant tracking in body composition for individuals persists from childhood to adulthood.
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              Pubertal alterations in growth and body composition. VI. Pubertal insulin resistance: relation to adiposity, body fat distribution and hormone release.

              To investigate the independent influence of alterations in fat mass, body fat distribution and hormone release on pubertal increases in fasting serum insulin concentrations and on insulin resistance assessed by the homeostasis model (HOMA). Cross-sectional investigation of pre- (n=11, n=8), mid- (n=10, n=11), and late-pubertal (n=10, n=11) boys and girls with normal body weight and growth velocity. Body composition (by a four-compartment model), abdominal fat distribution and mid-thigh interfascicular plus intermuscle (extramyocellular) fat (by magnetic resonance imaging), total body subcutaneous fat (by skinfolds), mean nocturnal growth hormone (GH) release and 06:00 h samples of serum insulin, sex steroids, leptin and insulin-like growth factor-I (IGF-I). Pubertal insulin resistance was suggested by greater (P 0.05) did not reliably improve r(2) beyond the physical characteristic and adiposity variables. In a second model, differences in sex and pubertal maturation were again held constant (r(2)=0.25), but body size differences were accounted for using percentage fat data. Sequential addition of percentage body fat (r(2)((inc)remental)=0.11, r(2)=0.36, P<0.05), then a block of fat distribution variables (percentage extramyocellular fat, percentage abdominal visceral fat, and percentage abdominal subcutaneous fat; r(2)(inc)=0.08, r(2)=0.44, P=0.058), and then a block of serum IGF-I and log((10)) leptin concentrations (r(2)(inc)=0.07, r(2)=0.51, P<0.05) increased r(2). Mean nocturnal GH release was not related to HOMA (r=-0.04, P=0.75) and therefore was not included in the hierarchical regression models. Increases in insulin resistance at puberty were most related to FM. Accumulation of fat in the abdominal visceral, subcutaneous and muscular compartments may increase insulin resistance at puberty beyond that due to total body fat. Serum concentrations of leptin and IGF-I may further modulate HOMA beyond the effects of adiposity and fat distribution. However, the results are limited by the cross-sectional design and the use of HOMA rather than a criterion measure of insulin resistance.
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                Author and article information

                Journal
                HRE
                Horm Res Paediatr
                10.1159/issn.1663-2818
                Hormone Research in Paediatrics
                S. Karger AG
                978-3-8055-7609-3
                978-3-318-00998-9
                1663-2818
                1663-2826
                2003
                July 2003
                17 November 2004
                : 60
                : Suppl 1
                : 36-45
                Affiliations
                Lifespan Health Research Center, Department of Community Health, Wright State University School of Medicine, Dayton, Ohio, USA
                Article
                71224 Horm Res 2003;60(suppl 1):36–45
                10.1159/000071224
                12955016
                © 2003 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 2, Tables: 2, References: 67, Pages: 10
                Categories
                Puberty

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