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      Body Mass Index as a Phenotypic Expression of Adiposity: Quantitative Contribution of Muscularity in a Population-Based Sample

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          Abstract

          ObjectiveAlthough widely applied as a phenotypic expression of adiposity in population and gene-search studies, body mass index (BMI) is also acknowledged to reflect muscularity even though relevant studies directly measuring skeletal muscle (SM) mass are lacking. The current study aimed to fill this important gap by applying advanced imaging methods to test the hypothesis that, after controlling first for adiposity, SM mass is also a significant determinant of BMI in a population-based sample.DesignWhole-body magnetic resonance imaging scans were completed in CARDIA Study subjects aged 33-45 years. Physical activity (PA) levels, alcohol intake, and adequacy of food intake were assessed by standardized questionnaires.Subjects58 African-American (AA) and 78 Caucasian (C) men; 63 AA and 64 C women.MeasurementsWhole-body AT and SM volumes.ResultsAT was significantly predicted by not only BMI, but PA and alcohol intake with total model R2s of 0.68 (p<0.0001) for men and 0.89 (p<0.0001) for women. Men had more SM than AT at all levels of BMI while SM predominated in women at lower BMIs (C <26 kg/m2; AA <28 kg/m2). Both AT and SM contributed a similar proportion of between-subject variation in BMI in men. In contrast, AT contributed ~30% more than SM to the variation in BMI in women. Developed allometric models indicated SM associations with AT, PA, and race after adjusting for height. There was little association of age, lifestyle factors, or race with BMI after controlling for both AT and SM.ConclusionVariation in muscularity provides a mechanistic basis for the previously observed non-specificity of BMI as a phenotypic expression of adiposity. These quantitative observations have important implications when choosing adiposity measures in population and gene-search studies.

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          Most cited references 38

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          Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence Report. National Institutes of Health.

           FX Pi-Sunyer (1998)
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            Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity.

            Obesity results from the interaction of genetic and environmental factors. To search for sequence variants that affect variation in two common measures of obesity, weight and body mass index (BMI), both of which are highly heritable, we performed a genome-wide association (GWA) study with 305,846 SNPs typed in 25,344 Icelandic, 2,998 Dutch, 1,890 European Americans and 1,160 African American subjects and combined the results with previously published results from the Diabetes Genetics Initiative (DGI) on 3,024 Scandinavians. We selected 43 variants in 19 regions for follow-up in 5,586 Danish individuals and compared the results to a genome-wide study on obesity-related traits from the GIANT consortium. In total, 29 variants, some correlated, in 11 chromosomal regions reached a genome-wide significance threshold of P < 1.6 x 10(-7). This includes previously identified variants close to or in the FTO, MC4R, BDNF and SH2B1 genes, in addition to variants at seven loci not previously connected with obesity.
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              Skeletal muscle mass and distribution in 468 men and women aged 18-88 yr.

              We employed a whole body magnetic resonance imaging protocol to examine the influence of age, gender, body weight, and height on skeletal muscle (SM) mass and distribution in a large and heterogeneous sample of 468 men and women. Men had significantly (P < 0.001) more SM in comparison to women in both absolute terms (33.0 vs. 21.0 kg) and relative to body mass (38.4 vs. 30.6%). The gender differences were greater in the upper (40%) than lower (33%) body (P < 0.01). We observed a reduction in relative SM mass starting in the third decade; however, a noticeable decrease in absolute SM mass was not observed until the end of the fifth decade. This decrease was primarily attributed to a decrease in lower body SM. Weight and height explained approximately 50% of the variance in SM mass in men and women. Although a linear relationship existed between SM and height, the relationship between SM and body weight was curvilinear because the contribution of SM to weight gain decreased with increasing body weight. These findings indicate that men have more SM than women and that these gender differences are greater in the upper body. Independent of gender, aging is associated with a decrease in SM mass that is explained, in large measure, by a decrease in lower body SM occurring after the fifth decade.
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                Author and article information

                Affiliations
                [1 ]Global Center for Scientific Affairs, Merck & Co, Rahway, NJ
                [2 ]Department of Medicine, University of California, San Francisco, CA, and the Metabolism Section, Veterans Affairs Medical Center, San Francisco, CA
                [3 ]Pediatric Unit, Verona University Medical School, Verona, Italy
                [4 ]University of Alabama, Birmingham, AL
                Author notes
                Address correspondence to: Steven B. Heymsfield, MD, Clinical Research, Metabolism, Merck Research Laboratories, 126 E. Lincoln Avenue, PO Box 2000, RY34A-A238, Rahway, NJ 07065-0900, Tel: 732-594-4448, Fax: 732-594-5179, Steven_Heymsfield@ 123456Merck.Com
                Journal
                101256108
                32579
                Int J Obes (Lond)
                International journal of obesity (2005)
                0307-0565
                1476-5497
                19 May 2010
                December 2009
                16 August 2011
                : 33
                : 12
                : 1363-1373
                3156622
                19773739
                10.1038/ijo.2009.184
                nihpa138252
                Funding
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 HL074814-07 ||HL
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 HL074814-06 ||HL
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 HL074814-05 ||HL
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 HL074814-04 ||HL
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 DK057508-03 ||DK
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 DK057508-02 ||DK
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 DK057508-01 ||DK
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: P30 DK026687-289012 ||DK
                Categories
                Article

                Nutrition & Dietetics

                ethnicity, body composition, obesity, body mass index

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