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Energy intake and energy expenditure among children with polymorphisms of the melanocortin-3 receptor^1,2,3,4

¹ From the Unit on Growth and Obesity, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD (DMS, MT-K, JCH, CN, RAS, CAR, LEW, KA, KSJ-G, REF, ELS, SB, and JAY); the Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD (MT-K and LEW); the Nutrition Department, Clinical Center, National Institutes of Health, Bethesda, MD (MK); and the Department of Nutritional Sciences, University of Wisconsin, Madison, WI (DAS).

² DMS and MT-K contributed equally to this work. JCH, MK, and JAY are commissioned officers in the US Public Health Service, Department of Health and Human Services.

³ Supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health (JAY), and by supplemental funding from the National Center on Minority Health and Health Disparities (JAY).

⁴ Adress correspondence to JA Yanovski, Unit on Growth and Obesity, Program on Developmental Endocrinology and Genetics, National Institute of Child Health and Human Development, National Institutes of Health, 10 Center Drive, Hatfield Clinical Research Center, Room 1-3330, MSC 1103, Bethesda, MD 20892-1103. E-mail: jy15i{at}nih.gov.

Background: Homozygosity for 2 protein-altering polymorphisms in the melanocortin-3 receptor gene (MC3R) coding sequence, C17A and G241A, has been reported to be associated with an obesity phenotype in children, yet how these polymorphisms affect energy homeostasis is unknown. Association between adult body weight and +2138InsCAGACC, another variant in the 3' untranslated region of MC3R, has also been described.

Objective: The objective of this study was to examine associations of C17A + G241A and +2138InsCAGACC MC3R variants with children's energy balance.

Design: Children aged 6–19 y were genotyped for MC3R C17A, G241A, and +2138InsCAGACC. Subjects underwent studies of energy intake from a 9835-kcal food array (n = 185), resting energy expenditure (REE) by using indirect calorimetry (n = 302), or total daily energy expenditure (TEE) by using doubly labeled water (n = 120). Linear regression was used to examine the associations between MC3R polymorphisms and the measures of energy balance.

Results: Body mass index and fat mass were greater in those with double homozygosity for C17A + G241A (P = 0.001). After accounting for covariates (including body composition), the number of minor C17A + G241A alleles was associated with significantly greater energy intake (β = +0.15, P = 0.02) but not altered REE or TEE. No significant associations were observed between +2138InsCAGACC and measures of either fat mass or energy balance.

Conclusions: C17A + G241A polymorphisms may be associated with pediatric obesity because of greater energy intake rather than because of diminished energy expenditure. +2138InsCAGACC does not appear to be associated with obesity or measures of energy balance in children.