Obesity is a complex disease influenced by genetic and environmental factors and their interactions. The current surge in childhood obesity in the U.S. is attributable to an interaction between a genetic predisposition toward efficient energy storage and a permissive environment of readily available food and sedentary behaviors [1]. Genetic architecture of common polygenic childhood obesity remains largely unknown. In genetic studies, the phenotypic description of the obese child usually has been limited to body mass index (BMI). BMI represents a composite trait of fat free mass (FFM) and fat mass (FM) and thus loci influencing BMI may differ from more direct measures of adiposity. In addition, markers of biological processes underlying the development of obesity such as dietary intake, energy expenditure and nutrient partitioning may be more effectual in identifying causal genetic variants [2]. In epidemiology studies, childhood obesity has been shown to be genetically correlated with glucose intolerance, hypertension, dyslipidemia, insulin resistance, chronic inflammation, and risk for fatty liver disease [3], [4]. Identification of genes underlying these distinct patterns of association also may unravel important biological pathways involved in the pathophysiology of childhood obesity.
