Obesity affects 25% to 30% of children. After adolescence african- american females have a higher prevalence of obesity, and as adults obese african-american females have increased morbidity and mortality compared to caucasian females. Obesity is caused by increased energy intake and/or decreased energy expenditure (EE). 24-hour BE can be divided into three components: resting EE, thermic effect of food, and energy cost of activity. Total BE can be determined in free-living subjects using the doubly-labeled (2H2 18O) stable isotope of water and in confined subjects using whole-room indirect calorimetry. 2H2 18O measures total EE; indirect calorimetry measures total EE and its components, and fuel utilization. The difference between the total EE from the two methods is an estimate of free-living physical activity. Low EE has been demonstrated before the period of rapid weight gain in pre-obese caucasian infants and children (aged 4 to 5 years), and in adult Pima Indians. In obese adult Pima Indians reduced EE aggregated in families and may be the physiologic basis for the inheritance of obesity. Other studies in Pima Indians suggest that reduced oxidation of fat leads to a positive fat balance, which may be another factor in the development of obesity. It is unknown 1) if EE is decreased in pre-obese prepubertal females (african-american or caucasian), and 2) which component of EE is decreased. The main hypothesis of this study is that low EE (adjusted for body composition) and a low rate of fat oxidation will predict more rapid weight gain in african-american or caucasian females with obese parents than in similar females with no familial predisposition to obesity. The second hypothesis is that low resting EE and low habitual activity are the EE components that best predict rapid weight gain. Using state-of-the-art methods of whole-room indirect calorimetry (never used in this age group) and 2H2 180, the components of 24-hour EE and habitual physical activity will be determined. Two baseline analyses (1-month apart) of EE and fat oxidation of 52 prepubertal nonobese african- american or caucasian females, aged 6 to 9 years, will be the starting point for a longitudinal follow-up of at least 2.5 years. 26 children (non-pre-obese) will be selected as having both biological parents with a measured body mass index (BMI) < 27.5 kg/m2. The other 26 children (pre-obese) will be selected as having both parents with a measured BMI > 30 kg/m2. All children will undergo repeat assessments of blood pressure, glucose tolerance, body fat pattern, and body composition after 2.5 years. Analyses of the data will allow comparisons of baseline EE and fat oxidation in children of nonobese and obese parents, as well as the relationship to subsequent weight gain and body fat pattern over at least 2.5 years. This study will provide valuable information for understanding which factors predispose certain individuals to obesity. This information is crucial to develop strategies for obesity prevention.
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