Variants of the FTO gene in obese children and their impact on body composition and metabolism before and after lifestyle intervention.

OBJECTIVE: To investigate the impact of variants of the FTO gene (rs1421085, rs17817449, rs9939609) in obese children before and after lifestyle intervention. DESIGN: Longitudinal, clinical intervention study with an increase in physical activity, and nutritional recommendations based on the 'Optimized Mixed Diet for German Children and Adolescents' (Research Institute of Child Nutrition, Germany). STUDY POPULATION: 75 overweight children (40 male, mean BMI 30.4±5.5 kg/m², mean age 12.6±2.6 years). MEASUREMENTS: Genotyping by means of a TaqMan SNP genotyping assay. Lean and fat mass were determined by means of DXA. RESULTS: For the whole study population, the 6-month lifestyle intervention resulted in a significant improvement (before intervention minus time point 6 months; mean±SD) in BMI-SDS (0.10±0.17, p<0.001), HOMA (1.41±3.19, p<0.001) and relative fat-mass-SDS (0.09±0.23, p=0.005). Before and after lifestyle intervention, there was no significant difference between heterozygote (n=52) and homozygote (n=21) carriers of the FTO gene in terms of BMI, body composition, and the metabolic profile (Insulin, HOMA, lipids, liver function tests). CONCLUSION: Variants in the FTO gene are common in obese children but have no impact on body composition and metabolism before and after lifestyle intervention.

The functional muscle-bone unit in obese children - altered bone structure leads to normal strength strain index.

UNLABELLED: Obese children have a twofold increased risk of fracture of the forearm compared to non-obese children. OBJECTIVE: To investigate bone strength and bone structure of the forearm, and the relationship between muscle and bone in obese children. METHODS: The study-group consisted of 84 (40 female) overweight children (mean (SD)) age 11.8 (3.2) years, BMI 29.0 (5.1) kg/m(2)). Bone geometry and strength were measured at the proximal radius of the non-dominant forearm (65% measurement site) by means of pQCT (XCT 2000). Bone mineral density and lean mass of the total body was determined by means of DXA (Lunar, DPXL/PED). Results were compared to reference values by calculating age (SDS(CA)) and height-age (SDS(HA)) dependent standard deviation scores (SDS). RESULTS: Cortical density, -1.11 (1.74) SDS(HA), -0.45 (1.52) SDS(CA); cortical thickness, -1.46 (1.33) SDS(HA), -1.01 (1.46) SDS(CA); cortical area, -0.42 (1.31) SDS(HA), 0.26 (1.58) SDS(CA); total bone area +2.21 (1.47) SDS(HA), 2.91 (1.80) SDS(CA), marrow area +3.12 (2.29) SDS(HA), 3.37 (2.38) SDS(CA); strength strain index +0.10 (1.10) SDS(HA), 0.95 (1.57) SDS(CA). These changes in bone structure were independent from pubertal stage. Measurements revealed correlations between muscle area and SSI (R(2)=0.67, p<0.001), and muscle mass and bone mineral content (DXA; R (2)=0.81, p<0.001). CONCLUSION: Low cortical density, normal cortical area and increased total bone area led to a normal strength strain index adjusted both for height and for age. We assume that this normal bone strength is not appropriate for the higher kinetic energy of impact in case of a fall in overweight children.

Investigation of myostatin serum levels before and after a 6-month lifestyle intervention program in obese children.

OBJECTIVE: To investigate the relationship between myostatin serum levels and muscle mass, fat mass and HOMA before and after a 6-month lifestyle intervention program in obese children and adolescents. DESIGN: A total of 57 overweight children and adolescents (female, n=27; age range, 6.0-16.1 years) were examined between 2007 and 2009. Mean BMI (±SD) was 31.1 (5.7) kg/m(2) corresponding to a mean BMI-SDS LMS of 2.2 (0.4). Muscle and fat mass were determined by means of DXA. Serum myostatin was measured by using a competitive ELISA. RESULTS [MEAN±SD]: After the 6-month intervention program, muscle mass (+2.1±2.7 kg, p<0.0001), and percentage myostatin serum levels (+23.7±26.7%, p<0.0001) were higher than before, whereas decreases in BMI (-0.4 kg/m(2)±1.5, p<0.0001), fat mass (-1.2±3.9 kg, p<0.0001), and HOMA insulin sensitivity index (-0.78±3.28 SD, p=0.0004) were observed. In 86% (n=49, p<0.0001) of all cases, the intervention program resulted in a higher level of myostatin. After lifestyle intervention, patients with the greatest increase of myostatin had a significantly lower increase of muscle mass (p=0.048) but did not differ for fat mass. There was no significant correlation between Myostatin and HOMA insulin sensitivity index before and after lifestyle intervention. CONCLUSION: Both muscle mass and serum myostatin increased concordantly. Patients with the greatest rise of myostatin had a significantly lower increase of muscle mass suggesting a negative feedback loop between myostatin and muscle tissue. In our study, the change of myostatin serum levels was not associated with the amount of fat mass or HOMA insulin sensitivity index.