Subjects were classified as obese, overweight and non-overweight according to the International Obesity Task Force . The non-overweight group includes normal weight (n = 533) and underweight (n = 2) children and for the purposes of this study has been called the normal weight group (n = 535). Table 1 summarises the baseline characteristics of a selection of lipid and anthropometric measures, comparing the overweight and obese children (n = 343) in the study to their normal weight counterparts (n = 535). Measures of blood pressure, insulin, TG, height and insulin resistance MK-2206 molecular weight were significantly higher (p < 0.0001) and HDL-C significantly lower
(p < 0.0001) in the overweight and obese group compared to their normal weight counterparts. The mean BMI of the mothers and fathers of the children was 24.6 ± 4.8 and 27.2 ± 3.6, respectively. Children whose parents were both overweight (BMI ≥ 25) had a BMI 2.2 units larger than children whose parents were both of a normal weight (BMI < 25) (p < 0.00001) ( Appendices Table 1a). Children of parents who were hypercholesterolemic (Cholesterol >240 mg/dl) had significantly higher cholesterol levels compared to children of parents who’s cholesterol PD0332991 levels were
normal (p < 0.00001) and the same observation was observed between parents and their children with LDL levels (p = 0.003) ( Appendices Table 1c and 1b, respectively). There were no allele frequency differences between boys and girls for any of the ten variants (data not shown). The genotype and minor allele frequency (MAF) for the ten variants are shown in Table 2. The genotype distribution of APOC3 1100C > T deviated from those expected under HWE (p = 0.02). There was a borderline statistically significant difference in allele frequency distribution of the LPL S447X variant between normal weight
children and their overweight and obese counterparts, MAF 0.14 (95% confidence intervals (CI) 0.11, 0.16) vs. 0.11 (95% CI 0.08, 0.14) (p = 0.02). Significant data for lipid and anthropometric variables, according to genotype, are presented in Table 3. APOE genotype, defined by two variant sites at residues 112 and 158 creating the ɛ2, ɛ3 and ɛ4 alleles, was significantly associated with TC (p = 0.0001) with ɛ2 carriers having TC plasma levels 11.3% lower Edoxaban than ɛ3/ɛ3 subjects (p < 0.001) and ɛ4 carriers with 1.3% higher TC plasma levels than ɛ3/ɛ3 subjects (p = 0.522). APOE genotype was also significantly associated with LDL-C (p < 0.0001). ɛ2 carriers had LDL-C plasma levels that were 17.6% lower than ɛ3/ɛ3 subjects (p < 0.001) and ɛ4 carriers had a mean LDL-C plasma level that was 2.8% higher than ɛ3/ɛ3 subjects (p = 0.258). ɛ2 carriers were also observed with a significantly lower mean TC: HDL-C ratio of 3.26 (95% CI 3.1, 3.5) compared to 3.62 (95% CI 3.6, 3.7) and 3.81 (95% CI 3.7, 4.