Table 3

Baseline measures of blood parameters and BMI-SDS in German fasted obese children and adolescents

Parameter

N¹

Genotype

N (%)

Mean ± SD

Additive genetic model²

Estimate

95% CI

p-value³

BMI-SDS⁷

519

TT

140 (27)

2.53 ± 0.49

0.025

-0.034...0.083

0.410

AT

238 (46)

2.60 ± 0.51

AA

141 (27)

2.58 ± 0.52

TGL [mg/dl]⁴

332

TT

94 (28)

115.15 ± 65.17

-0.008

-0.039...0.022

0.590

AT

159 (48)

107.89 ± 52.75

AA

79 (24)

109.52 ± 53.64

LDL [mg/dl]⁵

323

TT

93 (29)

104.18 ± 30.12

-0.001

-0.021...0.020

0.947

AT

153 (47)

106.52 ± 32.67

AA

77 (24)

103.42 ± 30.75

HDL [mg/dl]⁶

324

TT

93 (29)

50.25 ± 11.26

-0.004

-0.018...0.010

0.601

AT

153 (47)

50.92 ± 11.28

AA

78 (24)

49.33 ± 11.54

Glucose [mg/dl]⁷

480

TT

136 (28)

85.54 ± 9.09

-0.003

-0.009...0.003

0.350

AT

216 (45)

84.67 ± 9.54

AA

128 (27)

84.37 ± 8.60

¹ total number of obese individuals, from which baseline measures were available; ² linear regression analyses for log10-transformed parameters or BMI-SDS http://www.mybmi.de webcite including covariates age and sex; ³ two-sided p-value; ⁴ TGL: triglycerides; ⁵ LDL: low density lipoprotein; ⁶ HDL: high density lipoprotein; ⁷A trend towards a deviation from Hardy-Weinberg equilibrium was observable for genotype frequencies for BMI-SDS and glucose (exact p = 0.07; 0.03, respectively). This finding, however, is not surprising and expected in case of a true genetic association and indeed the number of homozygotes for the at-risk A-allele was increased in these patients compared to controls.

Müller et al. BMC Medical Genetics 2008 9:85   doi:10.1186/1471-2350-9-85