UCP-1 A-3826G Polymorphism and HDL-C in Relation to Obesity J Clin Med Res • 2011;3(6):319-324 Table 2. The Results of the Multivariate-adjusted Logistic Regression Analysis of Factors Associated With Low High- density Lipoprotein Cholesterolemia in the Non-obese and Obese Groups Factor Age (years) Gender (male) Current smoking (presence) BMI (kg/m2) SBP (mmHg) DBP (mmHg) T-chol (mmol/L) TG (mmol/L) HbA1c (%) G/G genotype (presence) Non-obese Obese OR (95% CI) 1.04 (0.98-1.09) 3.05 (0.86-10.78) 1.72 (0.43-6.83) 0.94 (0.70-1.27) 0.98 (0.94-1.02) 1.02 (0.94-1.10) 0.95 (0.93-0.97) 1.03 (1.02-1.05) 1.14 (0.79-1.65) 0.51 (0.13-1.96) P value 0.19 0.08 0.44 0.69 0.32 0.63 < 0.01* < 0.01* 0.49 0.33 OR (95% CI) 1.04 (0.98-1.11) 0.95 (0.19-4.75) 6.51 (0.71-59.9) 1.53 (1.05-2.21) 0.94 (0.89-0.99) 1.06 (0.98-1.16) 0.95 (0.92-0.99) 1.02 (1.01-1.03) 1.67 (0.51-5.46) 6.85 (1.65-28.49) P value 0.22 0.95 0.10 0.03* 0.03* 0.15 < 0.01* < 0.01* 0.40 < 0.01* OR: odds ratio; CI: conﬁdence interval; BMI: body mass index; SBP: systolic blood pressure; DBP: diastolic blood pressure; T- chol: total cholesterol; HDL-C: high-density lipoprotein cholesterol; TG: triglycerides; HbA1c: hemoglobin A1c. All the listed factors, including the G/G genotype of the uncoupling protein-1 gene A-3826G polymorphism (reference: the A/A + A/G genotypes), were entered into the multivariate-adjusted logistic regression analysis models. Signiﬁcant level: *: P < 0.05. total cholesterol (T-chol), triglycerides (TG) and HDL-C levels were enzymatically measured. Hemoglobin A1c (HbA1c) levels were measured using a high performance liq- uid chromatography method. Genomic DNA was extracted from the subject’s buccal mucosa cells obtained using cyto- brushes, and genotypes were determined by an intercalater- mediated ﬂuorescent allele-speciﬁc PCR method using spe- ciﬁc primers, as described previously [8]. The data were presented as the means ± standard de- viation (SD) or the medians plus interquartile range. The genotype and allele frequencies for Hardy-Weinberg equilib- rium were examined using the χ2-test. Differences between the genotype-based groups were compared using either the unpaired t-test, one way ANOVA (with a multi-comparison test), or χ2-test (with a residual analysis) in each group of non-obese and obese subjects. When the two groups by geno- type were compared, we divided subjects into the A/A + A/G genotype group and the G/G genotype group according to the earlier study [15]. The TG values were log-transformed because of their skewed distribution in this analysis. A mul- tivariate logistic regression analysis on the presence of low HDL-cholesterolemia, adjusted for all the measured factors including the G/G genotype (reference: the A/A + A/G geno- type), was performed to observe whether the genotype was associated with low HDL-cholesterolemia in each group of non-obese and obese subjects. Obesity was deﬁned as a BMI ≥ 25 kg/m2 according to the clinical guideline of the Japan society for the study of obesity [16], and low HDL-choles- terolemia was deﬁned as HDL-C < 1.04 mmol/L according to the clinical guideline of the Japan Atherosclerosis Society [17]. A P-value < 0.05 was considered to be signiﬁcant. Results Overall, the distributed number of A/A, A/G and G/G geno- types was 91 (31%), 131 (45%) and 72 (24%), respectively, among all subjects (n = 294). The frequency of the G-allele was 47%. This frequency was similar to earlier Japanese re- ports [12, 14, 15]. These frequencies were in Hardy-Wein- berg equilibrium (χ2 = 1.64, P = 0.45). In the non-obese group (n = 192), the subject number of A/A, A/G and G/G genotypes was 59 (31%), 88 (46%) and 45 (23%), while in the obese group (n = 102), the subject number of A/A, A/G and G/G genotypes was 32 (31%), 43 (42%) and 27 (27%), respectively. There was no signiﬁcant difference in the geno- type distribution between the non-obese and obese groups (P = 0.79). When the clinical characteristics of subjects were compared between the respective genotype carriers, signiﬁcant differences in HDL-C levels (A/A genotype: 1.37 ± 0.41 mmol/L, A/G: 1.42 ± 0.31 mmol/L, G/G: 1.20 ± 0.30 mmol/L; F = 3.54, P = 0.03) and the prevalence of low HDL-cholesterolemia (A/A genotype: 5 subjects, 16%, A/G: Articles © The authors | Journal compilation © J Clin Med Res and Elmer Press™ | www.jocmr.org 321