Abstract

BackgroundThis study aimed to investigate whether the body mass index (BMI) in combination with genetic variations in APOE and APOA5_‘T’ alleles modulates the risk of sHTG. MethodsThere were 255 moderate HTG (TG ≥2.26 and <5.65mmol/L) and 176 sHTG (TG ≥5.65mmol/L) and 304 controls (TG <2.26mmol/L) were recruited. APOE epsilon alleles were genotyped using sequence-specific primers; the APOA5_‘T’ allele (c.553G>T, rs2075291) was identified using a restriction site polymorphism. Overweight/obesity was defined as BMI ≥25kg/m2 and non-overweight as BMI <25kg/m2. ResultsMultivariate logistic regression analysis showed, in addition to APOA5_‘T’ allele, a significant interaction between BMI ≥25kg/m2 and APOE4 carriers on the risk of sHTG. Subjects with diagnosis of diabetes, current smoking, hypertension, levels of non-high density lipoprotein, and BMI ≥25kg/m2 were significant determinants of sHTG. The odds ratio (95% confidence intervals) of overweight/obese APOE4 carriers for sHTG was 13.56 (4.89–37.59) more than those of non-overweight non-APOE4 carriers, while the odds ratio for sHTG in overweight/obese patients with the APOA5_‘T’ allele was 15.83 (7.77–32.26) higher than those of non-overweight non-APOA5 carriers. ConclusionsOverweight/obesity may potentiate the genetic variants of the APOE4 and APOA5_‘T’ alleles on the risk of sHTG.

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