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. Author manuscript; available in PMC: 2011 Jan 7.
Published in final edited form as: Nat Genet. 2010 Jul 25;42(8):684–687. doi: 10.1038/ng.628

Table 2.

Genetic loci associated with HTG.

Locus SNP CHR Position Minor Allele HTG MAF Control MAF OR (95% CI) P-value
APOA5 rs964184 11 116.2 G 0.33 0.14 3.28 (2.61-4.14) 5.4 × 10-24
GCKR rs1260326 2 2.8 T 0.52 0.41 1.75 (1.45-2.12) 6.5 × 10-9
LPL rs7016880 8 19.9 C 0.03 0.10 0.32 (0.21-0.49) 2.0 × 10-7
APOB rs4635554 2 21.2 G 0.39 0.31 1.67 (1.38-2.02) 2.0 × 10-7

MLXIPL rs714052 7 72.5 G 0.07 0.13 0.44 (0.31-0.62) 0.000003
TRIB1 rs2954029 8 126.6 T 0.37 0.46 0.71 (0.59-0.86) 0.0004
ANGPTL3 rs10889353 1 62.9 C 0.27 0.32 0.73 (0.59-0.89) 0.002
NCAN rs17216525 19 19.5 T 0.07 0.09 0.71 (0.50-1.00) 0.05
FADS rs174547 11 61.3 C 0.40 0.33 1.20 (0.99-1.44) 0.07
XKR6 rs7819412 8 11.1 G 0.46 0.50 0.87 (0.72-1.05) 0.14
PLTP rs7679 20 44.0 C 0.20 0.19 1.17 (0.94-1.47) 0.16

CHR, chromosome; CI, confidence interval; HTG, hypertriglyceridemia; MAF, minor allele frequency; OR, odds ratio; SNP, single nucleotide polymorphism. Association was tested using an additive multivariate logistic regression model, entering sex, body mass index, diabetes status, and 10 principal components of ancestry as covariates. The top four loci surpassed a pre-specified threshold for genome-wide significance of P<5×10-7. Remaining loci were replicated from GWAS meta-analysis of population-based TG concentrations5, using a Bonferroni corrected significance threshold of P<0.005.