title: A genetic variant of apolipoprotein M increases susceptibility to coronary artery disease in a Chinese population.
abstract: 1. High-density lipoprotein (HDL) is widely accepted as a lipoprotein that protects against coronary artery and other atherosclerotic diseases. Recently, a new apolipoprotein encoded by the APOM gene, which plays an important role in affecting the intrinsic properties of HDL, has been reported. Genetic variations exist in the APOM gene, but their significance is presently unclear. The aim of the present study was to elucidate whether the APOM T-855C mutant allele is implicated in coronary artery disease (CAD). 2. In the present study, 418 patients with CAD and 372 controls were studied, all of whom were Han Chinese from Jiangsu Province, China. Plasma levels of triglycerides (TG), total cholesterol (TC), HDL-cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C) were evaluated. Genomic DNA from the whole blood from these subjects was subjected to polymerase chain reaction amplification and restriction enzyme digestion to determine genotype with respect to the APOM T-855C polymorphism. 3. The allelic frequencies were in Hardy-Weinberg equilibrium. Plasma HDL levels were significantly lower in subjects with CAD than in control subjects (1.08 +/- 0.31 vs 1.25 +/- 0.32, respectively; P < 0.001) and the distribution of genotypes and allelic frequencies was significantly different in the two groups (P = 0.013 and 0.005, respectively). Multiple logistic regression analysis after adjustment for age, gender, smoking, body mass index, hypertension and serum glucose showed that, compared with the wild-type TT genotype, carriers of the C allele had an increased risk of CAD (odds ratio = 1.819, 95% confidence interval 1.142-2.898; P = 0.012). 4. In conclusion, the results of the present study suggest that the APOM T-855C polymorphism carries an increased risk for CAD in this Chinese population.
authors.affiliation: Atherosclerosis Research Center, Nanjing Medical University, Nanjing, China.
authors.forename: Wei-Wei
authors.initials: WW
authors.lastname: Xu
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Yi-Bo
authors.initials: YB
authors.lastname: Tang
authors.forename: Ya-Lin
authors.initials: YL
authors.lastname: Xu
authors.forename: Han-Zhang
authors.initials: HZ
authors.lastname: Zhu
authors.forename: Albert
authors.initials: A
authors.lastname: Ferro
authors.forename: Yong
authors.initials: Y
authors.lastname: Ji
authors.forename: Qi
authors.initials: Q
authors.lastname: Chen
authors.forename: Le-Ming
authors.initials: LM
authors.lastname: Fan
mesh_terms: D000368:Aged; D000483:Alleles; D001053:Apolipoproteins / Q000235:genetics*; D000075243:Apolipoproteins M; D044466:Asian People / Q000235:genetics*; D016022:Case-Control Studies; D003327:Coronary Disease / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D014644:Genetic Variation; D005838:Genotype; D006801:Humans; D054834:Lipocalins; D008297:Male; D008875:Middle Aged; D012307:Risk Factors
chemical_list: C400523:APOM protein, human; D001053:Apolipoproteins; D000075243:Apolipoproteins M; D054834:Lipocalins