Conceived and designed the experiments: R-XY Y-YL. Performed the experiments: Y-YL W-YL LZ J-ZW. Analyzed the data: R-XY W-YL. Contributed reagents/materials/analysis tools: R-XY W-YL. Wrote the paper: R-XY. Epidemiological survey: R-XY J-ZW.
The authors have declared that no competing interests exist.
Little is known about the interactions of apolipoprotein (Apo) A5 gene polymorphisms and alcohol consumption on serum lipid profiles. The present study was undertaken to detect the interactions of ApoA5–1131T>C, c.553G>T and c.457G>A polymorphisms and alcohol consumption on serum lipid levels.
A total of 516 nondrinkers and 514 drinkers were randomly selected from our previous stratified randomized cluster samples. Genotyping was performed by polymerase chain reaction and restriction fragment length polymorphism. The levels of serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), ApoA1 and ApoB were higher in drinkers than in nondrinkers (
The differences in some serum lipid parameters between the drinkers and nondrinkers might partly result from different interactions of the ApoA5 gene polymorphisms and alcohol consumption.
Dyslipidemia has become a major health problem in many countries because of its high prevalence and a causal relationship with serious medical condition such as coronary artery disease (CAD), hypertension and stroke
Apolipoprotein (Apo) A5 is a secreted protein present in human serum and is associated with specific lipoprotein particles. It was detectable in very low-density lipoprotein (VLDL), HDL, and chylomicrons. Serum ApoA5 is very low compared with other apolipoproteins. Human serum ApoA5 concentrations range from 24 to 406 µg/l, with a mean value in normolipidemic persons of 157 µg/l
A total of 1030 unrelated subjects who reside in 16 villages in Napo County, Guangxi Zhuang Autonomous Region, People's Republic of China were randomly selected from our previous stratified randomized cluster samples
The survey was carried out using internationally standardized methods, following a common protocol
Venous blood samples (8 ml) were drawn from a forearm vein of every subject after venous occlusion for a few seconds in a sitting position, after an overnight fast of 12 h and abstention from alcohol use for at least 12 h. A part of the sample (3 ml) was collected into glass tubes and allowed to clot at ambient temperature, and used to determine serum lipid levels, and another part of the sample (5 ml) was transferred into tubes with anticoagulate solution (4.80 g/l citric acid, 14.70 g/l glucose, and 13.20 g/l tri-sodium citrate) and used to extract deoxyribonucleic acid (DNA). Immediately following clotting serum was separated by centrifugation for 15 min at 3000 rpm. The levels of serum total cholesterol (TC), TG, HDL-C, and LDL-C in samples were determined by enzymatic methods with commercially available kits, Tcho-1, TG-LH (RANDOX Laboratories Ltd., Ardmore, Diamond Road, Crumlin Co. Antrim, United Kingdom, BT29 4QY), Cholestest N HDL, and Cholestest LDL (Daiichi Pure Chemicals Co., Ltd., Tokyo, Japan); respectively. Serum ApoA1 and ApoB levels were assessed by the immunoturbidimetric immunoassay using a commercial kit (RANDOX Laboratories Ltd.). All determinations were performed with an autoanalyzer (Type 7170A; Hitachi Ltd., Tokyo, Japan) in the Clinical Science Experiment Center of the First Affiliated Hospital, Guangxi Medical University.
Total genomic DNA was isolated from peripheral blood leukocytes using the phenol-chloroform method
Sixteen samples (each genotype in two) detected by the PCR-RFLP were also confirmed by direct sequencing. The PCR product was purified by low melting point gel electrophoresis and phenol extraction, and then the DNA sequences were analyzed by using an ABI Prism 3100 (Applied Biosystems) in Shanghai Sangon Biological Engineering Technology & Services Co., Ltd., People's Republic of China.
The normal values of serum TC, TG, HDL-C, LDL-C, ApoA1, ApoB levels and the ratio of ApoA1 to ApoB in our Clinical Science Experiment Center were 3.10–5.17, 0.56–1.70, 0.91–1.81, 1.70–3.20 mmol/L, 1.00–1.76, 0.63–1.14 g/L, and 1.00–2.50; respectively
The data were recorded on a pre-designed form and managed with Excel software. The quantitative variables were presented as mean ± standard deviation (serum TG levels were presented as medians and interquartile ranges). The difference in general characteristics between the two groups was tested by the Student's unpaired
Parameter | Nondrinker(n = 516) | Drinker(n = 514) |
|
|
Male/female | 186/330 | 306/208 | 56.930 | 0.000 |
Age (years) | 41.26±19.53 | 45.35±15.38 | –3.733 | 0.000 |
Body mass index (kg/m2) | 21.66±2.71 | 21.95±2.39 | –1.821 | 0.069 |
Systolic blood pressure (mmHg) | 120.03±16.15 | 125.60±15.63 | –5.624 | 0.000 |
Diastolic blood pressure (mmHg) | 74.13±9.82 | 77.79±9.78 | –5.993 | 0.000 |
Pulse pressure (mmHg) | 45.95±11.89 | 47.83±12.01 | –2.525 | 0.012 |
Cigarette smoking [n (%)] | ||||
Nonsmoker | 414(80.2) | 292(56.8) | ||
<20 cigarettes/day | 62(12.0) | 106(20.6) | ||
≥20 cigarettes/day | 40(7.8) | 116(22.6) | 69.628 | 0.000 |
Alcohol consumption [n (%)] | ||||
Nondrinker | 516(100.0) | – | ||
<25 g/day | – | 396(77.0) | ||
≥25 g/day | – | 118(23.0) | ||
Total cholesterol (mmol/L) | 4.52±0.99 | 4.65±0.95 | –2.150 | 0.032 |
Triglyceride (mmol/L) | 0.97(0.57) | 1.09(0.61) | –2.488 | 0.013 |
HDL-C (mmol/L) | 1.98±0.45 | 2.14±0.49 | –5.458 | 0.000 |
LDL-C (mmol/L) | 2.40±0.70 | 2.41±0.70 | –0.229 | 0.819 |
Apolipoprotein (Apo) A1 (g/L) | 1.40±0.16 | 1.48±0.13 | –8.805 | 0.000 |
ApoB (g/L) | 0.89±0.22 | 0.92±0.20 | –2.290 | 0.022 |
ApoA1/ApoB | 1.68±0.57 | 1.69±0.46 | –0.310 | 0.757 |
HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol. The value of TG was presented as median (interquartile range). The difference between the two groups was determined by the Wilcoxon-Mann-Whitney test.
The levels of TC, TG, HDL-C, ApoA1 and ApoB were higher in drinkers than in nondrinkers (
After the genomic DNA of the samples was amplified by PCR and imaged by 2% agarose gel electrophoresis for the ApoA5 c.553G>T, the PCR product of 211 bp nucleotide sequences could be seen in the samples. The GG and GT genotypes were shown in
(A) ApoA5 c.553G>T. Lane M, 50 bp marker ladder; lanes 1 and 2, the PCR products of the samples (211 bp); lanes 3 and 4, GG genotype (176 bp and 35 bp); lanes 5 and 6, GT genotype (211 bp, 176 bp and 35 bp). TT genotype was not be detected in both groups. The 35 bp fragment was invisible in the gel owing to its fast migration speed. (B) ApoA5 –1131T>C. Lanes 1 and 2, the PCR products of the samples (188 bp); lanes 3 and 4, TT genotype (165 bp and 23 bp); lanes 5 and 6, TC genotype (188 bp, 165 bp and 23 bp); and Lanes 7 and 8, CC genotype (188 bp). The 23 bp fragment was invisible in the gel owing to its fast migration speed. (C) ApoA5 c.457G>A. Lanes 1 and 2, the PCR products of the samples (211 bp); lanes 3 and 4, GG genotype (211 bp); lanes 5 and 6, GA genotype (211 bp, 133 bp and 78 bp); and lanes 7 and 8, AA genotype (133 bp and 78 bp).
The results were shown as TT, TC and CC genotypes of the –1131T>C, GG and GT genotypes of the c.553G>T, and GG, GA and AA genotypes of the c.457G>A by PCR-RFLP, the genotypes were also confirmed by sequencing (
(A) ApoA5 –1131T>C: (1) TT genotype, (2) TC genotype, (3) CC genotype; (B) ApoA5 c.553G>T: (4) GG genotype, (5) GT genotype; (C) ApoA5 c.457G>A: (6) GG genotype, (7) GA genotype, (8) AA genotype.
The genotypic and allelic frequencies of the three SNPs are shown in
SNP | Group | n | Genotype [n (%)] | Allele [n (%)] | |||
AA AB BB | A B | ||||||
–1131T>C | Nondrinker | 516 | 268(51.9) | 208(40.3) | 40(7.8) | 744(72.1) | 288(27.9) |
(rs662799) | Drinker | 514 | 266(51.8) | 196(38.1) | 52(10.1) | 728(70.8) | 300(29.2) |
|
– | 1.925 | 0.411 | ||||
|
– | 0.382 | 0.521 | ||||
Drinker | |||||||
<25 g/day | 396 | 206(52.0) | 152(38.4) | 38(9.6) | 564(71.2) | 228(28.8) | |
≥25 g/day | 118 | 60(50.8) | 44(37.3) | 14(11.9) | 164(69.5) | 72(30.5) | |
|
– | 0.515 | 0.261 | ||||
|
– | 0.773 | 0.609 | ||||
c.553G>T | Nondrinker | 516 | 482(93.4) | 34(6.6) | – | 998(96.7) | 34(3.3) |
(rs2075291) | Drinker | 514 | 480(93.4) | 34(6.6) | – | 994(96.7) | 34(3.3) |
|
– | 0.000 | 0.000 | ||||
|
– | 0.988 | 0.988 | ||||
Drinker | |||||||
<25 g/day | 396 | 370(93.4) | 26(6.6) | – | 766(96.7) | 26(3.3) | |
≥25 g/day | 118 | 110(93.2) | 8(6.8) | – | 228(96.6) | 8(3.4) | |
|
– | 0.008 | 0.007 | ||||
|
– | 0.934 | 0.936 | ||||
c.457G>A | Nondrinker | 516 | 454(88.0) | 60(11.6) | 2(0.4) | 968(93.8) | 64(6.2) |
(rs3135507) | Drinker | 514 | 454(88.3) | 52(10.1) | 8(1.6) | 960(93.4) | 68(6.6) |
|
– | 4.168 | 0.147 | ||||
|
– | 0.125 | 0.701 | ||||
Drinker | |||||||
<25 g/day | 396 | 354(89.4) | 36(9.1) | 6(1.5) | 744(93.9) | 48(6.1) | |
≥25 g/day | 118 | 100(84.7) | 16(13.6) | 2(1.7) | 216(91.5) | 20(8.5) | |
|
– | 2.036 | 1.715 | ||||
|
– | 0.361 | 0.190 |
Allele A, –1131T, c.553G or c.457G; Allele B, –1131C, c.553T or c.457A; Genotype AA, –1131TT, c.553GG or c.457GG; Genotype AB, –1131TC, c.553GT or c.457GA; Genotype BB, –1131CC, c.553TT or c.457AA.
SNP | n | TC | TG | HDL-C | LDL-C | ApoA1 | ApoB | ApoA1/ApoB |
ApoA5 –1131T>C | ||||||||
Nondrinker TT | 268 | 4.48±0.92 | 0.91(0.56) | 1.98±0.41 | 2.37±0.71 | 1.40±0.13 | 0.88±0.21 | 1.71±0.61 |
TC | 208 | 4.55±1.13 | 1.00(0.62) | 1.97±0.50 | 2.43±0.72 | 1.40±0.19 | 0.91±0.22 | 1.62±0.42 |
CC | 40 | 4.64±0.60 | 0.99(0.57) | 2.00±0.44 | 2.45±0.60 | 1.41±0.12 | 0.87±0.25 | 1.83±0.87 |
Drinker TT | 266 | 4.68±0.92 | 0.89(0.53) | 2.15±0.47 | 2.35±0.72 | 1.47±0.14 | 0.89±0.20 | 1.74±0.50 |
TC | 196 | 4.83±0.82 | 1.12(0.73) | 2.13±0.51 | 2.42±0.65 | 1.48±0.13 | 0.94±0.20 | 1.66±0.42 |
CC | 52 | 5.17±0.93 | 1.38(0.94) | 2.15±0.55 | 2.66±0.69 | 1.50±0.10 | 1.03±0.20 |
1.52±0.30 |
|
– | 1.143 | 0.518 | 0.075 | 1.006 | 0.259 | 4.273 | 5.059 |
|
– | 0.319 | 0.596 | 0.928 | 0.366 | 0.772 | 0.014 | 0.007 |
ApoA5 c.553G>T | ||||||||
Nondrinker GG | 482 | 4.51±1.01 | 0.93(0.58) | 1.99±0.46 | 2.39±0.71 | 1.40±0.16 | 0.89±0.22 | 1.69±0.58 |
GT | 34 | 4.60±0.78 | 1.05(0.62) | 1.83±0.32 | 2.55±0.67 | 1.40±0.11 | 0.98±0.20 | 1.48±0.32 |
Drinker GG | 480 | 4.80±0.89 | 1.00(0.60) | 2.16±0.50 | 2.42±0.70 | 1.48±0.13 | 0.92±0.20 | 1.69±0.44 |
GT | 34 | 4.63±0.90 | 1.14(1.29) | 1.93±0.37 | 2.23±0.63 |
1.45±0.15 | 0.92±0.27 | 1.73±0.59 |
|
– | 1.155 | 1.214 | 0.476 | 4.084 | 0.770 | 3.600 | 3.990 |
|
– | 0.283 | 0.271 | 0.491 | 0.044 | 0.380 | 0.058 | 0.046 |
ApoA5 c.457G>A | ||||||||
Nondrinker GG | 454 | 4.55±0.97 | 0.97(0.58) | 1.99±0.45 | 2.41±0.69 | 1.40±0.15 | 0.90±0.22 | 1.67±0.57 |
GA/AA | 62 | 4.31±1.17 | 0.99(0.63) | 1.88±0.46 | 2.30±0.79 | 1.37±0.22 | 0.85±0.24 | 1.74±0.58 |
Drinker GG | 454 | 4.81±0.88 | 1.01(0.60) | 2.17±0.50 | 2.44±0.71 | 1.49±0.13 | 0.93±0.21 | 1.69±0.47 |
GA/AA | 60 | 4.63±0.97 | 0.95(0.49) |
1.94±0.40 | 2.22±0.57 | 1.41±0.14 | 0.87±0.17 | 1.70±0.45 |
|
– | 0.102 | 15.663 | 1.648 | 0.554 | 2.329 | 0.167 | 0.288 |
|
– | 0.750 | 0.000 | 0.200 | 0.457 | 0.127 | 0.683 | 0.591 |
SNP, single nucleotide polymorphism; TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B; ApoA1/ApoB, the ratio of apolipoprotein A1 to apolipoprotein B.
The values of
We observed four haplotypes: T-G-G, C-G-G, T-A-G, and C-G-T with frequencies ranging from 0.06 to 0.87, representing 100% of all haplotypes in the both groups (
Lipid | Haplotype | T-G-G | C-G-G | T-A-G | C-G-T | Haplotype global association | |
– | Frequency | 0.65 | 0.26 | 0.06 | 0.03 | – | – |
– | Frequency (carrier vsnoncarrier) | 898 vs 132 | 454 vs 576 | 122 vs 908 | 62 vs 968 |
|
|
TC | Carrier | 4.65±0.04 | 4.75±0.05 | 4.50±0.09 | 4.59±0.12 | ||
(mmol/L) | Noncarrier | 4.71±0.08 | 4.58±0.05 | 4.71±0.04 | 4.69±0.04 | ||
|
0.482 | 0.003 | 0.017 | 0.397 | <0.001 | 0.001 | |
TG | Carrier | 1.21 (0.06) | 1.32 (0.07) | 1.58 (0.12) | 1.41 (0.16) | ||
(mmol/L) | Noncarrier | 1.36 (0.11) | 1.16 (0.07) | 1.19 (0.06) | 1.21 (0.06) | ||
|
0.058 | <0.001 | 0.479 | 0.006 | < 0.001 | 0.001 | |
HDL-C | Carrier | 2.12±0.02 | 2.11±0.03 | 1.99±0.05 | 1.92±0.06 | ||
(mmol/L) | Noncarrier | 2.04±0.04 | 2.10±0.03 | 2.13±0.02 | 2.12±0.02 | ||
|
0.065 | 0.725 | 0.003 | <0.001 | < 0.001 | 0.001 | |
LDL-C | Carrier | 2.37±0.03 | 2.44±0.04 | 2.23±0.07 | 2.33±0.09 | ||
(mmol/L) | Noncarrier | 2.44±0.06 | 2.32±0.04 | 2.42±0.03 | 2.40±0.03 | ||
|
0.242 | 0.004 | 0.005 | 0.440 | 0.002 | 0.002 | |
ApoA1 | Carrier | 1.46±0.01 | 1.46±0.01 | 1.42±0.01 | 1.44±0.02 | ||
(g/L) | Noncarrier | 1.44±0.01 | 1.46±0.01 | 1.47±0.01 | 1.47±0.01 | ||
|
0.133 | 0.769 | 0.001 | 0.160 | 0.001 | 0.002 | |
ApoB | Carrier | 0.90±0.01 | 0.92±0.01 | 0.86±0.02 | 0.94±0.03 | ||
(g/L) | Noncarrier | 0.92±0.02 | 0.88±0.01 | 0.92±0.01 | 0.91±0.01 | ||
|
0.401 | 0.001 | 0.003 | 0.259 | < 0.001 | 0.001 | |
ApoA1/ | Carrier | 1.72±0.02 | 1.67±0.03 | 1.76±0.05 | 1.66±0.07 | ||
ApoB | Noncarrier | 1.69±0.05 | 1.75±0.03 | 1.70±0.02 | 1.71±0.02 | ||
|
0.499 | 0.005 | 0.199 | 0.475 | 0.129 | 0.155 |
TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B; ApoA1/ApoB, the ratio of apolipoprotein A1 to apolipoprotein B. The value was presented as median (interquartile range). The difference among the genotypes was determined by the Kruskal-Wallis test or the Wilcoxon-Mann-Whitney test.
Multiple linear regression analysis showed that the –1131T>C genotypes were correlated with serum TG levels, and c.553G>T and c.457G>A genotypes were associated with serum HDL-C levels in nondrinkers (
Lipid | Correlative factor | Unstandardized coefficient | Standard error | Standardized coefficient |
|
|
Nondrinker and drinker | ||||||
TC | ApoA5 c.457G>A genotype | –0.183 | 0.076 | –0.070 | –2.404 | 0.016 |
ApoA5 c.553G>T genotype | –0.248 | 0.114 | –0.065 | –2.184 | 0.029 | |
TG | ApoA5 –1131 T>C allele | 0.297 | 0.073 | 0.119 | 4.067 | 0.000 |
ApoA5 c.457G>A genotype | –0.853 | 0.383 | –0.248 | –2.231 | 0.026 | |
HDL-C | ApoA5 c.553G>T genotype | –0.207 | 0.058 | –0.107 | –3.569 | 0.000 |
LDL-C | ApoA5 –1131 T>C genotype | 0.079 | 0.032 | 0.074 | 2.476 | 0.013 |
ApoA5 c.457G>A genotype | –0.137 | 0.057 | –0.071 | –2.383 | 0.017 | |
ApoA1 | ApoA5 c.457G>A genotype | –0.047 | 0.012 | –0.112 | –3.872 | 0.000 |
ApoB | ApoA5 –1131 T>C genotype | 0.034 | 0.010 | 0.103 | 3.534 | 0.000 |
ApoA5 c.457G>A genotype | –0.040 | 0.017 | –0.068 | –2.312 | 0.021 | |
ApoA1/ApoB | ApoA5 –1131 T>C allele | –0.087 | 0.031 | –0.084 | –2.809 | 0.005 |
Nondrinker | ||||||
TG | ApoA5 –1131 T>C allele | 0.177 | 0.081 | 0.095 | 2.198 | 0.028 |
HDL-C | ApoA5 c.553G>T genotype | –0.170 | 0.077 | –0.094 | –2.214 | 0.027 |
ApoA5 c.457G>A genotype | –0.111 | 0.055 | –0.084 | –2.000 | 0.046 | |
Drinker | ||||||
TC | ApoA5 –1131 T>C genotype | 0.265 | 0.058 | 0.198 | 4.607 | 0.000 |
ApoA5 c.553G>T genotype | –0.340 | 0.154 | –0.095 | –2.200 | 0.028 | |
TG | ApoA5 –1131 T>C genotype | 0.320 | 0.091 | 0.143 | 3.502 | 0.001 |
ApoA5 c.457G>A genotype | –1.414 | 0.504 | –0.363 | –2.804 | 0.005 | |
ApoA5 c.553G>T genotype | 0.500 | 0.244 | 0.084 | 2.052 | 0.041 | |
HDL-C | ApoA5 c.553G>T genotype | –0.262 | 0.084 | –0.132 | –3.112 | 0.002 |
LDL-C | ApoA5 –1131 T>C genotype | 0.140 | 0.046 | 0.134 | 3.067 | 0.002 |
ApoA5 c.457G>A genotype | –0.202 | 0.078 | –0.111 | –2.598 | 0.010 | |
ApoA5 c.553G>T genotype | –0.282 | 0.121 | –0.101 | –2.335 | 0.020 | |
ApoA1 | ApoA5 c.457G>A genotype | –0.062 | 0.015 | –0.178 | –4.202 | 0.000 |
ApoB | ApoA5 –1131 T>C genotype | 0.059 | 0.013 | 0.192 | 4.579 | 0.000 |
ApoA5 c.457G>A genotype | –0.051 | 0.022 | –0.096 | –2.279 | 0.023 | |
ApoA1/ApoB | ApoA5 –1131 T>C genotype | –0.126 | 0.028 | –0.185 | –4.490 | 0.000 |
TC, total cholesterol; TG, triglyceride; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B.
Lipid | Correlative factor | Unstandardized coefficient | Standard error | Standardized coefficient |
|
|
Nondrinker and drinker | ||||||
TC | Body mass index | –0.409 | 0.073 | –1.098 | –5.614 | 0.000 |
Age | 0.014 | 0.002 | 0.253 | 8.586 | 0.000 | |
Weight | 0.211 | 0.032 | 1.915 | 6.623 | 0.000 | |
Height | –0.122 | 0.020 | –1.221 | –6.171 | 0.000 | |
Sex | 0.322 | 0.066 | 0.168 | 4.844 | 0.000 | |
TG | Weight | 0.410 | 0.041 | 2.849 | 9.958 | 0.000 |
Height | –0.250 | 0.026 | –1.910 | –9.730 | 0.000 | |
Body mass index | –0.846 | 0.094 | –1.738 | –8.959 | 0.000 | |
Sex | 0.262 | 0.088 | 0.105 | 2.976 | 0.003 | |
Alcohol consumption | 0.160 | 0.058 | 0.088 | 2.751 | 0.006 | |
Diastolic blood pressure | 0.008 | 0.004 | 0.062 | 2.055 | 0.040 | |
HDL-C | Alcohol consumption | 0.139 | 0.023 | 0.198 | 6.027 | 0.000 |
Age | 0.003 | 0.001 | 0.099 | 3.187 | 0.001 | |
Sex | 0.106 | 0.031 | 0.111 | 3.380 | 0.001 | |
Weight | –0.004 | 0.002 | –0.081 | –2.455 | 0.014 | |
Diastolic blood pressure | 0.003 | 0.002 | 0.067 | 2.101 | 0.036 | |
LDL-C | Body mass index | 0.052 | 0.008 | 0.192 | 6.460 | 0.000 |
Age | 0.007 | 0.001 | 0.185 | 6.308 | 0.000 | |
ApoA1 | Alcohol consumption | 0.066 | 0.007 | 0.302 | 9.701 | 0.000 |
Age | 0.001 | 0.000 | 0.170 | 5.811 | 0.000 | |
Sex | 0.046 | 0.009 | 0.153 | 4.980 | 0.000 | |
ApoB | Body mass index | 0.019 | 0.002 | 0.233 | 7.968 | 0.000 |
Age | 0.003 | 0.000 | 0.209 | 7.262 | 0.000 | |
ApoA1/ApoB | Body mass index | –0.030 | 0.006 | –0.150 | –4.912 | 0.000 |
Age | –0.003 | 0.001 | –0.106 | –3.513 | 0.000 | |
Nondrinker | ||||||
TC | Age | 0.016 | 0.002 | 0.320 | 7.825 | 0.000 |
Body mass index | 0.078 | 0.015 | 0.212 | 5.160 | 0.000 | |
Cigarette smoking | –0.212 | 0.068 | –0.127 | –3.096 | 0.002 | |
TG | Diastolic blood pressure | 0.015 | 0.004 | 0.156 | 3.576 | 0.000 |
Cigarette smoking | –0.179 | 0.068 | –0.115 | –2.635 | 0.009 | |
HDL-C | Sex | 0.212 | 0.041 | 0.226 | 5.169 | 0.000 |
Age | 0.004 | 0.001 | 0.154 | 3.637 | 0.000 | |
Height | –0.004 | 0.002 | –0.096 | –2.172 | 0.030 | |
LDL-C | Body mass index | 0.074 | 0.011 | 0.287 | 7.083 | 0.000 |
Age | 0.010 | 0.001 | 0.276 | 6.920 | 0.000 | |
ApoA1 | Sex | 0.054 | 0.016 | 0.166 | 3.424 | 0.001 |
Age | 0.002 | 0.000 | 0.243 | 5.932 | 0.000 | |
Body mass index | 0.014 | 0.004 | 0.238 | 3.716 | 0.000 | |
Cigarette smoking | –0.033 | 0.012 | –0.124 | –2.607 | 0.009 | |
ApoB | Body mass index | 0.023 | 0.003 | 0.286 | 7.080 | 0.000 |
Age | 0.003 | 0.000 | 0.291 | 7.326 | 0.000 | |
ApoA1/ApoB | Body mass index | –0.029 | 0.009 | –0.140 | –3.182 | 0.002 |
Age | –0.004 | 0.001 | –0.144 | –3.323 | 0.001 | |
Drinker | ||||||
TC | Weight | 0.026 | 0.006 | 0.227 | 4.483 | 0.000 |
Age | 0.007 | 0.003 | 0.118 | 2.675 | 0.008 | |
Sex | 0.189 | 0.087 | 0.104 | 2.180 | 0.030 | |
TG | Body mass index | –1.340 | 0.257 | –2.149 | –5.217 | 0.000 |
Weight | 0.650 | 0.110 | 3.397 | 5.930 | 0.000 | |
Height | –0.424 | 0.074 | –2.288 | –5.706 | 0.000 | |
HDL-C | Body mass index | –0.037 | 0.009 | –0.180 | –4.181 | 0.000 |
Diastolic blood pressure | 0.005 | 0.002 | 0.104 | 2.431 | 0.015 | |
Age | 0.003 | 0.001 | 0.086 | 1.996 | 0.046 | |
ApoA1 | Age | 0.001 | 0.000 | 0.136 | 2.986 | 0.003 |
Height | 0.002 | 0.001 | 0.103 | 2.315 | 0.021 | |
Body mass index | –0.007 | 0.002 | –0.120 | –2.773 | 0.006 | |
Diastolic blood pressure | 0.002 | 0.001 | 0.111 | 2.553 | 0.011 | |
ApoB | Body mass index | 0.012 | 0.004 | 0.141 | 3.361 | 0.001 |
ApoA1/ApoB | Body mass index | 0.264 | 0.081 | 1.387 | 3.252 | 0.001 |
Height | 0.090 | 0.023 | 1.592 | 3.835 | 0.000 | |
Weight | –0.126 | 0.035 | –2.158 | –3.635 | 0.000 |
TC, total cholesterol; TG, triglyceride; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B.
In the present study, we show that the levels of TC, TG, HDL-C, ApoA1 and ApoB were lower in nondrinkers than in drinkers. There was no significant difference in the levels of LDL-C and the ratio of ApoA1 to ApoB between the two groups. These results are consistent with those of our previous studies
The present study shows that there was no significant difference in the allelic and genotypic frequencies of the three SNPs in ApoA5 gene between the nondrinkers and drinkers. The frequency of the –1131C allele in our study populations was similar to that in Chinese (29.9%)
The association of ApoA5 gene polymorphisms and plasma or serum lipid levels in humans has been evaluated in a large number of studies
The interactions of ApoA5 gene polymorphisms and alcohol consumption on serum lipid levels are not fully known. In the present study, we detected an interaction between –1131T>C genotypes and alcohol consumption on serum ApoB levels and the ratio of ApoA1 to ApoB, between c.553G>T genotypes and alcohol consumption on serum LDL-C levels and the ratio of ApoA1 to ApoB, and between c.457G>A genotypes and alcohol consumption on serum TG levels. These findings suggest that some serum lipid parameters in our study subjects were partly influenced by the interactions of ApoA5 gene polymorphisms and alcohol consumption. Correlational studies have suggested that the relation between alcohol consumption and cardiovascular disease may be influenced by the type of alcohol drunk
There are several potential limitations in the present study. First, the sample size in both groups is a bit small. The individual with ApoA5 c.553TT genotype is not detected in our population, and the number of subjects with ApoA5 c.457AA genotype in both groups is also small. It has been postulated that an adequate analysis of the polymorphic variants of the ApoA1/ApoC3/ApoA4 gene complex requires a sample of at least 600 subjects to allow the detection of a twofold increased risk of disease
The present study shows that there was no significant difference in the genotypic and allelic frequencies of ApoA5 –1131T>C, c.553G>T and c.457G>A polymorphisms between the nondrinkers and drinkers. But the interactions of ApoA5 gene polymorphisms and alcohol consumption on serum lipid levels are different among the genotypes. The interactions between –1131T>C genotypes and alcohol consumption on serum ApoB levels and the ratio of ApoA1 to ApoB, between c.553G>T genotypes and alcohol consumption on serum LDL-C levels and the ratio of ApoA1 to ApoB, and between c.457G>A genotypes and alcohol consumption on serum TG levels were detected in the present study. The differences in some serum lipid parameters between the drinkers and nondrinkers might partly result from different interactions of the ApoA5 gene polymorphisms and alcohol consumption.