中文摘要：

目的 探讨重庆汉族男性载脂蛋白B基因（apolipoprotein B,ApoB）MspⅠ、XbaⅠ、EcoRⅠ位点的多态性与血脂水平的关系。方法 采用基因芯片技术,检测血脂异常组157人和健康对照组180人载脂蛋白B基因MspⅠ、XbaⅠ、EcoRⅠ位点的多态性,并分析其与血脂水平的关系。结果 血脂异常组和健康对照组组内比较,MspⅠ位点M＋M-基因型的总胆固醇（TC）水平高于M＋M＋基因型[异常组：（6.54±0.58）vs（5.58±0.83）mmol/L,P〈0.01;对照组：（5.43±0.17）vs（4.39±0.62）mmol/L,P〈0.01）];XbaⅠ位点X＋X-基因型的高密度脂蛋白胆固醇（HDL-C）水平和低密度脂蛋白胆固醇（LDL-C）水平分别低于和高于X-X-基因型[异常组HDL-C：（1.08±0.27）vs（1.22±0.44）mmol/L,P=0.03;LDL-C：（3.88±0.63）vs（3.46±0.83）mmol/L,P=0.01;对照组HDL-C：（1.31±0.43）vs（1.48±0.37）mmol/L,P=0.04;LDLC：（3.19±0.54）vs（2.94±0.59）mmol/L,P=0.02];EcoRⅠ位点E＋E-基因型的HDL-C水平低于E＋E＋基因型[异常组：（1.01±0.18）vs（1.21±0.43）mmol/L,P=0.01;对照组：（1.27±0.20）vs（1.47±0.40）mmol/L,P=0.03]。血脂异常组和对照组组间比较,异常组X＋X-基因型HDL-C水平和LDL-C水平分别低于和高于对照组X＋X-基因型[HDL-C：（1.08±0.27）vs（1.31±0.43）mmol/L,P=0.01;LDL-C：（3.88±0.63）vs（3.19±0.54）mmol/L,P〈0.01];异常组E＋E-基因型HDL-C水平低于对照组E＋E-基因型[（1.01±0.18）vs（1.27±0.20）mmol/L,P〈0.01]。多元线性回归分析结果显示,MspⅠ多态性与TC呈正相关,XbaⅠ多态性与HDL-C呈负相关、与LDL-C呈正相关。结论 ApoB基因MspⅠ和XbaⅠ多态性对血脂水平有一定的影响,M＋M-基因型有使TC水平升高的趋势,X＋X-基因型有使HDL-C水平降低、LDL-C水平升高的趋势。

英文摘要：

Objective To explore the relationship between apolipoprotein B （ApoB） gene Msp I/Xba I/EcoR I polymorphisms and the levels of serum lipid in male Han population in Chongqing. Methods The ApoB gene Msp I/Xba I / EcoR ] polymorphisms were detected by gene chip technology in 157 dyslipidemia cases and 180 healthy controls; and their relationship with serum lipids was analyzed in the dyslipidemia group and the controls. Results In both dyslipidemia group and control group, the total cholesterol （TC） levels with M＋ M- genotype at Msp I locus were signiicantly higher than those with M＋ M＋ genotype （dyslipidemia group： [6.54±0. 58] vs [5.58±0.83] mmol/L, P〈0.01; control group.. [5.43±0. 17] vs [-4.39±0. 62] retool/L, P〈0.01）; the high density lipoprotein cholesterol （HDDC） levels with X＋ X- genotype at Xba I locus were signi{icantly lower than those with X-X- genotype, whereas the low density lipoprotein cholesterol （LDL-C） levelswere significantly higher than those with X X genotype （dyslipidemia group HDL-C： [1.08±0. 27] vs [-1.22±0. 44] mmol/ L, P=0. 03; LDL-C： [3.88±0.63] vs [3.46±0. 83] mmol/L, P=0. 01; control group HDL-C： [-1.31±0. 43] vs [-1.48± 0. 37] mmol/L, P=0. 04; LDL-C： [3. 19±0. 54] vs [2. 94±0. 59] mmol/L, P=0. 02） the HDL-C levels with E＋E genotype at EcoR I locus were significantly lower than those with E＋ E＋ genotype （dyslipidemia group： [1. 01 ±0. 18] vs [1.21±0. 43] retool/L, P=0. 01; control group： [1.27±0. 20] vs [1.47±0. 40] mmol/L, P=0.03）. The HDL-C levels in dyslipidemia group with X＋ X- genotype were significantly lower than the control group with X＋ X- genotype, but the LDL-C levels were significantly higher than the control group with X＋X genotype （HDL-C： [-1.08~0. 27] vs [-1. 314-0.43] mmol/ L, P=0.01; LDL-C.. [3. 88±0. 63] vs [3. 19±0.54] mmol/L, P〈0.01） the HDL-C levels in the dyslipidemia group with E＋ E- genotype were significantly lower than those in the control group （[1.01±0. 18] vs [1.2