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目的探讨基因过氧化物酶增殖激活受体(PPAR)γC161T多态性对低出生体质量新生儿的影响。方法用横断面调查法,使用统一的调查表,对入住本院分娩的孕妇及其单胎、活胎的低出生体质量儿和健康对照新生儿进行调查,共得到有效样本268个母亲-新生儿对,并根据出生体质量和孕周进行分组,分为健康对照组和低出生体质量组,其中低出生体质量组包括早产儿组和小于胎龄儿组。使用多聚酶链-限制性片段长度多态性(PCR-RFLP)方法检测其外周血基因PPARγC161T单核苷酸多态性,分析不同基因型对其低出生体质量的影响。结果 1.根据双变量Logistic回归分析得出低出生体质量与父母的受教育水平、职业、家庭居住环境和氛围及维生素的补充相关,相关系数分别为-0.434、-0.337、-0.343、-0.269、-0.691、0.296、0.235。2.PPARγC161T多态性CC型、CT型与TT型基因频率分布在健康对照组、小于胎龄儿组和早产儿组分别为53.33%、14.44%、21.11%,75.00%、18.18%、6.82%和76.67%、20.00%、3.33%,早产儿组和小于胎龄儿组比较均无统计学差异,但与健康对照组比较均有统计学差异。携带C等位基因增加低出生体质量的风险,低出生体质量组携带CC基因型风险与健康出生体质量儿的OR值分别为1.938(95%CI:1.001～3.750,P=0.002)、2.122(95%CI:1.091～4.127,P=0.000)。结论低出生体质量是环境和遗传因素共同作用的结果,PPARγC161T多态性与低出生体质量有关,C等位基因可能是低出生体质量的遗传易感基因。
Objective To investigate the effect of genetic polymorphisms of peroxisome proliferator-activated receptor (PPAR) γC161T on neonates with low birth weight. Methods A cross-sectional survey and a unified questionnaire were used to survey pregnant women and their single birth and live births with low birth weight and healthy newborns admitted to our hospital. A total of 268 mothers - freshmen The groups were divided into healthy control group and low birth weight group according to birth weight and gestational age. Among them, low birth weight group included premature infant group and small gestational age child group. Polymerase chain-restriction fragment length polymorphism (PCR-RFLP) was used to detect the single nucleotide polymorphisms of PPARγC161T in peripheral blood, and the effect of different genotypes on the low birth weight was analyzed. According to the bivariate Logistic regression analysis, the correlations between low birth weight and parents’ education level, occupation, family living environment and atmosphere and vitamins were obtained. The correlation coefficients were -0.434, -0.337, -0.343, -0.269 , -0.691,0.296,0.235.2.The frequencies of PPARγC161T polymorphism CC, CT and TT genotypes were 53.33%, 14.44% and 21.11% respectively in healthy control group, less than gestational age group and premature infant group, 75.00%, 18.18%, 6.82% and 76.67%, 20.00% and 3.33% respectively. There was no significant difference between the premature infant group and the younger than gestational age child group, but there was a significant difference compared with the healthy control group. Carrying the C allele increased the risk of low birth weight, with OR values of 1.938 (95% CI: 1.001-3.750, P = 0.002), 2.122 for low birth weight children with CC genotype risk and healthy birth weight (95% CI: 1.091 to 4.127, P = 0.000). Conclusions Low birth weight is a result of the combination of environmental and genetic factors. Polymorphism of PPARγC161T is associated with low birth weight, and C allele may be a genetic predisposition to low birth weight.