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为探究脐带血中胰岛素样生长因子Ⅰ(insulin-like growth factor 1,IGF-1)的浓度和基因甲基化变化与巨大儿发生的关系,选择152名正常妊娠足月分娩的产妇和新生儿为对象,其中68名巨大儿,84名正常出生体重儿.收集产妇及新生儿的基本信息和脐带血样品.采用双抗体夹心ABCELISA法测定脐带血IGF-1蛋白浓度,基质辅助激光解吸附电离飞行时间质谱分析技术(MALDITOF)测定脐带血IGF-1基因启动子区CpG位点的甲基化水平.结果显示,脐带血IGF-1启动子区CpG位点均呈低甲基化状态.以所有研究对象出生体重的上四分位数(4 260 g)为拐点,出生体重<4 260g组的脐带血IGF-1浓度显著高于出生体重≥4 260 g组(P=0.015),且与出生体重呈正相关关系(r=0.242,P=0.011).表明在出生体重<4 260 g范围内,脐带血IGF-1浓度的增加贡献于出生体重的增长.但当胎儿过大时,存在负反馈调节机制,使脐带血IGF-1浓度降低,以限制胎儿过度增长.这些结果提示,脐带血IGF-1浓度与出生体重呈双向性关联,两者均与处于低甲基化状态的脐带血IGF-1的甲基化程度无关.
In order to explore the relationship between the concentration of insulin-like growth factor 1 (IGF-1) and gene methylation in umbilical cord blood and the occurrence of macrosomia, 152 pregnant women and newborns with term full-term childbirth , 68 males and 84 normal birth weight infants were collected.The basic information of maternal and newborns and cord blood samples were collected.The concentration of IGF-1 in umbilical cord blood was measured by double antibody sandwich ABC ELISA and the concentration of matrix-assisted laser desorption ionization MALDITOF was used to detect the methylation level of CpG locus in the promoter region of IGF-1 gene in umbilical cord blood. The results showed that CpG loci in IGF-1 promoter region of umbilical cord blood were hypomethylated The upper quartile of birth weight (4 260 g) was the inflection point for all subjects, and the cord blood IGF-1 concentration was significantly higher for birth weight <4 260 g than for birth weight ≥ 4 260 g (P = 0.015) (R = 0.242, P = 0.011) .It shows that in the range of birth weight <4 260 g, the increase of IGF-1 concentration in umbilical cord blood contribute to the growth of birth weight.But when the fetus is too large, there is a negative Feedback regulation mechanism, so that the concentration of cord blood IGF-1 decreased to limit Children excessive growth. These results suggest that cord blood IGF-1 concentrations and birth weight was associated with two-way, both with the umbilical cord blood in a low methylation status independent of IGF-1 degree of methylation.