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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Absence of the wild-type allele (192 base pairs) of a polymorphism in the promoter region of the IGF-I gene but not a polymorphism in the insulin gene variable number of tandem repeat locus is associated with accelerated weight gain in infancy.
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Absence of the wild-type allele (192 base pairs) of a polymorphism in the promoter region of the IGF-I gene but not a polymorphism in the insulin gene variable number of tandem repeat locus is associated with accelerated weight gain in infancy.

机译：IGF-1基因启动子区缺乏野生型等位基因（192个碱基对），而胰岛素基因可变数目的串联重复基因座不是多态性，与婴儿期体重增加有关。

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摘要

OBJECTIVE: Our goal was to investigate whether a polymorphism in the insulin-like growth factor I promoter gene (IGF-I, wild-type, 192 base pairs) and in the insulin gene (INS) variable number of tandem repeat locus influence birth weight and weight gain in infancy. PATIENTS AND METHODS: We obtained genomic DNA from 768 children. Exclusion criteria were multiple births, gestational diabetes, maternal diabetes, gestational age <37 weeks, >42 weeks, or unclear, and any condition potentially influencing weight gain. SD scores were calculated and adjusted for gestational age and gender. A gain in SD scores for weight between birth and 1 year >0.67 SD scores was defined as accelerated weight gain. Genotyping was performed by fragment length analysis (IGF-I) and by fragment length analysis after using a restriction enzyme-based assay (INS variable number tandem repeat). RESULTS: Accelerated weight gain was present in 205 of 768 children. IGF-I and INS variable number tandem repeat genotype were not associated with birth weight. The IGF-I 192-base pair allele was less frequent in children with accelerated weight gain and was shown to reduce the risk for accelerated weight gain in a logistic regression model. CONCLUSION: The IGF-I 192-base pair allele may reduce the risk for rapid weight gain in early infancy.
机译：目的：我们的目的是研究胰岛素样生长因子I启动子基因（IGF-1，野生型，192个碱基对）和胰岛素基因（INS）的可变数目的串联重复基因座的多态性是否影响出生体重和婴儿期的体重增加。患者与方法：我们从768名儿童中获得了基因组DNA。排除标准为多胎，妊娠糖尿病，母亲糖尿病，胎龄<37周，> 42周或不清楚，以及任何可能影响体重增加的疾病。计算SD分数并针对胎龄和性别进行调整。出生至1岁之间体重的SD得分增加> 0.67 SD得分被定义为体重增加。使用基于限制酶的测定法（INS可变数目串联重复），通过片段长度分析（IGF-1）和片段长度分析进行基因分型。结果：768名儿童中有205名体重增加。 IGF-1和INS可变数目串联重复基因型与出生体重无关。在体重增加加速的儿童中，IGF-I 192个碱基对的等位基因频率较低，在逻辑回归模型中显示可降低加速体重增加的风险。结论：IGF-I 192个碱基对等位基因可能降低婴儿早期体重快速增加的风险。

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