Han Tongyan, Wang Xinli, Cui Yunpu, Ye Hongmao, Tong Xiaomei, Piao Meihua
Department of Pediatrics, Third Hospital, Peking University, Beijing 100083, PR China.
Pediatrics. 2007 Jun;119(6):1089-94. doi: 10.1542/peds.2006-3297.
It was proposed that the association between low birth weight and adult insulin resistance is principally genetically mediated. The insertion/deletion polymorphism of the angiotensin-converting enzyme gene was associated with insulin sensitivity in adults.
Our goal was to investigate the relationship between angiotensin-converting enzyme gene insertion/deletion polymorphism and the insulin sensitivity in healthy newborns.
One hundred eighty healthy newborns, all of whom had a 1-minute Apgar score of > 7 and gestational age > 33 weeks, were enrolled in the study. Fasting glucose and insulin levels were measured on day 2 or 3 after birth, and angiotensin-converting enzyme genotype was determined.
The observed frequency distribution of angiotensin-converting enzyme genotypes did not deviate from that predicted by Hardy-Weinberg equilibrium in this group. There were no statistically significant differences in birth size and shape in different angiotensin-converting enzyme genotypes. Those carriers of the genotype homozygous for the deletion allele had the highest logarithmically transformed homeostasis model assessment compared with those who were heterozygous or homozygous for the insertion polymorphism. When compared with those with > or = 1 insertion allele, those of the genotype homozygous for the deletion allele had significantly higher logarithmically transformed fasting insulin and logarithmically transformed homeostasis model assessment results. Regarding birth weight, birth length, ponderal index, and fasting glucose concentration, there were no significant differences between the genotype homozygous for the deletion allele and the genotypes heterozygous or homozygous for the insertion allele.
In this study, the deletion allele was associated with relatively impaired insulin sensitivity in healthy neonates. It may be a clue to explain the association between the deletion allele and insulin resistance in the long-term.
有人提出低出生体重与成人胰岛素抵抗之间的关联主要由基因介导。血管紧张素转换酶基因的插入/缺失多态性与成人胰岛素敏感性相关。
我们的目标是研究血管紧张素转换酶基因插入/缺失多态性与健康新生儿胰岛素敏感性之间的关系。
180名健康新生儿纳入本研究，所有新生儿1分钟阿氏评分>7分且胎龄>33周。在出生后第2天或第3天测量空腹血糖和胰岛素水平，并确定血管紧张素转换酶基因型。
该组中血管紧张素转换酶基因型的观察频率分布未偏离哈迪-温伯格平衡预测值。不同血管紧张素转换酶基因型在出生大小和体型方面无统计学显著差异。与插入多态性杂合或纯合的个体相比，缺失等位基因纯合基因型的携带者具有最高的对数转换稳态模型评估值。与有≥1个插入等位基因的个体相比，缺失等位基因纯合基因型的个体对数转换空腹胰岛素和对数转换稳态模型评估结果显著更高。在出生体重、出生身长、体重指数和空腹血糖浓度方面，缺失等位基因纯合基因型与插入等位基因杂合或纯合基因型之间无显著差异。
在本研究中，缺失等位基因与健康新生儿相对受损的胰岛素敏感性相关。这可能是长期解释缺失等位基因与胰岛素抵抗之间关联的一条线索。
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