CAJ | 학술논문

目的：研究血管紧张素转化酶（ACE）基因插入或缺失（I /D）多态性与健康新生儿胰岛素敏感性的关系。方法180例健康新生儿（孕周>33周，1分钟 Apgar 评分>7分）在出生时测量体重、身长，生后2~3天上午8～9时哺乳前取足跟血，测空腹血糖（FG）和空腹胰岛素（FI）水平，提取 DNA 进行 ACE 基因分型，用 FI 和内稳态模式评估值（HOMA）衡量胰岛素敏感性。结果 ACE基因分布符合 Hardy-Weinberg 平衡定律（χ2=0.188，P =0.910）。不同 ACE 基因型间出生体格无差异。DD 基因型的 HOMA 对数值最高（0.21±0.45），但与 ID 和 II 基因型相比差异无显著性。DD 基因型与≥1个 I 等位基因（即 ID+II 基因型）比较，DD 基因型 FI 对数值较高（0.93±0.41比0.76±0.36, P=0.018），DD 基因型的 HOMA 对数值较高（0.21±0.45比0.01±0.38, P=0.010）。结论在健康新生儿， D 等位基因与相对差的胰岛素敏感性相关。这可能是解释远期胰岛素抵抗与 D 等位基因相关的线索。
목적：연구혈관긴장소전화매（ACE）기인삽입혹결실（I /D）다태성여건강신생인이도소민감성적관계。방법180례건강신생인（잉주>33주，1분종 Apgar 평분>7분）재출생시측량체중、신장，생후2~3천상오8～9시포유전취족근혈，측공복혈당（FG）화공복이도소（FI）수평，제취 DNA 진행 ACE 기인분형，용 FI 화내은태모식평고치（HOMA）형량이도소민감성。결과 ACE기인분포부합 Hardy-Weinberg 평형정률（χ2=0.188，P =0.910）。불동 ACE 기인형간출생체격무차이。DD 기인형적 HOMA 대수치최고（0.21±0.45），단여 ID 화 II 기인형상비차이무현저성。DD 기인형여≥1개 I 등위기인（즉 ID+II 기인형）비교，DD 기인형 FI 대수치교고（0.93±0.41비0.76±0.36, P=0.018），DD 기인형적 HOMA 대수치교고（0.21±0.45비0.01±0.38, P=0.010）。결론재건강신생인， D 등위기인여상대차적이도소민감성상관。저가능시해석원기이도소저항여 D 등위기인상관적선색。
Objective Our goal was to investigate the relationship between angiotensin-converting enzyme gene insertion/deletion polymorphism and the insulin sensitivity in healthy newborns. Method 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.Result 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 (HOMA) compared with those who were heterozygous or homozygous for the insertion polymorphism. When compared with those with ≥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. Conclusion 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.