In healthy neonates, the angiotensin-converting enzyme gene deletion allele homozygous genotype was associated with significantly impaired insulin sensitivity compared to insertion allele carriers.
Cross-Sectional (n=180)
Is the angiotensin-converting enzyme gene deletion polymorphism associated with impaired insulin sensitivity in healthy newborns?
The ACE gene deletion allele is associated with relatively impaired insulin sensitivity in healthy neonates, potentially linking it to long-term insulin resistance.
CONTEXT: 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. OBJECTIVE: Our goal was to investigate the relationship between angiotensin-converting enzyme gene insertion/deletion polymorphism and the insulin sensitivity in healthy newborns. PATIENTS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Han et al. (Fri,) conducted a cross-sectional in Healthy newborns (n=180). Angiotensin-converting enzyme gene deletion allele (homozygous) vs. Heterozygous or homozygous for the insertion allele was evaluated on Insulin sensitivity (logarithmically transformed homeostasis model assessment and fasting insulin). In healthy neonates, the angiotensin-converting enzyme gene deletion allele homozygous genotype was associated with significantly impaired insulin sensitivity compared to insertion allele carriers.
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