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IGF1 gene is epigenetically activated in preterm infants with intrauterine growth restriction
Masato Kantake1, Naho Ikeda2, Hirofumi Nakaoka3,4
1Neonatal Medical Center, Juntendo University Shizuoka Hospital, 1192 Nagaoka, Izunokuni, Shizuoka, 410-2295, Japan. kantake@juntendo.ac.jp.
Insights
Insulin-like Growth Factor 1 (IGF1) gene promoter methylation occurs during fetal development. This epigenetic change is reduced in infants with intrauterine growth restriction (IUGR), impacting growth and metabolism.
Area of Science:
- Endocrinology
- Epigenetics
- Developmental Biology
Background:
- Insulin-like Growth Factor 1 (IGF1) regulates growth and metabolism; low IGF1 causes growth restriction and adult metabolic diseases.
- IGF1 gene P2 promoter methylation leads to low IGF1 secretion, but the timing of this epigenetic event is unknown.
- Understanding IGF1 gene methylation timing during intrauterine development is crucial for infant health.
Purpose of the Study:
- To determine when IGF1 gene P2 promoter methylation occurs during intrauterine development.
- To investigate the relationship between IGF1 P2 promoter methylation and intrauterine growth restriction (IUGR).
Main Methods:
- Analysis of 56 preterm infants (<32 weeks gestation), including 19 with IUGR.
- Genomic DNA extraction from whole blood at birth.
- Bisulfite amplicon sequencing (MiSeq) to analyze methylation at six CpG sites in the IGF1 P2 promoter.
Main Results:
- IGF1 P2 promoter methylation positively correlated with birth weight and length in preterm infants.
- Infants with IUGR showed significantly reduced methylation at all six CpG sites.
- These findings suggest epigenetic activation of the IGF1 gene before 32 weeks gestation in IUGR infants.
Conclusions:
- The IGF1 gene is epigenetically activated before 32 weeks gestation in infants with IUGR.
- This activation may be suppressed later in gestation, impacting growth and metabolism.
- Insights may aid in preventing adult diseases and guiding nutritional management for preterm infants.
Background:
IGF1 is a key molecule in the regulation of growth and metabolism. Low IGF1 secretion is known to cause growth restriction in childhood, as well as deregulated lipid metabolism, cardiovascular disease, and diabetes in adulthood. The IGF1 gene P2 promoter is highly methylated, resulting in low secretion of IGF1 in small infants and children. However, it is unknown when this methylation occurs. The aim of study was to clarify the point when this epigenetic program occurs during intrauterine development. We analyzed 56 preterm infants born before 32 weeks of gestation, including 19 intrauterine growth restriction (IUGR) infants whose birth weights were lower than - 2SD calculated by the Japanese datasets. We extracted genomic DNA from whole blood at birth; methylation of the six CpG sites in the IGF1 P2 promoter was analyzed by the bisulfite amplicon method using the MiSeq platform.
Results:
In contrast to term infants and children, the methylation of all six CpG sites positively correlated with body weight and body length at birth. IGF1 P2 promoter methylation levels were significantly reduced in all six CpG sites in infants with IUGR.
Conclusions:
These findings indicated that the IGF1 gene is epigenetically activated before 32 weeks of gestation in infants with IUGR and that the activated gene may become suppressed after this time point. This study may provide new insights to prevent the onset of adult diseases and to aid in nutritional management for preterm birth infants in neonatal intensive care units.
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