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Cord Blood from SGA Preterm Infants Exhibits Increased GLUT4 mRNA Expression
Satoshi Narai1, Yuki Kawashima-Sonoyama1, Masanobu Fujimoto1
1Division of Pediatrics and Perinatology, Department of Multidisciplinary Internal Medicine, School of Medicine, Faculty of Medicine, Tottori University, Yonago 683-8503, Japan and.
Insights
Small-for-gestational age (SGA) preterm infants do not show hyperinsulinemia but have altered insulin/IGF signaling, specifically increased GLUT4 mRNA. This suggests prematurity or malnutrition impacts this crucial pathway in newborns.
Area of Science:
- Neonatal physiology
- Endocrinology
- Metabolic disorders
Background:
- Insulin and insulin-like growth factor (IGF) signaling are vital for fetal and infant growth and glucose regulation.
- Infants who are small-for-gestational age (SGA) and preterm infants exhibit abnormal growth and glucose metabolism.
- Previous research indicated abnormal insulin/IGF signaling in term SGA infants' cord blood.
Purpose of the Study:
- To investigate if preterm infants exhibit similar aberrations in cord blood insulin/IGF signaling as term SGA infants.
- To compare insulin/IGF signaling pathways between SGA preterm and appropriate-for-gestational age (AGA) preterm neonates.
Main Methods:
- Collected 41 preterm cord blood samples.
- Measured blood glucose, insulin, IGF-1, and C-peptide levels.
- Analyzed mRNA expression of IGF1R, INSR, IRS1, IRS2, and SLC2A4 (GLUT4) using quantitative RT-PCR.
Main Results:
- Included 34 AGA and 7 SGA preterm neonates.
- No significant differences in hyperinsulinemia, IGF1R, or INSR mRNA expression were found between SGA and AGA preterm groups.
- Preterm SGA infants showed increased GLUT4 mRNA levels, particularly those with hypoglycemia, compared to hypoglycemic preterm AGA infants.
Conclusions:
- Small-for-gestational age preterm birth does not lead to hyperinsulinemia.
- Insulin/IGF signaling components, such as GLUT4, are modified in the umbilical cord blood of SGA preterm infants.
- The findings suggest that prematurity or adaptation to malnutrition alters the insulin/IGF signaling pathway in newborns.
Background:
Insulin and insulin-like growth factor (IGF) signaling plays an important role in prenatal and postnatal growth and glucose metabolism. Both small-for-gestational age (SGA) and preterm infants have abnormal growth and glucose metabolism. However, the underlying mechanism remains unknown. Recently, we showed that term SGA infants have abnormal insulin/IGF signaling in cord blood. In this study, we examined whether preterm infants show similar aberrations in cord blood insulin/IGF signaling.
Methods:
A total of 41 preterm cord blood samples were collected. Blood glucose, insulin, IGF-1, and C-peptide concentrations were measured, and mRNA expression of IGF1R, INSR, IRS1, IRS2, and SLC2A4 (i.e., GLUT4) was analyzed by quantitative reverse-transcription PCR.
Results:
This study included 34 appropriate-for-gestational age (AGA) and 7 SGA preterm neonates. No hyperinsulinemia or any differences in IGF1R or INSR mRNA expression were detected between the two groups. However, GLUT4 mRNA levels were increased in preterm SGA. Moreover, the expression level in hypoglycemic preterm SGA was significantly higher than that in hypoglycemic preterm AGA. IRS2 mRNA expression did not show a statistically significant difference between preterm SGA and AGA neonates.
Conclusion:
SGA preterm birth does not induce hyperinsulinemia; however, it modifies insulin/IGF signaling components such as GLUT4 in umbilical cord blood. Our study suggests that prematurity or adaptation to malnutrition alters the insulin/IGF signaling pathway.
