Relationship between 11β-HSD2 mRNA and insulin sensitivity in term small-for-gestational age neonates after birth

Area of Science:

• Endocrinology
• Neonatal Metabolism
• Perinatal Medicine

Background:

• Small-for-gestational age (SGA) neonates often experience metabolic complications.
• Insulin resistance is a significant concern in SGA infants post-birth.
• The role of placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in SGA metabolic programming requires further investigation.

Purpose of the Study:

• To examine the association between placental 11β-HSD2 mRNA levels and insulin sensitivity in term SGA neonates.
• To compare metabolic profiles, including insulin sensitivity markers, between SGA and appropriate-for-gestational age (AGA) neonates.
• To identify correlations between placental 11β-HSD2 mRNA and key metabolic parameters.

Main Methods:

• Study included 38 term neonates divided into SGA and AGA groups.
• Measured placental 11β-HSD2 mRNA abundance.
• Assessed umbilical vein plasma levels of cortisol, glucose, insulin, adiponectin, visfatin, and IGF-1.
• Calculated Homeostatic Model Assessment for Insulin Resistance (HOMA-IR).

Main Results:

• SGA neonates showed significantly lower placental 11β-HSD2 mRNA and serum cortisol levels compared to AGA neonates.
• SGA infants presented with higher fasting insulin and HOMA-IR values.
• Serum adiponectin and IGF-1 were lower in SGA infants, while visfatin levels were higher.
• Placental 11β-HSD2 mRNA levels negatively correlated with fasting insulin, HOMA-IR, and visfatin.

Conclusions:

• Reduced placental 11β-HSD2 mRNA expression is associated with impaired insulin sensitivity in term SGA neonates.
• Altered cortisol metabolism and dysregulation of adipokines (adiponectin, visfatin) and IGF-1 may contribute to insulin resistance in SGA infants.
• These findings highlight the potential role of placental 11β-HSD2 in the metabolic programming of SGA infants.