Glucocorticoid-Induced Preterm Birth and Neonatal Hyperglycemia Alter Ovine β-Cell Development

Area of Science:

• Endocrinology
• Neonatal Physiology
• Metabolic Health

Background:

• Adults born preterm face higher risks of impaired glucose tolerance and diabetes.
• High blood glucose in late-gestation fetuses also increases adult diabetes risk.
• Preterm infants often experience hyperglycemia, potentially affecting pancreatic development.

Purpose of the Study:

• To investigate if preterm birth or postnatal hyperglycemia impacts later pancreatic function.
• To differentiate the effects of preterm birth from hyperglycemia on pancreatic beta-cell mass and function.

Main Methods:

• Singleton preterm lambs were made hyperglycemic (HYPER) or normoglycemic.
• Groups were compared to vehicle-treated preterm and term controls.
• Pancreatic beta-cell mass, insulin secretion, and gene expression were assessed.

Main Results:

• Preterm birth reduced beta-cell mass from 4 weeks post-term into adulthood.
• Reduced insulin secretion and mRNA expression were observed in preterm lambs.
• Postnatal hyperglycemia in preterm lambs further downregulated key pancreatic gene expression.

Conclusions:

• Reduced beta-cell mass following preterm birth is a key factor in elevated diabetes risk.
• Postnatal hyperglycemia in preterm infants can worsen pancreatic function and diabetes risk.
• Interventions to manage hyperglycemia in preterm infants may be crucial for long-term metabolic health.