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Published on: April 12, 2021
Impact of prematurity for pancreatic islet and beta-cell development
1Liggins InstituteUniversity of Auckland, Auckland, New Zealand f.bloomfield@auckland.ac.nz.
Insights
Preterm birth survivors face higher risks of developing diabetes later in life. Factors before, during, and after birth may impair pancreatic beta-cell development, increasing non-communicable disease risks.
Area of Science:
- Endocrinology
- Neonatalogy
- Developmental Biology
Background:
- Increasing survival rates of preterm infants highlight emerging health risks.
- Preterm birth is associated with neurodevelopmental issues and non-communicable diseases, notably diabetes.
Purpose of the Study:
- To investigate the impact of preterm birth on fetal and neonatal pancreatic beta-cell development.
- To identify factors contributing to altered beta-cell mass and increased diabetes risk in preterm survivors.
Main Methods:
- Review of epidemiological studies on preterm birth and diabetes incidence.
- Analysis of experimental evidence on factors affecting beta-cell development during critical prenatal and postnatal periods.
Main Results:
- Preterm birth, including late preterm and early term gestations, is linked to increased risks of both type 1 and type 2 diabetes.
- Factors related to the cause of preterm birth, the birth event itself, and postnatal care can negatively affect beta-cell development.
Conclusions:
- Altered pancreatic beta-cell development due to preterm birth exposures contributes to elevated diabetes risk.
- Understanding these developmental impacts may inform interventions to mitigate long-term diabetes risk in preterm populations.
Abstract:
As increasing numbers of babies born preterm survive into adulthood, it is becoming clear that, in addition to the well-described risks of neurodevelopmental sequelae, there also are increased risks for non-communicable diseases, including diabetes. Epidemiological studies indicate that risks are increased even for birth at late preterm and early term gestations and for both type 1 and type 2 diabetes. Thus, factors related to preterm birth likely affect development of the fetal and neonatal beta-cell in addition to effects on peripheral insulin sensitivity. These factors could operate prior to preterm birth and be related to the underlying cause of preterm birth, to the event of being born preterm itself, to the postnatal care of the preterm neonate or to a combination of these exposures. Experimental evidence indicates that factors may be operating during all these critical periods to contribute to altered development of beta-cell mass in those born preterm. Greater understanding of how these factors impact upon development of the pancreas may lead to interventions or management approaches that mitigate the increased risk of later diabetes.
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