Oxytocin signal contributes to the adaptative growth of islets during gestation

in Endocrine Connections
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  • 1 P Gu, Department of Neurology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
  • 2 Y Lin, Department of Pathology, Nanjing Medical University, Nanjing, China
  • 3 Q Wan, Department of Neurology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
  • 4 D Su, Department of Pathology, Nanjing Medical University, Nanjing, 210029, China
  • 5 Q Shu, Department of Obstetrics, Shanghai First Maternity and Infant Health Hospital, School of Medicine, Tongji University, Shanghai, China

Correspondence: Qun Shu, Email: cmihh2012@163.com

Background: Increased insulin production and secretion by pancreatic β-cells are important for ensuring the high insulin demand during gestation. However, the underlying mechanism of β-cell adaptation during gestation or in gestational diabetes mellitus (GDM) remains unclear. Oxytocin is an important physiological hormone in gestation and delivery, and it also contributes to the maintenance of β-cell function. The aim of this study was to investigate the role of oxytocin in β-cell adaptation during pregnancy.

Methods: The relationship between the blood oxytocin level and pancreatic β-cell function in patients with GDM and healthy pregnant women was investigated. Gestating and non-gestating mice were used to evaluate the in vivo effect of oxytocin signal on β-cells during pregnancy. In vitro experiments were performed on INS-1 insulinoma cells.

Results: The blood oxytocin levels were lower in patients with GDM than in healthy pregnant women and were associated with impaired pancreatic β-cell function. Acute administration of oxytocin increased insulin secretion in both gestating and non-gestating mice. A three-week oxytocin treatment promoted the proliferation of pancreatic β-cells and increased the β-cell mass in gestating but not non-gestating mice. Antagonism of oxytocin receptors by atosiban impaired insulin secretion and induced GDM in gestating but not non-gestating mice. Oxytocin enhanced glucose-stimulated insulin secretion, activated the mitogen-activated protein kinase pathway, and promoted cell proliferation in INS-1 cells.

Conclusions: These findings provide strong evidence that oxytocin is needed for β-cell adaptation during pregnancy to maintain β-cell function, and lack of oxytocin could be associated with the risk of GDM.

 

     European Society of Endocrinology

     Society for Endocrinology

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