Maternal adaptation to the metabolic demands placed upon the mother by pregnancy includes alterations in glucose homeostasis and adaptations by the pancreatic islets particularly beta cells. Defective adaptation results in the disease gestational diabetes. Due to practical and ethical constraints, studies in humans are relatively limited. In rodent models, beta-cell mass has been shown to change dynamically around pregnancy, expanding during gestation, and regressing back to pre-pregnancy levels in the postpartum period. Molecular mechanisms identified to date include beta-cell proliferation and increased insulin secretion. While lactogen signaling, and islet serotonin signaling contribute to these processes, detailed molecular understanding of pregnancy adaptation is still poorly understood, particularly signals early in pregnancy, and those driving postpartum regression, or about how other islet cell types adapt to pregnancy. Recent studies have also shown critical roles for cross talk with other maternal organs and the placenta. Little is known about adaptations in humans.
This Research Topic solicits articles investigating normal mechanisms underlying pregnancy adaptations of pancreatic islets at molecular level, how these are altered in gestational diabetes, particularly studies that address key gaps in the field, including but not limited to:
• New models of GDM in rodents or other model systems
• Evidence for genes specifically causing/associated with GDM (distinct from T2D)
• How do the various signaling pathways crosstalk within beta-cells during gestation?
• What is the mechanism of postpartum beta-cell mass regression?
• Do lactogens and PRL activate specific target genes, or is it sum of their activity?
• Mechanisms of crosstalk between islets and other maternal tissues or the fetus/placenta.
• How do non-beta endocrine cells adapt during pregnancy? Non-endocrine islet cells?
Maternal adaptation to the metabolic demands placed upon the mother by pregnancy includes alterations in glucose homeostasis and adaptations by the pancreatic islets particularly beta cells. Defective adaptation results in the disease gestational diabetes. Due to practical and ethical constraints, studies in humans are relatively limited. In rodent models, beta-cell mass has been shown to change dynamically around pregnancy, expanding during gestation, and regressing back to pre-pregnancy levels in the postpartum period. Molecular mechanisms identified to date include beta-cell proliferation and increased insulin secretion. While lactogen signaling, and islet serotonin signaling contribute to these processes, detailed molecular understanding of pregnancy adaptation is still poorly understood, particularly signals early in pregnancy, and those driving postpartum regression, or about how other islet cell types adapt to pregnancy. Recent studies have also shown critical roles for cross talk with other maternal organs and the placenta. Little is known about adaptations in humans.
This Research Topic solicits articles investigating normal mechanisms underlying pregnancy adaptations of pancreatic islets at molecular level, how these are altered in gestational diabetes, particularly studies that address key gaps in the field, including but not limited to:
• New models of GDM in rodents or other model systems
• Evidence for genes specifically causing/associated with GDM (distinct from T2D)
• How do the various signaling pathways crosstalk within beta-cells during gestation?
• What is the mechanism of postpartum beta-cell mass regression?
• Do lactogens and PRL activate specific target genes, or is it sum of their activity?
• Mechanisms of crosstalk between islets and other maternal tissues or the fetus/placenta.
• How do non-beta endocrine cells adapt during pregnancy? Non-endocrine islet cells?
