Gestational diabetes (GDM) affects up to ∼1 in 6 pregnancies worldwide, representing ∼18 million births each year. It causes excessively big babies and difficult deliveries. There is also a strong link with the development of type 2 diabetes in the mother in later life. A failure of the mother to produce enough insulin and/or respond to insulin and appropriately control her glucose levels during pregnancy are believed to be the main culprits for GDM pathogenesis and its associated health risks to mother and baby. However, increasing evidence suggests that the placenta and particularly the function of its mitochondria may play a role.
It is well recognised that mitochondria generate ATP to fuel placental development, macromolecule synthesis and substrate exchange during pregnancy. They also produce reactive oxygen species (ROS), which are important signalling molecules that control placental functions in normal and compromised gestational environments (Lu and Sferruzzi‐Perri, 2021). Although less studied, mitochondria are also responsible for the synthesis of steroid hormones, like progesterone and oestrogen, which control maternal insulin production and action during gestation (Napso et al. 2018, Sferruzzi‐Perri et al. 2020). Previous work has shown that mitochondrial functional capacity is aberrant in term placental tissue from women with GDM (Sobrevia et al. 2020). However, the placenta is a heterogeneous organ and to understand the aetiology of GDM and its associated health risks, it is paramount to define the cellular contribution of changes in placental mitochondrial function.
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