Inositol and its derivatives regulate insulin, glucose and lipid signalling and metabolism. Disrupted inositol metabolism is associated with pregnancy complications, and clinical trials of inositol supplementation during preconception and pregnancy demonstrate promising risk reductions in gestational diabetes and preterm birth, which affect ~20% and ~10% of deliveries respectively. Furthermore, elevated maternal glycaemia increases neonatal adiposity, which is attenuated by high placental inositol content. This suggests that inositol mitigates glucose’s pro-adipogenic effects in the fetus. However, to develop inositol as an intervention, we must understand how inositol moderates these risks.

We hypothesise that inositol modulates lipid transport, metabolism and signalling at the maternal-placental-fetal interface, and hence fetal nutrient transfer and pregnancy progression. Using a range of ex-vivo and in-vitro techniques (including tissue/cell culture, molecular biology, LC-MS lipidomics), we will correlate laboratory findings with multiple maternal and offspring measures (eg. BMI, birthweight) to understand inositol’s role at the maternal-fetal interface and its possible consequences for fetal growth and development. In doing so, we may be able to mitigate the long-term negative health implications associated with gestational diabetes, preterm delivery and aberrant fetal growth in the mother and her offspring.