Dr Simon Tunster

The fetus is entirely dependent upon a healthy, functional placenta to deliver sufficient nutrients to support normal growth. Fetal growth restriction (FGR), which describes a fetus that fails to achieve its genetic growth potential, affects approximately 10% of pregnancies in developed countries. Although the precise mechanisms are often unclear, FGR is frequently attributed to “placental insufficiency”, where the placental supply of nutrients fails to meet fetal demand.

Placental insufficiency typically results in asymmetric growth restriction, with brain growth spared at the expense of other organs such as the liver, and rapid catch-up growth observed in the first year. In addition to increased morbidity and mortality in the neonatal period, FGR is associated with an increased risk of developing metabolic diseases such as type 2 diabetes and obesity in adulthood. However, the mechanisms that drive this “fetal programming” of adult disease are poorly understood.

In humans, increased expression of the imprinted gene PHLDA2 is associated with FGR. My research uses mouse models in which expression of Phlda2 is either increased or knocked-out in order to understand how Phlda2 regulates placental development, function, and ultimately, fetal growth. I am currently investigating how placental nutrient transport is affected in the context of elevated Phlda2 expression.

Centre for Trophoblast Research

Society for Endocrinology

Isaac Newton Trust