The overall goal of our research is to understand the connection between maternal health and the placental regulation of nutrient metabolism and delivery, and fetal growth.
This is important because babies’ growth in the womb (organ development, fat accrual, lean tissue growth) can modify their metabolism, cardiovascular function, neurological development, and their risk of future disease. Ultimately, we seek to improve cardiometabolic health of offspring, and thus population health in the long-term.
This concept is referred to as the Developmental Origins of Health and Disease, or Barker, Hypothesis (so named after David Barker, MD)
Currently, we are studying the effect of maternal obesity on placental lipid handling. Lipids are critical for proper fetal development (think cell membranes!), but the fetus is unable to synthesize lipids at the rate required to fulfill its developmental requirements. The placenta is not capable of making these essential fatty acids either, and so the fetus relies on maternal supply and placental transfer of these critical nutrients for development. Thus, changes to placental fatty acid transport have serious implications for fetal growth and long-term health.
This is a big topic and we have several projects under this umbrella. Click on the links below to learn more about individual projects:
- Question: Is fatty acid uptake different between placentas of obese and non-obese women?
- Question: Does supplementation with fish oil during pregnancy affect placental function and fetal growth?
- Question: How does maternal obesity alter placental fatty acid metabolism?
Our second area of focus is how the placenta impacts metabolic adaptations to pregnancy, such as glucose-insulin regulation. Maternal insulin sensitivity is a key predictor of fetal fat accrual, but the mechanisms regulating insulin signaling during pregnancy are unknown. Insulin sensitivity improves 120% following delivery of the placenta, suggesting a placental factor may regulate insulin signaling during pregnancy. As placental growth and gene expression is sensitive to maternal insulin levels in early pregnancy, and correlated to adiposity at birth, we propose that maternal-placental crosstalk is key to fetal growth regulation.