Interactions between the placenta, fetus, and maternal environment can influence various outcomes for the newborn, both at birth and in the long term. For example, having too much fatty tissue at birth (i.e., high adiposity) is associated with a higher risk of developing obesity, diabetes, and heart disease. A pregnant person’s sensitivity to insulin—the hormone that regulates blood sugar levels—can contribute to the newborn’s adiposity and these future health risks. A team of scientists funded by NICHD through the Human Placenta Project (HPP) is working to decode how placental cells regulate insulin sensitivity during pregnancy.
Placental Crosstalk
The communication between the placenta and the pregnant person’s cells is regulated in part by microRNAs (miRNAs). In one study, a team of scientists led by Perrie O’Tierney-Ginn, Ph.D., evaluated placenta samples to look for miRNAs that are important for regulating insulin resistance. Insulin resistance occurs when cells do not respond to insulin and cannot use available blood sugars. The team found a particular miRNA, called miRNA-3940-3p, that is associated with maternal insulin resistance. They are now working to understand how it is involved in the regulation of insulin sensitivity.
Health Implications
Insulin resistance development is a natural adaptation during pregnancy to support fetal growth, but excessive insulin resistance can result in maternal gestational diabetes and increased adiposity in the offspring. Researchers aim to clarify the mechanisms behind the development and progression of insulin resistance during pregnancy to identify early diagnostic biomarkers and potential therapeutic targets.
Learn more about the team
Principal Investigator(s):
Learn more about the HPP-funded project :
Placental miRNAs paracrine and endocrine roles in insulin sensitivity in pregnancy
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