The placenta performs a range of crucial functions that support fetal growth during pregnancy, including facilitating the supply of nutrients and gases to the fetus, removal of waste products from the fetus, and the endocrine modulation of maternal physiology. The placenta also stores glucose in the form of glycogen, the function of which remains unknown. Aberrant placental glycogen storage in humans is associated with maternal diabetes during pregnancy and pre-eclampsia, thus linking placental glycogen storage and metabolism to pathological pregnancies. To understand the role of placental glycogen in normal and complicated pregnancies, we must turn to animal models. Over 40 targeted mutations in mice demonstrate defects in placental cells that store glycogen and suggest that placental glycogen represents a source of readily mobilised glucose required during periods of high fetal demand. However, direct functional evidence is currently lacking. Here, we evaluate these genetic mouse models with placental phenotypes that implicate glycogen trophoblast cell differentiation and function to illuminate the common molecular pathways that emerge and to better understand the relationship between placental glycogen and fetal growth. We highlight current limitations to exploring key questions regarding placental glycogen storage and metabolism and define how to experimentally overcome these constraints.
January 18, 2021
[Application of special acupoints for chronic gastritis in ancient literature of acupuncture and moxibustion].
September 24, 2020
- ACC 2020The American College of Cardiology decided to cancel ACC.20/WCC due to COVID-19, which was scheduled to take place March 28-30 in Chicago. However, ACC.20/WCC Virtual Meeting continues to release cutting edge science and practice changing updates for cardiovascular professionals on demand and free through June 2020.
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