A groundbreaking study from the University of Cambridge reveals how fetuses manipulate their mother’s body to secure more nutrients during pregnancy. This process involves a gene inherited from the father, which directs the mother’s metabolism to prioritize fetal growth.
The study uncovers a delicate “nutritional tug of war” where the fetus uses a paternal gene to influence the mother’s metabolic processes. While the baby pushes for increased nutrients to support its development, the mother must balance her own nutritional needs to sustain the pregnancy, maintain her health, and prepare for future pregnancies.
Hormonal Communication Through the Placenta
The placenta plays a central role in this process by releasing hormones that signal the mother’s body to favor the fetus’s growth. In their experiments, scientists worked with pregnant mice, modifying cells in the placenta responsible for regulating nutrient distribution. This allowed them to observe how the placenta’s hormonal signals directly affected nutrient supply.
Professor Amanda Sferruzzi-Perri, a lead researcher on the project, explained, “This is the first direct evidence that a gene from the father influences the mother to divert nutrients to the fetus.”
Gene Wars: The Battle Between Maternal and Paternal Influences
The study also delves into the conflict between maternal and paternal genes, which influence fetal growth in opposing ways. According to Dr. Miguel Constancia, another lead researcher, genes from the father are “greedy” and work to maximize fetal growth, sometimes at the mother’s expense. In contrast, maternal genes aim to limit fetal growth to ensure the mother’s health and reproductive potential.
Dr. Constancia said, “Pregnancy is mostly cooperative, but there’s an underlying conflict, particularly through the role of imprinted genes and the placenta.”
The study, conducted by Cambridge’s Centre for Trophoblast Research and the Wellcome-MRC Institute of Metabolic Science, was published in Cell Metabolism.
The Role of the Igf2 Gene
One critical gene in this process is Igf2, which is involved in fetal growth. Scientists found that when the function of Igf2 was altered in the placenta, it disrupted the mother’s ability to produce sufficient glucose and fats, leading to poor fetal growth.
Dr. Jorge Lopez-Tello, a key researcher in the study, stated, “When Igf2 is switched off, the mother doesn’t make enough glucose or lipids available, which directly affects the fetus’s growth.”
The study found that Igf2 influences the production of hormones that regulate the mother’s insulin sensitivity during pregnancy. This ensures that the mother’s body does not absorb too much glucose, leaving more for the fetus.
Impacts of Genetic Defects
Defects in the Igf2 gene can lead to abnormal fetal growth. Mice lacking functional Igf2 in their placental cells showed signs of growth restriction or overgrowth, with their offspring later exhibiting symptoms of diabetes and obesity.
Professor Sferruzzi-Perri emphasized, “Our research underscores how vital it is to control the allocation of nutrients to the fetus for its long-term health.”
The Lasting Legacy of Placental Function
The study also suggests that the placenta’s function leaves a lasting impact on the child’s health. Professor Sferruzzi-Perri concluded, “The placenta is a remarkable organ. Its influence during pregnancy shapes how the fetus develops and how its organs will function throughout life.”
Future research will focus on understanding how Igf2 controls placental hormones and how this process can be leveraged to improve health outcomes for both mothers and babies.
This study sheds light on the complex relationship between genetics, maternal health, and fetal development, offering new insights into pregnancy’s intricate biology.
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