Unborn babies use gene to control mom’s metabolism

How fetuses use a "greedy" gene to get more food?

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In a fascinating exploration of the intricate relationship between unborn babies and their mothers, recent scientific research has shed light on a remarkable phenomenon. Unborn babies possess a genetic predisposition, colloquially called the ‘greedy’ gene, which allows them to influence their mothers’ eating habits remotely. By manipulating their mothers’ food intake, these tiny occupants of the womb ensure their own nutritional needs are met for optimal growth and development.

A groundbreaking study at the University of Cambridge has revealed the fascinating dynamics between unborn babies and their mothers during pregnancy. The study shows that unborn babies can remotely control their mother’s metabolism, leading to a complex nutritional tug-of-war. While the mother’s body aims to ensure the baby’s survival, it must also maintain sufficient glucose and fats for her well-being, delivery, breastfeeding, and future reproductive capacities.

The research focused on understanding how the placenta communicates with the mother to support the baby’s growth, with hormones playing a crucial role in influencing maternal adaptation to meet the fetus’s nutritional needs. By manipulating signaling cells in the placenta, scientists demonstrated the direct influence of a gene inherited from the father, revealing the existence of imprinted genes that act as the baby’s “remote control system.” Unraveling these mechanisms holds promise for advancing prenatal care and promoting the well-being of both mothers and their unborn children.

Father-controlled genes are “greedy” and “selfish,” manipulating maternal resources for the benefit of the fetuses, while mother-controlled genes limit fetal growth. The conflict between mother and baby is possible, with imprinted genes and the placenta playing key roles. Researchers from Cambridge’s Centre for Trophoblast Research and the Wellcome-MRC Institute of Metabolic Science have published these findings in Cell Metabolism.

Professor Sferruzzi-Perri explained: “Those genes from the mother that limit fetal growth are thought to be a mother’s way of ensuring her survival, so she doesn’t have a baby that takes all the nutrients and is too big and challenging to birth. The mother also has a chance of having subsequent pregnancies potentially with different males in the future to pass on her genes more widely.”

Researchers deleted the expression of an imprinted gene called Igf2, which promotes fetal growth and is crucial for developing placenta, liver, and brain tissues. The absence of Igf2 resulted in insufficient glucose and lipid availability in the mother’s circulation, leading to improper fetal growth.

Deleting Igf2 also affected the production of insulin sensitivity and nutrient transfer hormones. Babies with Igf2 gene defects can exhibit abnormal growth and potential health issues like diabetes and obesity in adulthood. These findings were discovered by scientists from the University’s Department of Physiology, Development, and Neuroscience.

Professor Sferruzzi-Perri emphasized the importance of controlled nutrient allocation to the fetus for long-term offspring health, highlighting the significant role of the placenta. The placenta’s functioning during pregnancy leaves a lasting impact on fetal organ development and lifelong functionality.

The following research objective is to investigate the control of placental hormones by Igf2 and their specific functions. Understanding this could lead to new strategies for targeting the placenta and improving health outcomes for both mothers and babies. Mice are used in this research due to their genetic similarity to humans, including comparable gene expression and similar reproductive and nervous systems. They also share common diseases like obesity, cancer, and diabetes.

Journal Reference:

  1. Jorge Lopez-Tello, Hannah E.J. Yong et al., Fetal manipulation of maternal metabolism is a critical function of the imprinted Igf2 gene. Cell Metabolism. DOI: 10.1016/j.cmet.2023.06.00.
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