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Study: Unborn babies employ paternal ‘greedy’ gene to obtain increased nourishment from mothers

According to new research from the University of Cambridge, unborn babies possess a “greedy” gene inherited from the father that controls their mother’s behavior, compelling her to provide them with extra food. This gene allows the fetus to manipulate the mother’s metabolism, resulting in a nutritional tug of war between the two.

The mother’s body aims to ensure the baby’s survival while also maintaining enough glucose and fats for her own health, delivery, breastfeeding, and future reproductive abilities.



In the words of Dr. Miguel Constancia, a researcher at the University of Cambridge, “Genes controlled by the father are ‘greedy’ and ‘selfish’ and will tend to manipulate maternal resources for the benefit of the fetus, promoting their growth and development.”

According to Professor Amanda Sferruzzi-Perri, a leading author of the paper and an expert in fetal and placental physiology, it is the first conclusive evidence that a gene inherited from the father influences the mother’s allocation of nutrients to the fetus.

Dr. Miguel Constancia further explains that the baby’s genetic control system, operated by imprinted genes from both parents, plays a crucial role in the potential conflict between the mother and the baby during pregnancy.

The study conducted by University of Cambridge researchers focuses on how the placenta communicates with the mother by releasing hormones, enabling her to meet the growing demands of the fetus.

Using pregnant mice, scientists selectively manipulated the signaling cells in the placenta responsible for instructing mothers to allocate nutrients to their developing fetuses.

The genes controlled by the father generally promote fetal growth, while those controlled by the mother tend to limit it. This restriction ensures the mother’s survival and prevents the birth of an excessively large and challenging baby.

The study revealed that deleting a gene called Igf2, responsible for producing a protein called ‘Insulin-Like Growth Factor 2’, affects the mother’s glucose and lipid availability. This deficiency results in inadequate nutrient supply to the fetus, leading to improper growth.

Moreover, the deletion of the Igf2 gene also influences the production of other hormones and impacts the mother’s insulin production, as well as the responses of her liver and other metabolic organs.

Babies with Igf2 gene defects may experience overgrowth or stunted growth. Additionally, the researchers found that the Igf2 gene regulates the signaling to the mother regarding nutrient allocation, a previously unknown role.

The potential implications of these findings include the lifelong health of the offspring, emphasizing the crucial role of controlled nutrient allocation through the placenta.

Professor Sferruzzi-Perri concludes, “The placenta plays an extraordinary role. It not only nourishes the baby during pregnancy but also leaves a lasting impact on the development and function of the fetal organs throughout life.”

The results of this study have been published in the journal Cell Metabolism.

 

Reference

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