Unborn Babies Use their Father's “Greedy” Gene to “Remote Control” their Mothers and Obtain Additional Nutrition

Scientists have discovered that fetuses use a copy of a gene they inherit from their father to force their mothers to release as many nutrients as possible during pregnancy. The unborn child “controls” its mother’s metabolism, creating a battle for nutrients between the two. The mother’s body wants the child to survive, but it needs enough glucose and fats in its system for its own health so that it can give birth, breastfeed, and reproduce again.

Genes Controlled by the Father Can Manipulate the Mother’s Resources to Benefit the Fetuses

Research at the University of Cambridge investigated how the placenta communicates with the mother via hormone release so that she can adapt to her baby’s growth. The placenta is a vital organ that develops in pregnant women and other female mammals alongside the fetus to provide for the developing fetus. In pregnant mice, scientists specifically altered the signaling cells in the placenta that signal mothers to release nutrients to their developing fetuses. Professor Amanda Sferruzzi-Perri, Professor of Fetal and Placental Physiology, Fellow of St John’s College, and co-author of the study, said: “This is the first direct evidence that a gene inherited from the father signals the mother to pass nutrients to the fetus.”

Dr. Miguel Constancia, MRC researcher at the Wellcome-MRC Institute of Metabolic Science and co-author of the study, said: “The baby’s remote control system is controlled by genes that can be turned on or off depending on whether they are ‘father’ or ‘mother’ genes, known as imprinting genes. Genes controlled by the father are ‘greedy’ and ‘selfish’ and tend to manipulate the mother’s resources for the benefit of the fetuses so that they grow large and fit.” Although pregnancy is largely cooperative, there is considerable scope for potential conflict between mother and child, with imprinting genes and the placenta playing a key role. The results of the researchers at the Centre for Trophoblast Research at the Department of Physiology, Development and Neuroscience at the University of Cambridge and the Medical Research Council Metabolic Diseases Unit, which is part of the Wellcome-MRC Institute of Metabolic Science, were published in Cell Metabolism.

When the Function of Igf2 is Switched off by the Father in the Signaling Cells, the Mother Does Not Produce Enough Nutrients for the Baby

The baby’s genes controlled by the father tend to promote fetal growth, while those controlled by the mother tend to restrict fetal growth. Professor Sferruzzi-Perri explained: “It is believed that the mother’s genes that restrict fetal growth are a means for the mother to ensure her survival so that she does not have a baby that takes up all the nutrients and is too large and difficult to give birth to. “The mother also has the chance to have further pregnancies in the future, possibly with other men, to spread her genes further. The researchers deleted the expression of an important imprinted gene called Igf2, which provides instructions for making a protein called ”insulin-like growth factor 2.” Similar to the hormone insulin, which is responsible for producing and regulating glucose levels in our bloodstream, the gene promotes fetal growth and plays an important role in the development of fetal tissues, including the placenta, liver, and brain.

Dr. Jorge Lopez-Tello, one of the lead authors of the study at the University’s Institute of Physiology, Development and Neuroscience, said: “When the function of Igf2 is switched off by the father in the signaling cells, the mother does not produce enough glucose and lipids – fats – for her circulation. These nutrients therefore reach the fetus in insufficient quantities, which prevents it from developing properly.” The scientists found that removing Igf2 from the placenta’s signaling cells affects the production of other hormones that modulate the mother’s pancreas’ insulin production and the response of her liver and other metabolic organs. They found that Igf2 controls the hormones responsible for reducing the mother’s insulin sensitivity during pregnancy. This means that the mother’s tissue does not absorb glucose, leaving more nutrients available in the bloodstream for the fetus.

Developing New Strategies to Target the Placenta

Babies with Igf2 gene defects can be overweight or have growth disorders. Researchers did not know that part of the Igf2 gene’s job is to regulate signaling to the mother so that she passes nutrients on to the fetus.

The mice studied were smaller at birth and their offspring showed early signs of diabetes and obesity later in life. This research highlights the importance of controlled distribution of nutrients to the fetus for the lifelong health of the offspring and the direct role the placenta plays in this process. The placenta is an amazing organ. At the end of pregnancy, the placenta is expelled by the mother, but memories of its function leave lasting traces in the development of fetal organs and their later functioning. Future research could help scientists develop new strategies to target the placenta and improve the health of mothers and babies.