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How Babies In The Womb Could Control Their Mom’s Metabolism

Scientists found that the unborn baby remote controls its mom’s metabolism so the two are in a nutritional tug-of-war. 

Babies in the womb use a “greedy” gene from dads to “remote control” mom into feeding them extra food, reveals new research.

Cambridge University scientists have discovered that fetuses use a copy of a gene inherited from their father to force their mother to release as many nutrients as possible during pregnancy,

They found that the unborn baby “remote controls” its mom’s metabolism so the two are in a nutritional tug-of-war.

The mother’s body wants the baby to survive but needs to keep enough glucose and fats circulating in her system for her own health to be able to deliver the baby, breastfeed and to reproduce again.

The study, published in the journal Cell Metabolism, examines how the placenta communicates with the mother through the release of hormones so she will accommodate her baby’s growth.

The placenta is a vital organ that develops with the fetus in pregnant women and other female mammals to support the developing fetus.

In pregnant mice, scientists selectively altered the signaling cells in the placenta that tell mothers to allocate nutrients to their developing fetuses.

The mother’s body wants the baby to survive but needs to keep enough glucose and fats circulating in her system for her own health to be able to deliver the baby, breastfeed and to reproduce again. PHOTO BY PAVEL DANILYUK/PEXELS 

Co-senior author Professor Amanda Sferruzzi-Perri a Fellow of St John’s College, said: “It’s the first direct evidence that a gene inherited from the father is signaling to the mother to divert nutrients to the fetus.”

Co-senior author Dr. Miguel Constancia, based at the Wellcome-MRC Institute of Metabolic Science, said: “The baby’s remote control system is operated by genes that can be switched on or off depending on whether they are a “dad’s” or “mom’s” gene, the so-called imprinted genes.

“Genes controlled by the father are ‘greedy’ and ‘selfish’ and will tend to manipulate maternal resources for the benefit of the fetuses, so as to grow them big and fittest.

“Although pregnancy is largely cooperative, there is a big arena for potential conflict between the mother and the baby, with imprinted genes and the placenta thought to play key roles.”

The team explained that the baby’s genes controlled by the father tend to promote fetal growth and those controlled by the mother tend to limit fetal growth.

Professor Sferruzzi-Perri said: “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.”

The Cambridge team 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 making and controlling glucose levels in our circulation, the gene promotes fetal growth and plays a key part in the development of fetal tissues, including the placenta, liver and brain.

Study lead author Dr. Jorge Lopez-Tello said: “If the function of Igf2 from the father is switched off in signaling cells, the mother doesn’t make enough amounts of glucose and lipids – fats – available in her circulation.

“These nutrients therefore reach the fetus in insufficient amounts and the fetus doesn’t grow properly.”

The researchers found that deleting Igf2 from the placenta’s signaling cells affects the production of other hormones that modulate the way the mom’s pancreas produces insulin and how her liver and other metabolic organs respond.

Prof. Sferruzzi-Perri said: “We found Igf2 controls the hormones responsible for reducing insulin sensitivity in the mother during pregnancy.

“It means the mother’s tissues don’t absorb glucose so nutrients are more available in the circulation to be transferred to the fetus.”

She said babies with Igf2 gene defects can be overgrown or growth-stunted, adding: “Until now, we didn’t know that part of the Igf2 gene’s role is to regulate signaling to the mother to allocate nutrients to the fetus.”

The mice studied were smaller at birth and their offspring showed early signs of diabetes and obesity in later life.

Prof. Sferruzzi-Perri said: “Our research highlights how important the controlled allocation of nutrients to the fetus is for the lifelong health of the offspring and the direct role the placenta plays.

“The placenta is an amazing organ. At the end of pregnancy, the placenta is delivered by the mother, but the memories of how the placenta was functioning leaves a lasting legacy on the way those fetal organs have developed and then how they’re going to function through life.”

She said future research could help scientists discover new ways to target the placenta to protect moms and babies.

Produced in association with SWNS Talker

Edited by Saba Fatima and Asad Ali

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