Unborn Baby Controls Moms for Extra Food

Because the unborn baby’remote controls’ its mother’s metabolism, the two are in a nutritional tug of war. The mother’s body wants the baby to survive but also needs to keep adequate glucose and lipids flowing in her system for her own health, in order to deliver the baby, breastfeed, and reproduce again.

A new study from the University of Cambridge published today looks at how the placenta interacts with the woman by releasing hormones so she can adapt her baby’s growth. The placenta is a critical organ that develops alongside the fetus in pregnant women and other female mammals to nourish the developing fetus. Scientists manipulated the signaling cells in the placenta that tell moms to allocate nutrition to their developing offspring in pregnant mice.

Professor Amanda Sferruzzi-Perri, Professor in Fetal and Placental Physiology, a Fellow of St John’s College and co-senior author of the paper, said: “It’s the first direct evidence that a gene inherited from the father is signalling to the mother to divert nutrients to the fetus.”

Dr Miguel Constancia, MRC Investigator based at the Wellcome-MRC Institute of Metabolic Science and co-senior author of the paper, said: “The unborn 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 ‘mum’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 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 findings were reported in Cell Metabolism by researchers from Cambridge’s Department of Physiology, Development, and Neuroscience and the Medical Research Council Metabolic Diseases Unit, which is part of the Wellcome-MRC Institute of Metabolic Science.

The genes controlled by the father of the infant tend to encourage fetal growth, whereas those controlled by the mother tend to inhibit fetal growth.

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 suppressed the expression of a key imprinted gene called Igf2, which encodes a protein called ‘Insulin Like Growth Factor 2’. The gene promotes fetal growth and plays an important role in the development of fetal tissues such as the placenta, liver, and brain, similar to the hormone insulin, which is responsible for creating and controlling glucose levels in our blood.

Dr Jorge Lopez-Tello, a lead author of the study based at the University’s Department of Physiology, Development and Neuroscience, said: “If the function of Igf2 from the father is switched off in signalling 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 discovered that removing Igf2 from the placenta’s signaling cells impacts the synthesis of other hormones that influence how the mother’s pancreas generates insulin, as well as how her liver and other metabolic organs respond.

“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,” said Professor Sferruzzi-Perri.

Babies with Igf2 gene defects can be overgrown or growth-stunted. “Until now, we didn’t know that part of the Igf2 gene’s role is to regulate signalling to the mother to allocate nutrients to the fetus,” added Professor Sferruzzi-Perri.

The mice investigated were smaller at birth, and their pups developed diabetes and obesity early in life.

Professor 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.”

The next stage is to understand how Igf2 regulates placental hormones and what those hormones do. Future study could assist scientists in developing novel techniques to target the placenta in order to enhance health outcomes for mothers and babies.

Mice are utilized in research because their DNA organization and gene expression are similar to humans, with 98 percent of human genes having a mouse counterpart. They have reproductive and neurological systems that are comparable to humans’, and they suffer from many of the same ailments, including as obesity, cancer, and diabetes.

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