New Study Reveals Sneaky Genetic Trickery in Mice Fetus to Manipulate Mother’s Nutrient Delivery
Genetic inheritance is the fundamental link that connects us to our birth parents, with two sets of chromosomes combining to form our unique set of molecular instructions for life. However, new research in pregnant mice has unveiled a fascinating example of genetic trickery that manipulates the mother’s response to glucose, ensuring that more sugary nutrients are delivered to their growing fetus.
This manipulation, known as “genetic imprinting,” involves one copy of an inherited gene being suppressed by removable molecules, allowing the other copy to be freely expressed. In this recent study conducted by researchers, it was discovered that mouse fetuses use a copy of an imprinted gene inherited from the father to divert nutrients away from the mother through the placenta.
“It’s the first direct evidence that a gene inherited from the father is signaling to the mother to divert nutrients to the fetus,” says Amanda Sferruzzi-Perri, a reproductive biologist from the University of Cambridge and co-author of the study.
The parents’ genes play a significant role in fetal growth, with genes from the father promoting growth and those from the mother restricting it. While a mother nourishes her baby throughout pregnancy, she must also ensure her own survival. This dynamic creates an arena for potential conflict between the mother and the baby, with genetic imprinting and placental hormones believed to be key factors in this nutritional “tug-of-war.”
Scientists previously hypothesized that fetuses possess clever ways of meeting their nutritional needs, just as mothers prioritize their own. One hormone, insulin-like growth factor 1 (Igf2), was particularly intriguing due to its powerful effects on fetal growth. However, the exact mechanisms of how it operates remained unclear, as the placenta – where Igf2 and other hormones are produced – remains one of the least understood organs in the body.
To unravel this mystery, the team of researchers from the University of Cambridge conducted animal experiments. They manipulated the gene encoding Igf2, which resembles the hormone insulin. Insulin is responsible for helping cells absorb glucose from the blood, but during the later stages of pregnancy, expectant mothers become insulin-resistant to prioritize their babies’ nutrient absorption.
The mouse experiments revealed that Igf2 produced in the placental cells increases a pregnant mother’s insulin resistance. This, in turn, diverts more glucose towards the fetus by preventing the mother’s tissues from absorbing it.
“It means the mother’s tissues don’t absorb glucose so nutrients are more available in the circulation to be transferred to the fetus,” explains Sferruzzi-Perri.
Mice that lacked a functional copy of their father’s Igf2 gene in placental cells were smaller at birth, indicating that their mothers did not provide enough nutrients. These findings could explain the mechanisms behind certain human growth disorders.
Additionally, the researchers observed that the offspring of these mice showed early signs of diabetes and obesity later in life, further emphasizing the importance of understanding the intricate dynamics of maternal metabolism during pregnancy.
While this study provides crucial insights into how Igf2 manipulates maternal metabolism in mice, further research is needed to explore its full extent in humans at different stages of pregnancy and its interactions with other placental hormones.
The study has been published in Cell Metabolism, shedding light on the fascinating world of genetic inheritance and the complex interplay between mothers and their unborn children.