Genetic inheritance is a physical link that tethers our birth parents; one-half of two sets of chromosomes meshing together to form our own unique set of molecular instructions for life.

As cooperative as this sounds, the stakes for each parent aren't the same, making those chromosomes a battleground over the mother's and offspring's future.

New research in pregnant mice reveals an example of genetic trickery that manipulates the mother's response to glucose so that more sugary nutrients are delivered to their growing fetus.

This trickery is not so sinister and really quite common. Called 'genetic imprinting', it results in one copy of an inherited gene being smothered by removable molecules to allow the other copy to be freely expressed.

In this new study, researchers found mice fetuses use a copy of an imprinted gene inherited from their dad to siphon nutrients away from their mother via 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 University of Cambridge reproductive biologist Amanda Sferruzzi-Perri who co-authored the study.

Of the genes a baby inherits, copies from the father tend to promote fetal growth while those from the mother limit it. Even as a mother nourishes a baby through pregnancy, she must ensure her own survival.

"Although pregnancy is largely cooperative, there is a big arena for potential conflict between the mother and the baby," says co-senior author Miguel Constancia, an epigeneticist at the University of Cambridge.

Genetic imprinting, along with hormones produced in the placenta, is thought to play key roles in the nutritional 'tug-of-war' that is pregnancy, Constancia adds.

Scientists figured that evolution had equipped fetuses with sneaky ways of meeting their nutritional needs, just like mothers preserved their own. Researchers had even honed in on a hormone called insulin-like growth factor 1 (Igf2), noting its "powerful effects of fetal growth".

But the exact mechanisms remained unclear: the placenta, where Igf2 and many other hormones are produced and operate, "is arguably the most important organ of the body, but paradoxically the most poorly understood," a 2015 review article explained.

In a series of animal experiments, University of Cambridge physiologist Jorge Lopez-Tello lead a team of colleagues in tinkering with the gene encoding Igf2, which resembles the hormone insulin.

Insulin helps cells absorb glucose from the blood, and expectant mothers become insulin-resistant in the later stages of pregnancy, to ensure their cells don't absorb the nutrients their babies need.

The mouse experiments showed that indeed, Igf2 produced in placental cells raises a pregnant mother's resistance to insulin, thereby shunting more glucose on to the fetus.

"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.

"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," she adds.

Mice without a working copy of their father's Igf2 gene in placental cells were smaller at birth, their mother's not sending enough nutrients their way.

This mechanism, if accurate, would neatly explain what we see in some human growth disorders.

The animal's offspring also showed early signs of diabetes and obesity in later life, the researchers found.

Further studies looking at earlier and later stages of pregnancy are still needed to understand the full extent by which Igf2 manipulates maternal metabolism in humans, and how it interacts with other placental hormones.

The study has been published in Cell Metabolism.