Amazing stuff!
"... A new study ... examines how the placenta communicates with the mother through the release of hormones so she will accommodate her baby’s growth. ... scientists selectively altered the signalling cells in the placenta that tell mothers to allocate nutrients to her developing fetuses. ...
“It’s the first direct evidence that a gene inherited from the father is signalling to the mother to divert nutrients to the fetus.” ...
“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. ..."
“It’s the first direct evidence that a gene inherited from the father is signalling to the mother to divert nutrients to the fetus.” ...
“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. ..."
"Fetuses use a copy of a gene inherited from their dad to force their mum to release as much nutrients as possible during pregnancy, Cambridge scientists have discovered.
The unborn baby ‘remote controls’ its mother’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. ..."
From the highlights and abstract:
"Highlights
• Placenta endocrine cell (Jz) IGF2 loss impairs maternal adaptation in pregnant mice
• Jz IGF2 loss reduces maternal glucose and lipid availability for fetal growth
• IGF2 regulates metabolism, protein synthesis, and hormone secretion of Jz cells
• Lack of Jz IGF2 programs offspring for postnatal metabolic dysfunction
Summary
Maternal-offspring interactions in mammals involve both cooperation and conflict. The fetus has evolved ways to manipulate maternal physiology to enhance placental nutrient transfer, but the mechanisms involved remain unclear. The imprinted Igf2 gene is highly expressed in murine placental endocrine cells. Here, we show that Igf2 deletion in these cells impairs placental endocrine signaling to the mother, without affecting placental morphology. Igf2 controls placental hormone production, including prolactins, and is crucial to establish pregnancy-related insulin resistance and to partition nutrients to the fetus. Consequently, fetuses lacking placental endocrine Igf2 are growth restricted and hypoglycemic. Mechanistically, Igf2 controls protein synthesis and cellular energy homeostasis, actions dependent on the placental endocrine cell type. Igf2 loss also has additional long-lasting effects on offspring metabolism in adulthood. Our study provides compelling evidence for an intrinsic fetal manipulation system operating in placenta that modifies maternal metabolism and fetal resource allocation, with long-term consequences for offspring metabolic health."
Fetal manipulation of maternal metabolism is a critical function of the imprinted Igf2 gene (open access)
Graphical abstract
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