Oxytocin, a hormone primarily associated with childbirth, lactation, and maternal bonding, has now been linked to a potential new role in mammalian reproduction, particularly in delaying embryo development. A recent study, conducted by researchers at NYU Langone Health, reveals that oxytocin may influence a process known as “diapause,” which can halt embryonic growth following conception.
Published in Science Advances in a special edition on women’s health, this groundbreaking research suggests that diapause—where an embryo temporarily ceases development before attaching to the uterine wall—could provide new insights into pregnancy and fertility issues in humans. The delay in embryonic development could be a crucial factor in understanding infertility, premature birth, and miscarriage.
The study’s lead researchers investigated the biological mechanism behind diapause, a phenomenon observed in several species, including armadillos, pandas, and seals. Diapause is thought to serve as an adaptive mechanism, allowing mothers to delay birth and conserve limited resources until conditions are more favorable for raising offspring.
In mammals, including humans, a form of diapause has been suggested, although its causes and mechanisms were not fully understood until now. The researchers discovered that maternal stress—particularly through lactation—could trigger diapause. In lactating rodents, the gestation period, typically lasting 20 days, was delayed by nearly a week, likely due to the increased demands on the mother’s body to nourish both newborns and developing embryos.
One of the key findings of the study was the role of oxytocin in this process. As lactation occurs, oxytocin levels rise, which appeared to delay embryonic implantation by as much as three days. In experiments, exposing embryos to small doses of oxytocin caused significant delays in their attachment to the uterine lining.
More strikingly, when oxytocin surges occurred at levels similar to those seen during nursing, it caused pregnancy loss in nearly all the rodents. According to Moses Chao, Ph.D., a professor at NYU Grossman School of Medicine, these findings shed new light on how oxytocin regulates diapause and suggests that disruptions in oxytocin production may contribute to issues like infertility, delayed pregnancy, or miscarriage.
The researchers also identified the mechanism through which embryos respond to oxytocin. They found that the hormone binds to receptors on the trophectoderm, a layer of cells surrounding the early embryo that later forms the placenta. In experiments where oxytocin receptors were disabled in mouse embryos, implantation rates into the placenta significantly decreased. This highlights the importance of the embryo’s ability to respond to oxytocin in order to survive and successfully implant.
Robert Froemke, Ph.D., the study’s senior author, emphasized the importance of understanding the factors behind infertility and pregnancy complications. “Infertility and developmental issues during pregnancy, while common, remain poorly understood,” he said. Our research provides a step toward addressing these challenges and improving reproductive health care.
Looking ahead, Froemke’s team plans to further investigate how embryos resume growth after diapause, as well as how diapause affects the health of offspring after birth. However, he cautioned that while mice and humans share some reproductive similarities, significant differences remain between the two species, and further studies are needed to assess the role of other pregnancy-related hormones, such as estrogen and progesterone, in the diapause process.
This study offers a promising new direction in reproductive medicine, with the potential to improve treatments for infertility and complications during pregnancy.
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