Jerusalem, 18 November, 2025 (TPS-IL) — A Study released on Tuesday reveals how gestational diabetes can affect children even before they are born, uncovering molecular changes in the placenta that were previously unknown, Israeli scientists announced.
Gestational diabetes mellitus (GDM), a form of diabetes that develops during pregnancy, is increasingly common worldwide. It creates a disrupted metabolic environment for the fetus, including elevated maternal blood sugar. This can lead to complications at birth, such as babies being too large or too small for their gestational age, preterm delivery, and higher rates of cesarean sections. Children born to mothers with GDM also face long-term risks, including obesity and type 2 diabetes.
A global estimate using standardized criteria found that 14.0% of pregnancies were affected by GDM in 2021. Its increase is attributed to rising rates of obesity, delayed childbearing, and improved screening.
Currently, gestational diabetes is managed through diet, exercise, and insulin therapy, which help control blood sugar but do not address the underlying molecular disruptions.
Until now, the biological reasons behind these outcomes were poorly understood. A team of researchers led by Prof. Maayan Salton from the Faculty of Medicine at the Hebrew University of Jerusalem and Dr. Tal Schiller of Hebrew University’s Faculty of Medicine, Kaplan Medical Center, and Wolfson Medical Center at Tel Aviv University has identified a key mechanism at the molecular level. Their findings, published in the peer-reviewed journal Diabetes, focus on how the placenta processes genetic instructions.
The study shows that gestational diabetes disrupts a process called RNA splicing, which determines how genetic messages are assembled into instructions for making proteins. Using RNA sequencing data from European and Chinese pregnancy cohorts, the team found that hundreds of these messages were misassembled in placentas affected by GDM. Many of the affected genes are involved in metabolism and diabetes-related pathways, offering a direct molecular explanation for some of the complications seen in children.
A central discovery involved the protein SRSF10, which helps regulate RNA splicing. When researchers blocked SRSF10 in laboratory placental cells, the same splicing errors appeared as those seen in gestational diabetes. “This shows that SRSF10 may act as a master regulator of placental function,” said Salton. “By understanding how gestational diabetes disrupts the placenta at the molecular level, we can begin to imagine new ways to protect the offspring.”
Schiller added, “By pinpointing specific molecular players, like SRSF10, we can start thinking about how to translate this knowledge into real-world strategies to improve pregnancy outcomes.”
The study could pave the way for new interventions to protect babies from the effects of gestational diabetes. By targeting SRSF10, future therapies might correct the molecular errors in the placenta, reducing complications for the fetus even when maternal blood sugar is elevated. Additionally, abnormal splicing patterns or SRSF10 activity could serve as early biomarkers, helping doctors identify pregnancies at higher risk and enabling closer monitoring or timely intervention.
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