Sons of mothers with type 1 diabetes show early signs of vascular dysfunction
A new study reveals that sons born to mothers with type 1 diabetes may develop early vascular dysfunction – independently of metabolic health. The finding may help shape future strategies to prevent cardiovascular disease early in life.
Children of women with type 1 diabetes are known to be at increased risk of developing cardiovascular diseases. A new study by researchers from Stockholm University and Karolinska Institutet and others is the first to show that the risk is linked to early dysfunction in blood vessel cells in sons, even before any metabolic issues arise. The study is published in Cell Reports Medicine.
The researchers used a combination of animal models, Swedish and Danish health registries, and a small clinical study to explore the link. Results show a sex-specific effect: only sons displayed early vascular changes.
“Our work shows that vascular function is affected before metabolic dysfunction appears, which challenges current assumptions,” says study author Qiaolin Deng, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University and Department of Physiology and Pharmacology, Karolinska Institutet.
The study found that the dysfunction is driven by oxidative stress in endothelial cells, a potential early sign of future cardiovascular disease. The findings could help clinicians better assess risk and focus on preventive measures.
“We observed that early intervention can restore vascular function in affected animals, pointing to new opportunities for disease prevention later in life,” adds first author Allan Zhao, Stockholm University and Karolinska Institutet.
The team is now investigating the long-term effects of maternal diabetes, with a particular focus on why sons seem to be affected earlier than daughters.
Read the study “Maternal diabetes programs sexually dimorphic early-onset cardiovascular dysfunction in metabolically healthy offspring” in Cell Reports Medicine.
DOI: 10.1016/j.xcrm.2025.102454.
Last updated: November 12, 2025
Source: Communications Office