Costa, Bruder, et al., Published In American Journal of Physiology-Endocrinology and Metabolism

Maternal diabetes in can result in a predisposition to high-salt (HS) dietary-induced vascular dysfunction and inflammation in adulthood, according to a new study out of our Center for Pediatrics Research in Obesity and Metabolism (CPROM), in collaboration from the Divisions of Nephrology and Endocrinology, as well as the Vascular Medicine Institute with the University of Pittsburgh. 

While prenatal exposure to maternal diabetes has generally been understood to be a significant cardiovascular risk factor in the emergence of high blood pressure, atherosclerosis, and heart disease later in life, the effects of a HS diet in this circumstance have been unknown. 

In this study, titled, “In utero exposure to maternal diabetes exacerbates dietary sodium intake-induced endothelial dysfunction by activating cyclooxygenase 2-derived prostanoids,” and published in the American Journal of Physiology-Endocrinology and Metabolism, our researchers designed a novel mouse model of prenatal exposure to maternal type 1 diabetes, for the first time observing that prenatal exposure results in HS dietary-induced vascular dysfunction. 

This research implies a stronger connection between diet and vascular outcomes for patients exposed to maternal type 1 diabetes. It also unveiled potential treatments in the form of ex vivo antioxidant inhibitors, which demonstrated potential to improve or revert endothelial dysfunction in animal models. 

Study authors included Rafael Costa, Debora Malta Cerqueira, PhD, Lydia Francis, Ariane Bruder-Nascimento, PhD, MS, Juliano V Alves, Sunder Sims-Lucas, PhD, Jacqueline Ho, MD, MSc, and Thiago Bruder-Nascimento, PhD.

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