This is why we study the development and function of pancreatic beta-cells. What determines the number of beta-cells? How is insulin secretion regulated? What causes beta-cell dysfunction? Answers to these questions help us to understand the molecular mechanism underlying the pathogenesis of diabetes and to ultimately improve the foundations of metabolic health.
Our main fields of research interest concern topics in:
Our team focuses on the impact of gestational diabetes on fetal growth and development. Our clinical studies dive into the relationship between maternal insulin sensitivity and fetal development. Our preclinical studies aid in the development of nutritional and/or pharmaceutical solutions to reduce the adverse effects of maternal obesity and GDM on both mother and child. By creating animal models for diseases such as gestational diabetes (GDM), we are acquiring new knowledge of the underlying foundation of GDM and the impact on offspring.
Progressive loss of beta-cells is the key characteristic of type 1 diabetes (T1D). Immune-mediated beta-cell destruction drives the disease, however, early pathogenesis of T1D is still poorly understood. This hampers successful therapies to prevent or reverse T1D. Although human studies indicated that genetic predisposition is required, the factors triggering loss of immune regulation are unknown. We hypothesise that defects in pancreatic beta-cells may play a causal or enabling role in the development of T1D. In preclinical studies, we study the role of intrinsic beta-cell fragility in initiating T1D.
UMCG
Department of Pediatrics (HPC CA84)
Hanzeplein 1
Postbus 30 001
9700 RB Groningen
The Netherlands
Visiting address
UMCG
Hanzeplein 1
Room Y2.147
9700 RB Groningen
The Netherlands
