My research covers translational and basic research in the field of type 1 diabetes (T1D) pathobiology. My objective is to increase our insight into the cellular and molecular mechanisms involved in the immune-mediated beta cell destruction in T1D. By understanding the genes, proteins, and factors affecting T1D risk at the beta cell level, the long-term perspective is to circumvent beta cell destruction in individuals at risk for T1D and/or to boost and maintain residual beta cell function in newly diagnosed T1D subjects.
Understanding the “beta cell genetics” of type 1 diabetes
The function of candidate risk genes is evaluated by loss and gain of function studies in pancreatic beta cells and immune cells.
Pro-inflammatory and pro-apoptotic signal transduction
The mechanisms underlying cytokine-induced beta cell apoptosis are investigated.
The levels of pro- and anti-inflammatory factors including cytokines and chemokines in the blood are determined to identify biomarkers of beta cell function and late-stage complications in T1D.
Gut hormone islet biology
The effects of gut hormones (GIP, GLP-1 and GLP-2) on islet function and survival and the underlying mechanisms are investigated.
- SKAP2 in type 1 diabetes
Aim: To examine if the T1D candidate gene SKAP2 modulates beta cell vulnerability to apoptotic cell death and to investigate if SKAP2 affects residual beta cell function in recent-onset T1D patients.
Collaborators: AK Cardozo, B. Holst, HB Mortensen.
- Genetic interactions in T1D and T2D
Aim: To reveal if genes associated with T1D and T2D interact in common networks in islets to mutually disrupt beta cell survival.
- Inflammatory biomarkers of residual beta cell function T1D
Aim: To identify circulating markers of beta cell function during first year after T1D diagnosis.
Collaborators: J Johannesen, JOB Madsen.
- Deciphering the effects of GIP and GLP-2 on human islet function
Aim: To examine the effects of GIP and GLP-2 on alpha and beta cell function under various glucose and inflammatory conditions mimicking diabetes.
Collaborators: FK Knop, TF Dejgaard, SM Heimbürger, A Lund, M Christensen.