Stephan Speier - Islet Cell Regeneration
1994 – 2000 Diploma degree in Human Biology, Philipps-University Marburg, Institute for Normal and Pathological Physiology, Marburg, Germany
2001 – 2004 PhD Thesis, European Neuroscience Institute Göttingen / Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
2004 – 2005 Postdoctoral Research Fellow, European Neuroscience Institute Göttingen / Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
2005 – 2009 Postdoctoral Research Fellow, The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institute, Stockholm Sweden
since 2009 Group Leader, CRTD
Our group is funded by the Emmy-Noether program of the Deutsche Forschungsgemeinschaft (DFG).
Previous and current research
Type I and type II diabetes are characterized by the inability of beta-cells, the major cell type in pancreatic islets of Langerhans, to secret a sufficient amount of insulin to counteract hyperglycemia. In type I diabetes this is due to a pure loss of beta-cells as result of an autoimmune process, whereas in type II diabetes it is the consequence of a combination of beta-cell loss, beta-cell dysfunction and insulin resistance. Substitution of the failing insulin secreting beta-cell by regeneration is considered a promising alternative for the treatment of diabetes. Therefore, understanding the mechanisms leading to neogenesis and replication of islet cells is of great importance to develop new therapeutic approaches.
Our lab studies the mechanisms leading to regeneration of islet cells in mouse and human. To achieve this, our group puts special emphasis on the use of in situ and in vivo technical platforms to study this complex, interactive process and overcome the limitations of commonly used in vitro methods. In particular, we have developed sophisticated methods to visualize and quantify beta cell expansion over time in animal models. We are especially interested under which physiological and pathophysiological conditions neogenesis and/or proliferation contribute to beta-cell mass expansion. Furthermore, we want to investigate the origin of pancreatic endocrine progenitor cells and assess the role of specific regulatory molecules in the signaling pathways, leading to replication of islet cells.
Future prospects and goals
- Assessing the contribution of neogenesis and proliferation to islet-cell regeneration
- Evaluating the role of specific regulatory molecules of beta-cell proliferation
- Development of novel techniques and tools for the study of islet-cell regeneration
- Translation of basic research topics into clinical studies in collaboration with the groups of the Diabetes Research Area of the CRTD
Group Members
Selected Publications
Nyqvist, D., Speier, S., Rodriguez-Diaz, R., et al. (2011). "Donor islet endothelial cells in pancreatic islet revascularization." Diabetes. [In Press]
Speier, S. (2011). "Experimental Approaches for High-Resolution In Vivo Imaging of Islet of Langerhans Biology." Curr Diab Rep. [Epub ahead of print]
Solimena, M. and Speier, S. (2010). "Insulin release: shedding light on a complex matter." Cell Metab 12(1): 5-6.
Speier, S., Nyqvist, D., Kohler, M., et al. (2008). "Noninvasive high-resolution in vivo imaging of cell biology in the anterior chamber of the mouse eye." Nat Protoc 3(8): 1278-1286.
Cabrera, O., Jacques-Silva, M. C., Speier, S., et al. (2008). "Glutamate is a positive autocrine signal for glucagon release." Cell Metab 7(6): 545-554.
Speier, S., Nyqvist, D., Cabrera, O., et al. (2008). "Noninvasive in vivo imaging of pancreatic islet cell biology." Nat Med 14(5): 574-578.
Speier, S., Gjinovci, A., Charollais, A., et al. (2007). "Cx36-mediated coupling reduces beta-cell heterogeneity, confines the stimulating glucose concentration range, and affects insulin release kinetics." Diabetes 56(4): 1078-1086.
