Beta cell death and the related loss of insulin production underlies the need for insulin replacement therapy in T1D. Understanding the mechanisms that control cell survival and cell death in the beta cell could illuminate new therapeutic approaches to preserve beta cells in T1D. In most cell types, cell survival is controlled by proteins from a particular group called Bcl. Certain proteins from this group had previously been implicated in beta cell survival under stress conditions. In this study, Dr. James Johnson and his team further investigated the role of these proteins in normal beta cell function. They found that the pro-survival proteins in this group function not only in promoting beta cell survival, but also in normal beta cell function and insulin secretion; providing a novel link between the activation of cell death pathways and beta cell dysfunction. This new connection has helped provide a new framework in the search for specific steps in the process that can prevent beta cell death while maintaining normal beta cell function and steps that may be controlled with novel therapeutics.
Ramifications for Individuals with T1D:
This early stage basic research helps to map the biological processes that control beta cell survival and death along with normal beta cell function and insulin secretion. This knowledge is now being used to identify steps in these processes that can be controlled with drug therapies to prevent the unwanted loss of beta cells in T1D while maintaining normal beta cell function.
This work was supported, in part, by a JDRF Career Development Award to Dr. Johnson.
Dan S. Luciani, Sarah A. White, Scott B. Widenmaier, Varun V. Saran, Farnaz Taghizadeh,
Xiaoke Hu, Michael F. Allard, and James D. Johnson (2013) Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic Beta-Cells. Diabetes 62(1):170-82 (Epub 2012 Aug 28).
Investigators and Institutions:
This work was led by Dr. James Johnson at the University of British Columbia.