The therapeutic treatment of type 1 and type 2 diabetes mellitus (T1DM, T2DM) has vastly improved over the past decades; however complete normalization of glucose remains elusive without proper functioning pancreatic β cells. Truly, sustained and effective treatment of T1DM and T2DM must involve retaining/replacing the function of pancreatic β cells. To this end, we must understand the molecular mechanisms that govern β cell development and function along with understanding the molecular progression of the disease.

The Stein lab and others have focused on the large Maf transcription factors, MafA and MafB, and their role in the β cell. Loss of MafB impedes normal β cell development in mouse models whereas loss of MafA restricts normal adult β cell function. In recent published data, we have shown that MafA and MafB are lowered in db/db mouse models and T2DM donor samples. Collectively, this data reveals the importance of MafA and MafB in normal β cell function and presents an area of research that needs to be further examined. 

Using nPOD, we are currently characterizing transcription factor levels and investigating coregulator interactions in T1DM and T2DM donor samples. This data is crucial to the understanding of the human β cell situation and vital for β cell replacement therapy protocols.