Both Type 1 (T1D) and Type 2 diabetes (T2D) are caused by a relative insufficiency in functional β-cell mass. Current therapeutic options for diabetes include daily insulin injections to maintain normoglycemia, pharmacological agents to stimulate β-cell function and enhance insulin sensitivity, or islet transplantation. A major obstacle to greater application of islet transplantation therapy is the scarcity of human islets. Thus, new methods for expansion of β-cell mass, applied in vitro to generate the large numbers of human islet cells needed for transplantation, or in situ to induce expansion of the patients remaining β-cells, could have broad therapeutic implications for this disease. To this end, our lab is interested in delineating the molecular pathways that increase β-cell proliferation, enhance glucose stimulated insulin secretion, and protect against β-cell death. I am also interested in the molecular changes that result in insulinoma formation and cancers that are associated with diabetes
