One contributing factor to the worsening of type 2 diabetes is the death of insulin-secreting pancreatic beta-cells through apoptosis, a regulated form of cell death.

In a study published online on March 4 in Developmental Cell, Richard N. Kitsis, M.D., and colleagues describe a molecular mechanism that drives beta-cell death in mice, and potentially humans with diabetes. The researchers identified a pathway in which a pool of ARC (a cell death inhibitor that normally maintains beta-cell viability) migrates to the nucleus to induce beta-cell apoptosis. The mechanism involves downregulation of the production of alpha-1 antitrypsin, a serine protease inhibitor that normally maintains beta-cell viability. The researchers showed that administering alpha-1 antitrypsin, an FDA-approved drug, to a mouse model of type 2 diabetes decreases beta-cell death and delays the progression of disease.

Dr. Kitsis is professor of medicine and of cell biology, director of the Wilf Family Cardiovascular Research Institute, and holds The Dr. Gerald and Myra Dorros Chair in Cardiovascular Disease at Einstein.