Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets.

Loss of functional pancreatic β-cell mass and increased β-cell apoptosis are fundamental to the pathophysiology of type 1 and type 2 diabetes. Pancreatic islet transplantation has the potential to cure type 1 diabetes but is often ineffective due to the death of the islet graft within the first few years after transplant. Therapeutic strategies to directly target pancreatic β-cell survival are needed to prevent and treat diabetes and to improve islet transplant outcomes.

Cation-Independent Mannose 6-Phosphate Receptor Deficiency Enhances β-Cell Susceptibility to Palmitate.

Palmitate attenuates insulin secretion and reduces the viability of insulin-producing cells. Previous studies identified the aberrant palmitoylation or mispalmitoylation of proteins as one mechanism by which palmitate causes β-cell damage. In this report, we identify a role for lysosomal protein degradation as a mechanism by which β cells defend themselves against excess palmitate.