ABSTRACT
Columbia, Vancouver, BC, Canada James D. Johnson, Ph.D., Assistant Professor (jimjohn@interchange.ubc.ca)
Dan S. Luciani, Ph.D., Post-doctoral Fellow (dan.luciani@gmail.com) Diabetes Research Group, Dept. of Cellular and Physiological Sciences
& Dept. of Surgery University of British Columbia, 5358 Life Sciences Building, 235 Health Sciences
Mall, Vancouver, BC, Canada, V6T 1Z3
Diabetes is a devastating disease caused by the dysregulation of glucose homeostasis. Normally β-cells, a highly specialized cell type located in the pancreas, release the hormone insulin whenever glucose levels are high, thus signalling to tissues such as the muscle, liver and fat to store nutrients. Diabetes occurs when β-cells no longer function properly or have been destroyed. In type 1 diabetes, the body’s own immune system attacks the β-cells and causes them to undergo programmed cell death. Apoptotic loss of β-cells also contributes to type 2 diabetes. Pancreatic β-cell death can be induced by a variety of stress factors in both forms of diabetes. Th ere is also evidence that β-cells can undergo apoptosis as a result of defects in the folding and processing of proinsulin. Th ere are also several rare forms of diabetes caused by mutation or dysregulation of genes that are essential to the survival of β-cells under stressful conditions. A promising treatment for diabetes, islet transplantation, is limited by excessive β-cell apoptosis. Th us, a more complete understanding of the factors that control pancreatic β-cell survival is required in order to eff ectively prevent and treat this disease. Indeed, scientists and
pharmaceutical companies have dedicated substantial resources to this topic and new therapies have emerged that may infl uence β-cell apoptosis. In this chapter, we will review the factors that infl uence the β-cells’ life and death decisions and the impact of β-cell apoptosis on the initiation and progression of several forms of diabetes.
