The Importance of β-Cell Failure in the Development and Progression of Type 2 Diabetes

Abstract

The pathogenesis of type 2 diabetes is complex and in most instances clearly requires defects in both β-cell function and insulin sensitivity (1). Together, these abnormalities result in increased rates of glucose release by the liver and kidney as well as decreased clearance from the circulation (2, 3). For the last decade, a great deal of attention has been directed at further understanding the role of insulin resistance as an important contributor to the development and maintenance of the hyperglycemia of type 2 diabetes. During this same period, the well described vital role of the pancreatic islet, and specifically the β-cell, in this process has been largely neglected.