Matthew J. Brady
Abstract
|
Full text
|
PDF
T
he etiology of type 2 diabetes is characterized by obesity, insulin and leptin resistance, and compensatory β cell hyperplasia followed by islet degeneration, resulting in the eventual dysregulation of glucose and lipid homeostasis. The recent identification of insulin receptor substrate 2 (IRS2) as a central player in the pathophysiology of many of these processes suggests a potentially unifying molecular link underlying the initiation and progression of type 2 diabetes.
