Type 2 Diabetes-a Matter of ß-Cell Life and Death?

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Abstract
In type 2 diabetes, the β cells of the pancreas fail to produce enough insulin to meet the body's demand, in part because of an acquired decrease in β-cell mass. In adults, pancreatic β-cell mass is controlled by several mechanisms, including β-cell replication, neogenesis, hypertrophy, and survival. Here, I discuss evidence supporting the notion that increased β-cell apoptosis is an important factor contributing to β-cell loss and the onset of type 2 diabetes. Interestingly, a key signaling molecule that promotes β-cell growth and survival, insulin receptor substrate 2 (IRS-2), is a member of a family of proteins whose inhibition contributes to the development of insulin resistance in the liver and other insulin-responsive tissues. Thus, the IRS-2 pathway appears to be a crucial participant in the tenuous balance between effective pancreatic β-cell mass and insulin resistance.