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      Type 2 diabetes-a matter of beta-cell life and death?

      Science (New York, N.Y.)

      Adaptation, Physiological, Animals, Apoptosis, Cell Count, Cell Division, Cell Size, Cell Survival, Cytokines, metabolism, Diabetes Mellitus, Type 2, physiopathology, Homeostasis, Humans, Hyperglycemia, Hyperlipidemias, Insulin, Insulin Receptor Substrate Proteins, Insulin Resistance, Intracellular Signaling Peptides and Proteins, Islets of Langerhans, cytology, physiology, Lipid Metabolism, Obesity, Phosphoproteins, Signal Transduction

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          Abstract

          In type 2 diabetes, the beta cells of the pancreas fail to produce enough insulin to meet the body's demand, in part because of an acquired decrease in beta-cell mass. In adults, pancreatic beta-cell mass is controlled by several mechanisms, including beta-cell replication, neogenesis, hypertrophy, and survival. Here, I discuss evidence supporting the notion that increased beta-cell apoptosis is an important factor contributing to beta-cell loss and the onset of type 2 diabetes. Interestingly, a key signaling molecule that promotes beta-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 beta-cell mass and insulin resistance.

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          Journal
          15662003
          10.1126/science.1104345

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