Molecular biology of pancreatic islet β cell proliferation and failure

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(1) High glucose levels or glucose stimulation predominantly control pancreatic β cell IRS-2 levels. (2) A transcription factor CREB is critical for regulating β cell IRS-2 expression levels. Calmodulin dependent kinase 4 is stimulated by glucose, and the kinase appears to be the key component of complex regulation of CREB activation in pancreatic β cells. (3) In models of pancreatic β cell failure, such as db/db mice, critical molecules of glucose sensing, including glucokinase and glucose transporter 2, are downregulated, thus leading to a net decrease in glucose flux to β cells. With resultant reduction in IRS-2 levels, pancreatic β cell lose a key component of adaptive β cell proliferation and survival.