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Plasticity of the β cell insulin secretory competence: preparing the pancreatic β cell for the next meal

It is well established that the acute rise in plasma glucose and in the incretin hormones glucose‐dependent insulinotropic peptide (GIP) and glucagon‐like peptide‐1 (7–36) amide (GLP‐1), as occurs during a meal, is of pivotal importance in regulating the minute‐to‐minute output of insulin from pancreatic β cells. In addition to this well studied acute effect, both glucose and incretin hormones have been recently observed to determine the future secretory responsiveness of the cells. Such plasticity of the insulin secretory competence would imply that glucose and incretins not only act during the present meal, but also help to prepare the β cells to function during the subsequent meal. Evidence supporting this hypothesis is growing as a result of physiological studies of cultured β cells (either primary cells or β cell lines), as well as from an increasing number of large‐scale gene expression studies, exploring transcriptional and post‐transcriptional events in genes regulated by glucose and incretins. On the basis of this hypothesis, one can speculate that genetic or environmental disturbances of plasticity of the insulin secretory competence is one aspect of β cell dysfunction that can contribute to the aetiology of type 2 diabetes.