ID’ing a Novel Inhibitor of b-Cell Function, Id1

It is well established that loss of b-cell mass andcompromised b-cell function are telltale indicatorsof the development of type 2 diabetes (1). Even in-dividuals at risk for developing diabetes show b-cell dysfunction such as reduction of first-phase insulin release (2). An early response to increased insulin demand, as brought about in states of insulin resistance such as obe-sity or pregnancy, is a compensatory upregulation of the pancreatic b-cell mass and function. However, when this compensation fails and an inadequate amount of insulin is released in response to a meal, diabetes develops. The inability of b-cells to compensate for insulin resistance is associated with several abnormalities in b-cell function such as mitochondrial stress and reactive oxygen species production, insufficient proinsulin-to-insulin processing, and increased expression of islet amyloid polypeptide. Many of these abnormalities are believed to be the result of a combination of genetic and environmental factors. I