Glucose toxicity of the pancreatic beta cell is considered to play
a secondary role in the pathogenesis of type II diabetes mellitus.
To gain insights into possible mechanisms of action of glucose
toxicity, we designed studies to assess whether the loss of
insulin secretion associated with serial passages of HIT-T15
cells might be caused by chronic exposure to high glucose levels
since these cells are routinely cultured in media containing supramaximal
stimulatory concentrations of glucose.