Pancreatic β-cells secrete insulin when blood glucose levels become high. However, when β-cells
are chronically exposed to hyperglycemia, their function gradually deteriorates. Although such phenomena
are called as β-cell glucose toxicity, its molecular mechanism remained unclear. This manuscript describes
the possible mechanism for such β-cell dysfunction. In the diabetic state, nuclear expression levels of pancreatic
transcription factors PDX-1 and MafA are decreased. In addition, incretin receptor expression in β-
cells is decreased, which is likely involved in the impairment of incretin effects in diabetes. Taken together, it is likely that
down-regulation of pancreatic transcription factors and/or incretin receptors are involved in β-cell dysfunction observed in
type 2 diabetes.
Keywords: Pancreatic β-cells, reactive oxygen species, PDX-1, MafA, GLP-1 receptor.
Rights & PermissionsPrintExport