β-Cell Dysfunction under Hyperglycemic Stress: A Molecular Model

摘要

BackgroundPancreatic β cells respond to chronic hyperglycemia by increasing the synthesis of proinsulin (the precursor molecule of insulin). Prolonged stimulations lead to accumulation of misfolded proinsulin in the secretory track, delayed insulin secretion, and release of unprocessed proinsulin in the blood. The molecular mechanisms connecting the state of endoplasmic reticulum overloading with the efficiency of proinsulin to insulin conversion remain largely unknown.