DIABETIC HYPERGLYCEMIA - LINK TO IMPAIRED GLUCOSE-TRANSPORT IN PANCREATIC BETA-CELLS

Glucose uptake into pancreatic beta-cells by means of the glucose transporter GLUT-2, which has a high Michaelis constant, is essential for the normal insulin secretory response to hyperglycemia. In both autoimmune and nonautoimmune diabetes, this glucose transport is reduced as a consequence of down-regulation of the normal beta-cell transporter. In autoimmune diabetes, circulating immunoglobulins can further impair this glucose transport by inhibiting functionally intact transporters. Insights into mechanisms of the unresponsiveness of beta-cells to hyperglycemia may improve the management and prevention of diabetes.