TY - JOUR
T1 - Diabetic hyperglycemia
T2 - Link to impaired glucose transport in pancreatic β cells
AU - Unger, Roger H
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1991
Y1 - 1991
N2 - Glucose uptake into pancreatic β 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 β-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 β cells to hyperglycemia may improve the management and prevention of diabetes.
AB - Glucose uptake into pancreatic β 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 β-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 β cells to hyperglycemia may improve the management and prevention of diabetes.
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U2 - 10.1126/science.2006409
DO - 10.1126/science.2006409
M3 - Article
C2 - 2006409
AN - SCOPUS:0025736821
SN - 0036-8075
VL - 251
SP - 1200
EP - 1205
JO - Science
JF - Science
IS - 4998
ER -