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.
Unger
R H
RH
Center for Diabetes Research, Gifford Laboratories, Dallas, TX.
D000328:Adult; D000368:Aged; D002648:Child; D003920:Diabetes Mellitus / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000378:metabolism*; D007515:Islets of Langerhans / Q000378:metabolism*; D008875:Middle Aged; D008954:Models, Biological; D009004:Monosaccharide Transport Proteins / Q000235:genetics / Q000378:metabolism*
D009004:Monosaccharide Transport Proteins; D005947:Glucose