GLUT2 may play an important role in pancreatic β-cell glucose metabolism. A decrease
in glucose uptake due to underexpression of GLUT2 has been considered as the cause
of β-cell dysfunction in diabetes with different pathogenesis. However, this view
has been challenged by recent studies, in which the underexpression of GLUT2 was not
accompanied by a decrease in glucose uptake. Our present aim is to evaluate the presumed
importance of GLUT2 in maintaining the efficiency of β-cell glucose uptake. We studied
the kinetic characteristics of 3-O-methylglucose uptake in two β-cell lines. One of
these is the βTC3 cell line which expresses GLUT1 and the other is the βHC9 cell line
which expresses both GLUT1 and GLUT2. Under equilibrium exchange conditions, 3-O-methylglucose
transport in these two cell lines showed similar values of Km and Vmax. The apparent IC50 of cytochalasin B for inhibiting 3-O-methylglucose transport in βHC9 cells was nine
times as high as in βTC3 cells, indicating that GLUT1 is the critically important
glucose transporter in the βTC3 cell line and GLUT2 in the βHC9 cell line. In both
cell lines, the rates of glucose uptake were at least three times as fast as that
of glucose phosphorylation. Our results suggest that GLUT1 is able to compensate for
GLUT2 loss as it occurs in βTC3 and maintains a commensurately high capacity of glucose
uptake to sustain glucose metabolism in pancreatic β-cells.
Key words
Pancreatic Islet - Glucose Uptake - Glucose Metabolism
