GLUT1 is Adequate for Glucose Uptake in GLUT2-Deficient Insulin-Releasing β-Cells

 

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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 K_m and V_max. 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.