Effect of cytochalasin B on glucose uptake, utilization, oxidation and insulinotropic action in tumoral insulin-producing cells.

Cytochalasin B (17-3 microM) virtually abolished 3-O-methyl-D-[U-14C]glucose uptake and D-[5-3H]glucose utilization in tumoral insulin-producing cells of the RINm5F line. This coincided with a marked decrease in D-[U-14C]glucose oxidation and suppression of the stimulant action of D-glucose upon insulin release. Cytochalasin B, however, augmented basal insulin release by the tumoral cells. The RINm5F cells appeared much more sensitive than normal islet cells to cytochalasin B, as judged by the relative magnitude of inhibition in either hexose uptake or utilization. In both cell types, the inhibitory action of cytochalasin B upon glucose metabolism seemed to be competitive, being more marked at low than high glucose concentration. These results are interpreted in support of the view that a decreased efficiency of hexose transport across the plasma membrane represents an essential deficiency of the RINm5F cells.