抄録
The effect of alloxan on pancreatic islets of the rat was studied by following the change in the incorporation of uridine diphospho (UDP) D-[U-14C] galactose into glycoproteins (chloroform/methanol-insoluble fraction) and glycolipids (chloroform/methanol-soluble fraction). Islets exposed to either alloxan or alloxan plus D-glucose anomers (16.7 mM) at 37° for 5 min, were incubated in a medium containing UDP-[U-14C] galactose at 37°for 120 min. The incorporation of UDP-[U-14C] galactose into glycoproteins and glycolipids was unaffected by 1.25 mM alloxan, but was slightly reduced by 6.25 mM alloxan. Alloxan at 31.2 mM severely inhibited the incorporation. The combination of alloxan (31.2 mM) plus the α anomer abolished the inhibitory effect of alloxan to a considerable extent, while the β anomer provided no protection against the action of alloxan. The label distribution on polyacrylamide gel electrophoresis of islets incubated with UDP-galactose was similar to that obtained after labeling with galactose oxidase and NaB3H4. In conclusion, the present data indicate that pancreatic islets of the rat can transfer galactose from UDP-galactose on the plasma membrane and that the α anomer of glucose is more effective than the β anomer in overcoming the inhibitory effect of alloxan.
