ArticleGunnarsson R.
Diabete Metab. 1977 Sep;3(3):149-53.
Isolated pancreatic islets obtained from spontaneously diabetic mice were recently shown to have a considerably reduced rate of insulin biosynthesis in response to glucose. This defect has now been further evaluated by in vitro measurements of the effects of glucose on the islet RNA metabolism. An increase of the glucose concentration from 3.3 mM to 16.7 mM more than doubled the incorporation of 3H-labelled uridine into the islet RNA in the normal mice. By contrast, no stimulation was observed in the diabetic mice. Electrophoretic separation, on polyacrylamide gels, of RNA from normal mouse islets indicated that glucose stimulated the incorporation mainly into RNA bigger than 4S. Furthermore the fraction of islet RNA which bound the poly (U) was stimulated in the normal mice but not in the diabetic animals. Taken together these findings indicate a deficient glucose regulation of the RNA metabolism in the diabetic mice which conforms to the previously reported low rate of insulin biosynthesis in response to glucose in these animals.