IN-SITU GLUCOSE-UPTAKE AND GLUCOKINASE ACTIVITY OF PANCREATIC-ISLETS IN DIABETIC AND OBESE RODENTS

The present study evaluated the involvement of glucose transport and p hosphorylation in glucose-stimulated insulin release from pancreatic i slets. Using quantitative histochemical techniques, we investigated ba sal islet glucose content, islet glucose uptake in situ during acute e xtreme experimental hyperglycemia, and islet glucokinase activity in s everal animal models of diabetes and obesity. The basal islet glucose content in anaesthetized diabetic or obese rodents was either the same or higher than that in their relevant controls. The rate of glucose u ptake of islet tissue in these animals after an i.v. glucose injection was different. The db(+)/db(+) mouse and the obese Zucker rat exhibit ed significantly reduced islet glucose uptake rates. RIP-cHras transge nic mice, BHE/cdb rats and partially pancreatectomized rats showed nor mal islet glucose uptake rates. The activity of islet glucokinase was increased to a different degree related to the blood glucose level. Al l five animal models of diabetes or obesity exhibited either a delay o r a reduction of insulin release in response to supra maximal glucose stimulation. Our results indicate that the impairment of glucose-induc ed insulin release in diabetes is not consistently associated with a r eduction of islet glucose uptake nor a change of glucokinase activity.