No abstract

No abstract

The authors have reported that alloxan, a ^-cytotoxic agent, inhibited glucose oxidation and glucose-induced 4s Ca uptake of pancreatic |3-cells; the non-0-cell mass was not inhibited by alloxan pretreatment. Therefore, it is feasible to assess glucose metabolism and Ca uptake in the mass composed of (3cells alone, by subtracting glucose oxidation and Ca uptake in the alloxan treated islets from the non-alloxan treated islets. In order to elucidate the interrelationship between glycolysis, glucose-induced Ca uptake and insulin release in the pancreatic 0-cell mass, but not in the pancreatic islets, we investigated 14 CO2 formation from 14 C-U-D-glucose, glucoseinduced 4s Ca uptake and insulin release in alloxan treated and non-alloxan treated islets. In vitro incubation of collagenase digested isolated islets of Langerhans was employed. The relationships between the three parameters in the presumed pancreatic (?-cell mass (14 C02 formation from 14 C-U-D-glucose, glucose-induced 45 Ca uptake and insulin release) and glucose concentration in the media were clearly sigmoidal. The threshold values of the three parameters are approximately 5 raM of glucose. The half maximum rates of 14 CO 2 formation, 4S Ca uptake and insulin release required 13.4 mM, 13.6 mM and 12.8 mM of glucose, respectively. The near maximum stimulation of the three parameters was obtained at 20 mM of glucose. The highly corelated concentration-response relationship between the three parameters in the presumed pancreatic (3-cell mass and glucose concentration in the media, strongly suggests that glycolysis of (3-cells controls Ca mobilization in (3-cells, which initiates insulin release.

SynopsisThe effects of alloxan on glucose oxidation and the protection by anomers of D-glucose from alloxan inhibition of glucose oxidation in the pancreatic islets were investigated using in vitro incubation of rat isolated islets.The pretreatment by alloxan (5-30mg/dl) for6minutes inhibits significantly14CO2 formation from 14C-U-D-glucose (10mM) and the addition of a-anomer of D-glucose (8.3mM) to alloxan (20mg/dl) completely reverses alloxan inhibition of glucose oxidation.These findings seem to be incompatible with the recent view that alloxan acts at the glucose receptor on the plasma membrane of pancreatic without affecting glucose metabolism in the pancreatic islets.