Significant Increase In Insulin Release Research Articles

Inhibition of calcium uptake by somatostatin in isolated rat islets of Langerhans.

Somatostatin (1 mug/ml) inhibited glucose (16.7 mM)-stimulated 45Ca uptake by isolated rat islets incubated in media containing no added calcium or calcium at a low concentration (0.2mM). Epinephrine (50 mug/ml) and mannoheptulose (20mM) also inhibited 45Ca uptake by islets incubated in the presence of calcium (0.2mM). Addition of glucose (16.7 mM) caused a small but significant increase in insulin release from islets incubated in media containing no added calcium. In the presence of a low concentration of calcium (0.2 mM), glucose caused a much greater increase in insulin secretion which was inhibited by addition of somatostatin, epinephrine or mannoheptulose.

Effects of mannoheptulose and DL-glyceraldehyde on glucose induced insulin release and adenosine 3',5'-monophosphate levels in isolated islets of rat pancreas.

The effects of mannoheptulose and DL-glyceraldehyde on glucose-induced insulin release and cycli AMP levels in islets isolated from rat pancreas were investigated. Mannoheptulose inhibition on glucose-induced insulin release was observed after only 5-min incubation period, indicating an inhibitory effect on the early phase of insulin release. This inhibition on insulin release was accompanied with the simultaneous depression of cyclic AMP levels in islets. By the addition of DL-glyceraldehyde to the medium in which glucose and mannoheptulose were present, the depressed cyclic AMP levels in islets were recovered to the control level completely but the restoration of insulin release in the early phase was not complete. In the absence of glucose, DL-glyceraldehyde did not demonstrate a significant increase of insulin release during 5 min incubation, though a marked stimulation was observed after 30-min incubation. Cyclic AMP levels in islets were not affected by DL-glyceraldehyde. When DL-glyceraldehyde was added to the medium with glucose, significant inhibition of glucos-induced insulin release in its early phase was observed without the reduction of cyclic AMP levels in islets. From these findings, the following possibilities are suggested and discussed. 1. Maintenance of the cyclic AMP levels in islets is a necessary but insufficient condition for glucose-induced insulin release particularly for its early phase. 2. Glucose-induced insulin release seems to depend on both the binding of glucose with glucoreceptor and the supply of some metabolites. Mannoheptulose inhibits both mechanisms. DL-glyceraldehyde may supply metabolites but competitively inhibit the binding of glucose to the glucoreceptor.

Effect of 6-aminonicotinamide on insulin release and C-14 glucose oxidation by isolated pancreatic rat islets: difference between glucose, tolbutamide and aminophylline.

Collagenase—isolated pancreatic islets collected from adult rats were incubated with glucose, tolbutamide or aminophylline (a soluble salt of theophylline). Indices of activity were insulin released into the medium, and oxidation of glucose labeled either in the C–l or C–6 position. Whereas glucose alone (16.5mM) produced a highly significant increase in insulin release, tolbutamide (0.1 mg/ml) or aminophylline (1 or 10mM) were ineffective by themselves. Both, however, potentiated the effect of glucose. If production of 14–CO2 from labeled glucose (SA 1.0 μi/mg) was measured in the presence of glucose, addition of neither tolbutamide nor aminophylline changed the number of 14–CO2 counts. If the islets were obtained from animals pretreated with 6–Aminonicotinamide, glucose released significantly less insulin, and less C–l carbon was incorporated into 14–CO2, indicating possible interference with adequate functioning of the pentose phosphate shunt. Addition of tolbutamide did not restimulate oxidation of gl...