1994 Volume 41 Issue 3 Pages 309-313
Aminoguanidine (AG) is a potential therapeutic agent for preventing the generation of advanced glycation end products in diabetes mellitus. In this study, the effect of AG on insulin secretion was investigated in in vitro rat pancreatic islets. The islets were aseptically isolated and cultured in fissure culture medium 199 for 48h with or without AG. After the culture, batches of 10 islets were incubated in Krebs-Ringer bicarbonate buffer containing 3.3mM or 16.7mM glucose. Islets previously exposed to 0.18mM AG or 0.45mM AG showed similar insulin release to control islets at a 16.7mM glucose concentration, but high glucose-stimulated insulin release was inhibited in the islets exposed to 1.8mM. In the perifusion experiment, insulin release caused by 16.7mM glucose from the islets previously exposed to 1.8mM AG was not significantly different from that of the control islets. However, culture of the islets with higher AG concentrations, 4.55mM and 9.1mM, significantly inhibited glucose -stimulated insulin release (<0.02 and 0.002, respectively). These results suggest that AG at high concentrations impairs pancreatic B-cell response to a high concentration of glucose.
