Differential insulin secretory activity in rat pancreatic islets and HIT cells.

We compared insulin secretory activity from rat pancreatic islets with that from a hamster beta-cell line (HIT-T). Insulin release from HIT cells was maximally stimulated with glucose at a concentration of 11.1 mM, and rather inhibited by higher concentrations of glucose. Blunted insulin release induced by glucose was shown in the isolated rat islets exposed to either streptozotocin (2.2 mM) for 30 min or alloxan (2 mM) for 5 min, whereas glucose-induced insulin release from HIT cells was not affected by pre-treatment with such beta-cell toxin. When pancreatic islets and HIT cells were cultured for 7 days with 10 mM nicotinamide, an inhibitor of poly (ADP-ribose) synthetase, glucose-induced insulin release from the islets was inhibited, whereas insulin release from HIT cells was rather enhanced. Insulin release induced by either arginine or leucine was also enhanced in HIT cells cultured with nicotinamide. These findings indicate that the multiple components of insulin stimulus-secretion coupling in HIT cells are considerably different from those in rat pancreatic islets.