Insulin secretion from islets of GK rats is not impaired after energy generating steps.

Insulin secretory responses of intact and electrically permeabilised islets of Goto-Kakizaki (GK) rats, a novel model of non-insulin dependent diabetes mellitus, and Wistar (control) rats were compared to investigate the mechanism of the impairment of insulin secretion from pancreatic islets of GK rats. Insulin secretion from intact islets in response to glucose, glyceraldehyde, succinate monomethylester and tetramethyl p-phenylenediamine, which reduces cytochrome c directly, was significantly impaired in GK rats compared to control rats (P < 0.05, P < 0.01, P < 0.05 and P < 0.05, respectively). However, Ca(2+)-induced insulin release from electrically permeabilised islets of GK rats was higher than that of control rats. Moreover, insulin secretion from intact islets in response to 50 mM KCl, which depolarises islet cells, was not impaired in GK rats. These results indicate that insulin secretion from islets of GK rats is not impaired after energy generating steps of metabolism.