Our previous work has shown that triphenyltin compound induces the diabetogenic effects, such as hyperglycemia and hypertriglyceridemia, on hamsters, but not on ra ts. In the present study, it is examined whether the species differences in the metabolic fate of triphenyltin exist for susceptibility between hamsters and rats. Triphenyltin chloride was orally dosed to hamsters and rats, and triphenyltin and its metabolites, mono- and diphenyltin, and inorganic tin, in liver, kidney, pancreas, brain, and blood were determined by gas chromatography periodically for 96 h after the treatment. Triphenyltin levels in the tissues of both species were almost maxima within 24 h after treatment. Although there were relatively high levels of triphenyltin in the tissues of hamsters dosed with triphenyltin chloride, compared with those in the rats, the proportion of metabolites to triphenyltin were lower than those in the rats. In particular, hamsters were more susceptible than rats to the pancreatic accumulations of triphenyltin and good correlation exists between the tin concentrations in the pancreas and the plasma glucose levels in triphenyltin-treated hamsters. These findings suggest that the dearylation of absorbed triphenyltin in hamsters is slower than that in rats and that triphenyltin-induced hyperglycemic action depends upon the amount of tin compounds absorbed into the pancreas. Furthermore, most of the tin compounds in the brains of both species were triphenyltin. This result shows that the metabolism of triphenyltin in the brains of both species was different from that in other tissues.