Zinc (Zn) is a trace element with anti-diabetes mellitus (anti-DM) effects. Zn complexes exhibit stronger insulin-like activity than Zn ions. Bis(hinokitiolato)zinc complex (Zn(hkt)2) was recently reported to be a potent anti-DM candidate. We examined the effects of Zn(hkt)2 on insulin resistance and pancreatic islet cells through in vivo long-term ingestion studies. In an in vivo study, we performed 4-month long-term Zn(hkt)2 administration experiments in KK-Ay mice as a type 2 DM animal model. Ingestion of Zn(hkt)2 resulted in lower blood glucose levels compared with the non-treated KK-Ay mice (control group). Additionally, Zn(hkt)2 treatment decreased plasma insulin concentration compared with that of the non-treated KK-Ay group. Zn(hkt)2 treatment resulted in a significant suppression of islet cell enlargement and a significantly decreased number of insulin-positive cells compared with the non-treated KK-Ay control group. The Zn(hkt)2 treatment group showed the increasing tendency in the amount of Zn levels in peripheral organs; liver, muscle, adipose, and pancreas, compared with the non-treated KK-Ay control group. However, the Zn level in the pancreas of the Zn(hkt)2 treatment group did not show the significant increase compared with the non-treated KK-Ay control group. This accumulation of Zn in pancreas suggested that Zn(hkt)2 mainly effects on the peripheral tissue, and Zn(hkt)2 has the less effect on the pancreas directly. Thus, we concluded that Zn(hkt)2 exerted the main effect on peripheral organs by ameliorating insulin resistance.