In 1997, a group of Australian researchers proposed (based on a study in rats) that oxycodone acts on KORs, unlike morphine, which acts upon MORs. Further research by this group indicated the drug appears to be a high-affinity κ2b-opioid receptor agonist. However, this conclusion has been disputed, primarily on the basis that oxycodone produces effects that are typical of MOR agonists. In 2006, research by a Japanese group suggested the effect of oxycodone is mediated by different receptors in different situations. Specifically in diabetic mice, the KOR appears to be involved in the antinociceptive effects of oxycodone, while in nondiabetic mice, the μ1-opioid receptor seems to be primarily responsible for these effects.