Researchers at the Samuel Lunenfeld Research Institute of Toronto's Mount Sinai Hospital have discovered the first genetic evidence that the elimination of the gene for glycogen synthase kinase-3 (GSK-3) in mice sensitizes the animals to insulin.

In people suffering type 2 diabetes, the pancreas does not produce enough insulin, or it is not properly used. As a result, sugar accumulates in the blood rather than being absorbed, stored or burned for energy.

The study found by eliminating GSK-3 in mouse models, more sugar became stored in the liver in response to increased insulin sensitivity, indicating insulin had become more effective.

"While potential human treatments are likely still years down the road, this study provides strong evidence that chemical inhibitors of this enzyme will be useful for increasing the effective potency of insulin," said Jim Woodgett, director of the Lunenfeld Institute.

The study, co-authored by Drs. Katrina MacAulay and Bradley Doble, is featured in the Oct. 3 issue of the journal Cell Metabolism.