Johns Hopkins team finds a new drug target for diabetes

Scientists at Johns Hopkins say they've identified a link between high blood sugar and an interference with mitochondria that could make for a prime new target in the field of diabetes drug research.

Mitochondria play a key role in the life of a cell, generating the energy they need to survive. Following up on earlier observations that high blood sugar disrupts the activity of mitochondria, the team compared enzymes that either added or removed a molecule called O-GlcNAc to proteins. And they compared rats that had diabetes and a group of healthy rodents.

There was a fundamental imbalance, they say, with higher levels of O-GlcNAc transferase--which adds O-GlcNAc to proteins–and lower levels of O-GlcNAcase, which removes the molecule.

That kind of imbalance creates a cascade of events. Energy production became inefficient, causing damage to the molecule which in turn triggered greater production of glucose, further elevating levels of blood sugar.

Johns Hopkins postdoctoral fellow Partha Banerjee

"We expected the enzyme levels to be different in diabetes, but we didn't expect the large difference we saw," said postdoctoral fellow Partha Banerjee in a statement.

Their conclusion: Find a drug that balances the enzyme, and you have a new approach to preventing or treating diabetes. The research was funded by the National Heart, Lung and Blood Institute and the National Institute of Diabetes and Digestive and Kidney Diseases.

- here's the release

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