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