Salk scientists eye 2 new targets against Type 2 diabetes

Salk Institute experts and others have identified two new potential drug targets to treat insulin-resistant Type 2 diabetes. Both molecules control sugar production in the liver, determining by way of a genetic switch whether larger or smaller amounts of glucose are made. This is big, because controlling their activity helped treat diabetic mice.

Details are published in the journal Nature. The researchers note that new treatments for the disease couldn't come soon enough, considering that 26 million Americans have Type 2 diabetes and as many as 79 million more are at risk of developing it. We agree, considering how deadly the disease can be, and as the researchers note, that it costs $116 billion annually to treat. More testing must be done, however, considering that results in mice aren't always repeatable in human trials. And we won't know for some time if the treatment works in people, but we hope additional trials can be launched soon.

"We obviously have a lot of work to do to find out whether such a strategy might work in humans," said study co-author Marc Montminy, head of the Salk Institute's Clayton Foundation Laboratories for Peptide Biology, in a statement. But he seems to think his team has hit pay dirt, noting: "If you control these switches, you can control the production of glucose, which is really at the heart of the problem of Type 2 diabetes."

Montminy and the research team focused on glucagon, a hormone produced by pancreatic islet cells released during fasting that turns on the CRTC2 genetic switch, telling the liver to make glucose for the brain. After eating, those same pancreatic islets release insulin, which in healthy people tells the liver to stop its glucose production. But in patients with insulin-resistant Type 2 diabetes, the CRTC2 switch produces too much glucose. Montminy and his colleagues believe that a potential drug could be used to reduce the activity of the IP3 molecular receptor, which is on the outside of liver cells. Triggered by glucagon, IP3 begins a process that activates a molecule known as calcineurin, which in turn triggers CRTC2 to produce more glucose, the researchers found. Such a compound would also be used to target the calcineurin accelerator.

The technique generated promise in liver cells and in mice.

- here's the release
- check out the journal abstract

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