Researchers said they learned that pain receptors don't secrete enough chemical elements found in the brain to keep insulin-producing pancreatic islets working normally. By supplying the chemical element to diabetic-prone mice, "the research group learned how to treat the abnormality ... and even reversed established diabetes," Salter said.

The team found that abnormal nerve endings in the insulin-producing cells of the pancreas initiated a chain of events that caused type 1 diabetes in mice. When they removed the nerve cells, the mice did not develop the disorder.

That means diabetes may be a disease of the nervous system, not just an autoimmune disease, said Hans Michael Dosch, a senior scientist at Toronto's Hospital for Sick Children and the study's principal investigator.

Research until now has mostly focused on the immune system and why it attacks and destroys insulin-producing islet cells. But Dosch, working with colleagues at Sick Kids, the University of Calgary and Maine's Jackson Laboratory, identified a control circuit between islet cells and their related sensory nerves. Disrupting this control circuit led to inflammation around the islets and eventually to their destruction. Without these cells, the mice could not make insulin. "This control circuit is the real cause of diabetes," said Dosch.

Experts say the findings, reported last week in the journal Cell, will change the way scientists think about diabetes. "It really is a breakthrough for the diabetes community," said Pam Ohashi, a professor of immunology at the University of Toronto and a senior scientist at the Campbell Family Institute for Breast Cancer Research. Dosch has immediate plans to move his research from mice to humans.

He is launching a clinical trial in January to determine if patients who have a high risk of type 1 diabetes have the same sensory nerve abnormalities. The researchers extended the studies to Type 2 diabetes. They said they believed treating the islet-sensory nerve circuits could normalize insulin resistance.

"If they do, then we have fantastic new therapeutic strategies," said Dosch, who is also a professor of pediatrics and immunology at the University of Toronto.

In the lab mice, so-called TRPV1 sensory neurons produced a specific kind of neuropeptide responsible for maintaining a healthy environment for the insulin-producing islet cells. If the balance was disrupted in any way, the immune system launched an attack on the islets, triggering type 1 diabetes. Eliminating these neurons -- or stopping their signals to the immune system -- prevented the chain of events that initiate type 1 diabetes.

Dr. Dosch added, that the discovery that nerves are involved in regulating the pancreas opens up new avenues of research. "We have a whole new target for therapy," he said. "It's always been the pancreas or the immune system. Now we have a new player."

the journal Cell, December 14, 2006

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