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Friday, December 15th 2006

Diabetes Would Be A Lovely Disease To Cure

This is a link from Drudge. Have scientists in Toronto cured the mouse equivalent of Type I Diabetes? That would be a lovely “breakthrough” considering Diabete’s toll.

Apparently, and this is the National Post reporting, there are

around the insulin-producing islets [cells of the Pancreas] an “enormous” number of nerves, pain neurons primarily used to signal the brain that tissue has been damaged.

Suspecting a link between the nerves and diabetes, [Dr. Dosch] and Dr. Salter used an old experimental trick — injecting capsaicin, the active ingredient in hot chili peppers, to kill the pancreatic sensory nerves in mice that had an equivalent of Type 1 diabetes.

And voila! The mice were literally cured, apparently.

Diabetic mice became healthy virtually overnight…

“I couldn’t believe it,” said Dr. Michael Salter, a pain expert at the Hospital for Sick Children and one of the scientists. “Mice with diabetes suddenly didn’t have diabetes any more.”

The researchers caution they have yet to confirm their findings in people, but say they expect results from human studies within a year or so. Any treatment that may emerge to help at least some patients would likely be years away from hitting the market.

This of course challenges the autoimmune understanding of Type 1 diabetes.

While pain scientists have been receptive to the research, immunologists have voiced skepticism at the idea of the nervous system playing such a major role in the disease. Editors of Cell put the Toronto researchers through vigorous review to prove the validity of their conclusions, though an editorial in the publication gives a positive review of the work.

The National Post article makes it sound like this might change the thinking about many autoimmune diseases if the results are repeated.

Personally I cannot find the study in the current or immediate past Cell issues or on Ovid through my school, but maybe this is a preview of publication in Volume 128 which will be out on December 28th.

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