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WASHINGTON — Scientists aiming to cure and prevent insulin- dependent diabetes have discover- ed what goes wrong in the bodies of a special breed of mice prone to the affliction and, using that knowl- edge, have developed a way to pre- vent the disease in the rodents.
Because mouse diabetes is al- most identical to human “Type I diabetes” — also called insulin-de- pendent or juvenile-onset diabetes — the researchers say they may be ready to test their techniques on humans in five years and that a treatment for patients in the early stages of the disease could be ready to test in two years.
The findings, published in Thurs- day’s issue of Nature, were ob- tained by two research groups working independently. One was led by Daniel L. Kaufman, a mo- lecular biologist at the University
of California at Los Angeles, and the other by Hugh O. McDevitt of Stanford University.
“There’s great excitement at the prospects for this research,” said James Gavin, a diabetes specialist and president of the American Dia- betes Association. “These are studies you have to call convinc- ing. They’re clearly likely to have human applications.”
Gavin said it was also significant that the new work was a product of basic science and could not have been accomplished without experi- menting on laboratory animals.
Type I diabetes has long been known to be an autoimmune dis- ease — an ailment in which the immune system, instead of defend- ing the body against invading mi- crobes, mistakenly attacks part of the body. In diabetes, it kills the special cells in the pancreas that make insulin. Without insulin, cells cannot take in sugar. The body is deprived of sugar’s energy and its accumulation in the bloodstream damages nerves and other tissues. The potential new treatments would either stop the immune sys- tem from making a mistake or sup- press an existing erroneous response.
Perhaps the most intriguing sci- entific finding is Kaufman’s expla- nation of a long-suspected link between Type I diabetes and Cox- sackie virus infections which cause colds, sore throats and sometimes more serious symptoms.
His group found that the virus carries a protein that is uncannily similar to another protein on cells in the pancreas that make insulin. The studies suggest that once the immune system has learned to rec- ognize the virus as a foreign in- vader and to attack it, the same defense mechanism mistakenly identifies insulin-making cells as enemies and goes on to destroy them as well.
Kaufman said Coxsackie virus infections, which are relatively common in childhood, may ac- count for a significant percentage of diabetes cases but not all of them.
Type I diabetes, which usually arises between the ages of 10 and 14, is the less common form of the disease, afflicting an estimated 300,000 Americans, who must re- ceive insulin injections for life. By contrast, 12 million people are thought to have Type II diabetes, which usually starts after age 40 and becomes more common with age. It is not an autoimmune dis- ease and can usually be controlled with diet and exercise.
“The bottom line is we’re able to completely prevent the disease” in mice, Kaufman said.
He said researchers hope to show within five years that the method is safe enough to try on human beings who have a high risk of developing Type I diabetes, which runs in families. Once iden- tified, Kaufman suggested, chil- dren might be tested regularly, and if necessary, they would be given an injection to prevent the onset of the disease.
Within two years, he said, it may be possible to start testing an ap- proach for those who are already in the early stages of getting diabetes.
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