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Synthetic Antioxidant Prevents Diabetes in Mice

Stopped or warded off disease, but at high levels

FRIDAY, Jan. 25, 2002 (HealthDayNews) -- A synthetic version of a potent antioxidant prevented Type I diabetes from developing in mice by protecting their insulin-producing cells, say researchers from the National Jewish Medical and Research Center and the University of Colorado Health Sciences Center.

The study was small, though, and the mice were given high doses of the antioxidant. Although any application to humans would be years away, the research opens a door for a way to ward off the disease.

As study co-author Jon Piganelli explains, in diabetes the immune system mistakenly identifies the beta cells in the pancreas (the insulin producers) as foreign invaders -- enemies that must be destroyed. Beta cells, however, are far from lethal. They are, in fact, necessary to produce insulin, a hormone that helps us metabolize sugar.

As the destruction of the beta cells begins, however, the attacking cells of the immune system give off a kind of chemical inflammation via the production of something called free radicals. In much the way rust wears away at those metal lawn chairs you leave out in winter, the oxygen-rich free radicals "eat away" chunks of the beta cells, crippling and eventually destroying them, says Piganelli. He worked with the Colorado team, and is now an associate professor of pediatrics at the University of Pittsburgh's Diabetes Institute.

The antioxidants work to prevent this entire process from occurring, he says.

"The antioxidant not only mops up the inflammation-causing free radicals emitted by the attack cells, but more importantly, when present in large enough amounts, the antioxidant also helps keep the immune system in line, reducing its desire to attack the beta cells by helping it to recognize these cells are not foreign invaders," says Piganelli.

Endocrinologist and diabetes specialist Dr. Loren Wissner-Greene deems the study provocative because it opens up a whole new approach to diabetes treatment and prevention.

"The idea that diabetes could be prevented in high-risk individuals is an exciting idea, because we do have some ability to identify who those children might be," says Wissner-Greene, clinical associate professor of medicine at New York University Medical Center.

But, she cautions, not only is the study small, but it was also done only on rodents. At best, it "has a very, very long way to go before it's applicable to humans," she says. Nonetheless, she says, the research is valuable.

"It may help us to learn more about how and why the immune system turns on the beta cells to begin with -- and when we find that out, we have the key to preventing this disease, or at least stopping it at the very earliest stages," says Wissner-Greene.

Type I diabetes is a chronic disease also known as juvenile diabetes because the onset usually occurs in children. Currently, the only known treatment is insulin, usually in the form of injections, which must be taken several times a day. While the cause of diabetes remains unknown, doctors do know that a close family history of the disease increases the risk, with siblings of children diagnosed with Type I diabetes the most likely to be affected.

The new study, which appears in the February issue of the journal Diabetes, involved just 15 mice, all of which received a medical procedure designed to induce diabetes quickly.

Before the procedure, 10 of the 15 mice also received injections of a synthetic compound designed to mimic a naturally occurring antioxidant known as superoxide dismutase. After the diabetes-inducing treatment, the researchers continued to treat the 10 mice with the antioxidant therapy four more times over the course of nine days. The five remaining mice served as control group and received no therapy either before or after the diabetes-inducing treatment.

By day 13, all five of the control mice had developed diabetes. Of the mice treated with the antioxidant, five developed diabetes, but not until day 21. None of the remaining five mice treated with the antioxidant developed diabetes at all, even after a four-week follow-up.

"The mice remained healthy for almost two weeks after the treatment ended," says Piganelli. This, he adds, strongly suggests that the use of the antioxidant compound affected the cells of the immune system, so that they no longer viewed the important beta cells as something to be destroyed.

This, says Wissner-Greene, is the essence of preventing diabetes from occurring.

"If we can stop the body from turning on itself, and from destroying the cells of the pancreas, we have stopped diabetes," she says.

What To Do

Doctors caution that before you run out and fill your shelves with antioxidant vitamins, remember that the study is only experimental and the results may not translate to humans. Moreover, the doses used in the study were considered pharmacological -- much higher than what you could ingest by taking vitamins.

For more information on diabetes, visit the American Diabetes Association or the National Institute of Diabetes and Digestive and Kidney Diseases.

SOURCES: Interviews with Jon Piganelli, Ph.D., associate professor, department of pediatrics, Diabetes Institute, Children's Hospital, University of Pittsburgh; Loren Wissner-Greene, M.D., endocrinologist, and clinical associate professor of medicine, New York University Medical Center, New York; February 2002 Diabetes
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