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Beta-cell break benefits diabetics.

Beta-cell break benefits diabetics

Patients with insulin-dependent diabetes mellitus (IDDM) gradually lose their ability to produce insulin, a hormone required for proper maintenance of blood sugar levels. But a two-week treatment with very large doses of insulin can delay for more than a year the demise of insulin-producing pancreatic beta cells in patients newly diagnosed with IDDM, researchers report.

Increasingly, scientists believe IDDM results from an immune reaction against some part of the insulin-making machinery in beta cells or against insulin itself. Indeed, treatment with immunosuppressive drugs has proved useful in delaying IDDM progression in some nely diagnosed diabetics (SN: 11/7/87, p.292). But the new research suggests the beneficial effects of this immunosuppressive therapy may result not from the drugs themselves but from the large doses of insulin routinely administered along with those drugs. Physicians typically give large amounts of insulin with immunosuppressive steroids because these drugs tend to raise blood sugar concentrations to dangerous levels.

Shirish C. Shah and his colleagues at the University of South Florida Health Sciences Center in Tampa treated two groups of newly diagnosed IDDM patients for one year. They kept 14 patients on conventional doses of insulin to hold blood sugar levels under control. But they hospitalized 12 other new patients and gave them insulin doses four times higher than normal for two weeks, before sending them home and putting them on conventional insulin therapy for the rest of the year. Tests showed that during the two-week period of high-dose insulin therapy, the hospitalized patient's beta cells got a "rest," producing only one-seventh the amount of insulin produced by the patients on normal insulin doses.

After one year, the experimental group's beta cells were producing almost twice as much insulin as those of the conventionally treated group. Reporting in the March 2 NEW ENGLAND JOURNAL OF MEDICINE, the researchers attribute the difference to the rest period granted beta cells during the two weeks of megadose insulin therapy. They hypothesize that too much beta-cell activity early in the disease process somehow triggers or exacerbates the body's autoimmune reaction. By giving the cells a rest during that critical period, they say, a full-blown autoimmune reaction can be set back by as much as a year or more.

"We think it is insulin itself that is the antigen that causes the immune system to attack the beta cells," says Shah. "And when we give megadoses of can produce tolerance in the body." Immune tolerance is a poorly understood mechanism by which the body, when exposed to large amounts of foreign material, comes to accept it rather than reject it.

Shah says unpublished follow-up studies with 12 other patients indicate the autoimmune process eventually comes back, necessitating repeat megadoses ofinsulin every six to 12 months. The treatment is not simple: While being treated with the abnormally high doses of the sugar-lowering homrone, patients must remain on an "artificial pancreas" to keep their blood sugar levels normal. However, Shah says, the results are striking. "We have one girl who has been treated three times now and she's beyond two years [since diagnosis] and she can make more insulin now than she was making three months after she was diagnosed." the girl is scheduled for a fourth treatment this summer, Shah says.

"Our ultimate goal is to try this treatment before they become insulin dependent," he adds, nothing it's now possible to predict "with reasonable certainty" those who will develop diabetes. "If we treat prediabetic high-risk individuals and if we can stop the progression, then they may never have to take [daily] insulin. That's what we'd like to achieve."
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Publication:Science News
Date:Mar 11, 1989
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