An experimental new combination therapy has reversed type I diabetes in mice, thanks in part to a novel focus on combating insulin resistance in this form of the disease, US researchers said Monday.
Insulin resistance has long been a recognized feature of type II or late-onset diabetes, but has only recently been identified as a component of juvenile or type I diabetes.
AdvertisementWith this study, investigators have shown for the first time that treating inflammation related to insulin resistance as well as the autoimmune component of the disease can successfully reverse the disease, if it is caught early enough.
"We believe this is the first study to show inflammation in insulin sensitive tissues plays an important role in this disease," said Terry Strom, a professor of medicine at Harvard Medical School and co-author of the paper.
Type I diabetes is an autoimmune disorder in which the body's own immune system attacks the pancreatic cells that produce the hormone insulin which regulates blood sugar.
The result is that the patient cannot produce enough insulin of their own, and has to supplement with synthetic versions of the hormone, typically by injection.
The condition raises an individual's risk for a host of complications, including heart disease, blindness and nerve damage.
In this experiment, investigators treated newly diabetic mice with a cocktail of three substances that prevented the body's own T-cells from destroying the pancreatic cells that produce insulin and also eliminated the inflammation that impaired the ability of tissues in the muscles, fat and liver to metabolize insulin properly.
The mice were treated for a period of 14 or 28 days, and within five to seven weeks, 95 percent of them had normal blood sugar levels and were able to control their blood sugar for 300 days.
In contrast, the untreated diabetic mice became hypoglycemic and most died within seven weeks even with insulin treatment.
The results suggest any therapy that hopes to arrest the development of diabetes in humans must not only tackle the T-cell disorder, it must also restore insulin responsiveness in tissues affected by an inflammatory disorder.
Otherwise, the body's remaining insulin-producing beta cells have to work twice as hard to regulate blood sugar levels.
"The remnants of the beta cells have to work overtime to try and maintain blood sugar levels," explained Strom.
Strom said that clinical trials of the treatment in humans would begin within 12 months.
The study appears in the Proceedings of the National Academy of Sciences.
Maria Koulmanda, an assistant professor of surgery at Harvard Medical School, and colleagues at the Joslin Diabetes Center and Beth Israel Deaconess Medical School in Boston worked on the project.
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