Gene therapy may help slow the progression of type 1 diabetes

Type 1 diabetes is an autoimmune disorder that occurs when an individual's body attacks its own insulin-producing cells.

While there are several diabetes treatments that may help people who have the condition manage their blood sugar levels, there is no cure.

However, a recent study published in the Journal of Clinical Investigation found that a type of gene therapy may help stop the process of beta cell elimination in diabetic mice.

The researchers explained that they inserted a gene called CCL22 into a breed of laboratory rodents that is known to develop diabetes. The gene stimulated the production of its corresponding protein, which attracted T-regulatory cells and thereby inhibited the rodents' immune systems from attacking their insulin-producing beta cells.

The study's results showed that this method of gene therapy prevented the onset of type 1 diabetes in the majority of mice.

"It's a novel way to turn down the immune system specifically in the region of the beta cells inside the pancreas, and that may be a big advantage over general immune suppression, which can have significant side effects," said lead researcher Dr Bruce Verchere.

The scientists noted that this strategy may help slow the progression of type 1 diabetes in people who are in what they called the "honeymoon" stage of the disease, meaning that they still have some beta cells that have not been eliminated by their immune systems. Another potential benefit may be for individuals with type 1 diabetes who undergo pancreas transplants, they added.

According to the American Diabetes Association, patients with type 1 diabetes account for only 5 percent of the more than 25 million diabetic people in the U.S.

While individuals with type 2 diabetes may be able to manage their condition with a diabetic diet and exercise regimen alone, those with type 1 diabetes often require an insulin pump or multiple daily injections of the hormone in order to maintain healthy blood glucose levels.