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Diabetes Biotechnology

Diabetes Cured without Side Effects

6 years, 11 months ago

39143  0
Posted on May 08, 2017, 6 a.m.

Scientists cure diabetes in mice for one year, without side effects, by boosting pancreatic cells that secrete insulin.

Researchers at the University of Texas Health Science Center at San Antonio have found a way to cure diabetes in mice. This finding is particularly important because the cure does not spur any side effects. The medical team's new technique boosts cells within the pancreas that emit insulin.

The Importance of the Findings

If the cure works for humans without side effects, it will be the first-ever cure for Type 1 diabetes that does not produce any related problems. Furthermore, the research team's novel approach might help Type 2 diabetics cease insulin shots. The researchers aim to perform human clinical trials within the next three years. However, in order to do so, they must first test the strategy on large animals. If these studies go well, testing will move on to human beings.

It is interesting to note that the studies conducted on large animals are estimated to cost upwards of $5 million. Large animals are the next logical stepping stone as their physiology is fairly similar to that of human beings. In particular, large animals and humans share a similar endocrine system. The cure's co-inventor, Bruno Doiron, Ph.D. indicates these studies will likely occur before he submits an application to the United States Food and Drug Administration for Investigational New Drug approval.

The Cure's Potential Commercialization

The research group secured a United States patent back in January. UT Health San Antonio is generating a company to hasten efforts to commercialize the cure. It is expected that the cure will work for human beings as it did for mice. According to Dr. Doiron, his team's strategy worked “perfectly” in mice. He states the mice were cured for a full year without side effects. This success is acclaimed as a monumental breakthrough as no one has even come close to an entire year without side effects.

About the Therapy

The pancreas has numerous cell types beyond beta cells. The research team's approach is to modify these cells so they generate insulin. However, the goal is for insulin to be secreted only in response to sugar. In essence, the aim is to have non-beta cells function similar to beta cells. Beta cells are the only cells that create insulin. Insulin is important as it decreases blood sugar levels. The immune system of a Type 1 diabetes patient destroys beta cells. As a result, the patient lacks insulin. Patients plagued by Type 2 diabetes have failed beta cells and a resulting drop in insulin. Type 2 diabetes also causes inefficient use of insulin to boot.

The therapy involves a technique known as “gene transfer”. A virus serves as a carrier that sends selected genes to the pancreas. These genes spur digestive enzymes and other types of cells to produce insulin. Gene transfer with a viral vector has been approved numerous times by the United States Food and Drug Administration with the hope that it would treat an array of different diseases. Indeed, this technique has proven successful for treating certain childhood diseases.

The cell populations aside from beta cells co-exist with the human body's natural immune defenses. Type 1 diabetes patients who have lived with these cells for decades will enjoy the newly secreted insulin without any sort of harmful immune system response.

Precise Sugar Control

The therapy controls blood sugar in an incredibly precise manner. This appears to be a significant improvement over conventional insulin therapy as well as diabetes medications that send blood sugar too low. The research team's gene transfer allows for the modified cells to match the characteristics of beta cells so low blood sugar does not result.

Current Pharmaceutical Biotechnology, Beta Cell Formation in vivo Through Cellular Networking, Integration and Processing (CNIP) in Wild Type Adult Mice, Author(s): Bruno Doiron, Wenchao Hu, Ralph A DeFronzo.

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