Prolonged Exposure to a Toxin Produced by A Bacteria may Cause Type-2 Diabetes

In an important research that could lead to the development of vaccine to prevent one of the most prevalent diseases of our time - Type-2 diabetes, US researchers have found that toxins produced by a bacterium may cause the disease. The researchers found that prolonged exposure to a toxin produced by Staphylococcus aureus (staph) bacteria causes rabbits to develop the hallmark symptoms of Type-2 diabetes, including insulin resistance, glucose intolerance, and systemic inflammation.

"We basically reproduced Type-2 diabetes in rabbits simply through chronic exposure to the staph super antigen," said lead researcher Patrick Schlievert, professor at University of Iowa in the US.

The findings suggest that therapies aimed at eliminating staph bacteria or neutralizing the super antigens - toxins produced by all strains of staph bacteria - might have potential for preventing or treating Type 2 diabetes.

"I think we have a way to intercede here and alter the course of diabetes," Schlievert said. "We are working on a vaccine against the super antigens and we believe that this type of vaccine could prevent the development of Type-2 diabetes," Schlievert said.

The findings also explain why obesity that leads to changes in the ecosystem of bacteria that colonize our bodies is a risk factor for Type-2 diabetes.

"What we are finding is that as people gain weight, they are increasingly likely to be colonized by staph bacteria - to have large numbers of these bacteria living on the surface of their skin," Schlievert said. "People who are colonized by staph bacteria are being chronically exposed to the super antigens the bacteria are producing," Schlievert added.

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The researchers found that toxins produced by all strains of staph bacteria interact with fat cells and the immune system to cause chronic systemic inflammation and this inflammation leads to insulin resistance and other symptoms characteristic of Type-2 diabetes.

The study was published in the journal mBio.

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Source-IANS