There is a strong link between obesity and type 2 diabetes, where fat cells contribute to development of the disease by changing metabolism and chronic inflammation. Now, a new study suggests that obesity’s effect on the microbiome – the ecosystem of bacteria and other microbes that live on and in our bodies and affect our health – could be involved.

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The more overweight people are, the more likely they are to have large amounts of staph bacteria living on their skin

The study, published in the journal mBio, adds to growing evidence about the role of bacteria and viruses in causing noninfectious diseases, such as cervical cancer (human papillomavirus) and stomach ulcers (H. pylori bacteria).

Microbiologists at the University of Iowa (UI) found that when rabbits are chronically exposed to a toxin produced by Staphylococcus aureus (staph) bacteria, they develop the hallmarks of type 2 diabetes, such as insulin resistance, glucose intolerance and inflammation.

Lead researcher Patrick Schlievert, professor of microbiology at the UI Carver College of Medicine, says:

“We basically reproduced Type 2 diabetes in rabbits simply through chronic exposure to the staph superantigen.”

The study is important because we already know that the human microbiome changes with obesity and that one of these changes is the increase in staph colonization and infections. Now, the new findings suggest the bacterium may play a role in the progression to type 2 diabetes.

Prof. Schlievert notes that as people gain weight, they are likely to have large amounts of staph bacteria living on their skin, and:

“People who are colonized by staph bacteria are being chronically exposed to the superantigens the bacteria are producing.”

In previous work, Prof. Schlievert and colleagues had shown that superantigens – the toxins that staph bacteria produce – disrupt the immune system and are also the main reason why staph infections like toxic shock syndrome, sepsis and endocarditis can kill.

In their new study, the team shows that superantigens cause inflammation by interacting with fat cells and the immune system. This systemic inflammation is what leads to insulin resistance and other hallmarks of type 2 diabetes.

The researchers found that levels of staph superantigens in people heavily colonized with the bacterium were comparable to those that caused the rabbits in their study to develop type 2 diabetes symptoms.

They suggest therapies that eliminate staph bacteria – or at least neutralize its superantigens – may also prevent or treat type 2 diabetes.

Prof. Schlievert explains:

I think we have a way to intercede here and alter the course of diabetes. We are working on a vaccine against the superantigens and we believe that this type of vaccine could prevent the development of type 2 diabetes.”

He and his colleagues are now planning to test a gel that could be used to eliminate staph from human skin. The gel contains glycerol monolaurate, which is known to kill staph bacteria on contact. Then, they plan to test whether use of the gel will improve blood sugar levels in pre-diabetics.

Grants from the Carver Trust Collaborative helped fund the study.

Meanwhile, Medical News Today recently reported another study that showed how changes in the eye microbiome of contact lens wearers may increase infections. The study also found that the composition of the eye microbiome of contact lens wearers is more similar to that of their skin than that of non-lens wearers.