Gene responsible for metabolic syndrome discovered

The absence of a gene called TLR5 on the intestinal surface leads to alterations in gut bacteria and promotes inflammation, leading to metabolic syndrome, says a study.

Metabolic syndrome is a combination of risk factors that increases a person's risk for heart disease, diabetes and stroke.

"They (the results) confirm the concept that altered microbiota can promote low-grade inflammation and metabolic syndrome and advance the underlying mechanism," said Andrew Gewirtz, professor at Georgia State University.

"We have filled in a lot of the details about how it works," Gewirtz added.

"It is the loss of TLR5 on the epithelium, the cells that line the surface of the intestine and their ability to quickly respond to bacteria. That ability goes away and results in a more aggressive bacterial population that gets closer in and produces substances that drive inflammation," Gewirtz explained.

Normally, the bacteria are in the mucous layer at a certain distance away from epithelial cells.

The researchers showed that altered gut microbiota is more aggressive in infiltrating the host and gets very close to the epithelium.

This altered population produces substances, namely flagellin and lipopolysaccharide that further promote inflammation, the findings showed.

For the study, the research team compared mice that were siblings and littermates, making all conditions in the study the same.

The mice only differed by whether they were missing a specific gene, TLR5.

"These results suggest that developing a means to promote a more healthy microbiota can treat or prevent metabolic disease," Gewirtz pointed out.

The findings were published in the journal Gastroenterology.