A person with metabolic syndrome is twice as likely to develop heart disease and five times as likely to develop diabetes.
Researchers at Georgia State University and Cornell University did a follow-up on their previous research published in journal Science, using an improved technical approach to make the results more significant.
In the previous study, researchers showed altered gut microbiota plays a role in promoting metabolic syndrome.
Gut microbiota performs key functions in health and when it becomes dysregulated it can promote chronic inflammatory diseases such as Crohn's disease and ulcerative colitis.
"We've filled in a lot of the details about how it works," said Dr Andrew Gewirtz, a professor in the Institute for Biomedical Sciences at Georgia State.
"It's 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 said.
Normally, the bacteria are in the mucous layer at a certain distance away from epithelial cells. The researchers showed altered gut microbiota is more aggressive in infiltrating the host and gets very close to the epithelium.
The research team improved the study by comparing 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.
Previously, the researchers studied mice that were from two different strains and lived in separate environments.
In the new study, they found the absence of TLR5 on the intestinal surface leads to alterations in bacteria that drive inflammation, leading to metabolic syndrome.
"These results suggest that developing a means to promote a more healthy microbiota can treat or prevent metabolic disease," Gewirtz said.
"We showed that the altered bacterial population is more aggressive in infiltrating the host and producing substances, namely flagellin and lipopolysaccharide, that further promote inflammation," Gewirtz said.
The findings are published in the journal Gastroenterology.
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