Metabolic syndrome is a condition where a person is exposed to the risks of developing heart diseases, diabetes and even stroke. A person who suffers from metabolic syndrome has a large waistline coupled with high blood sugar levels, increased blood pressure as well as unstable cholesterol levels. Metabolic syndrome is accompanied with high triglyceride and fasting sugar levels as well as low level of HDL cholesterol levels. These factors together make a person much susceptible and vulnerable to coronary artery disease, heart diseases, etc. It occurs due to inability of the body to utilize and store energy.
A recent research conducted by a team of experts at Georgia State University and Cornell University establishes that the bacteria that live in the intestine can help treat or prevent metabolic syndrome.
The experts conducted a follow-up on their previous research published in the journal Science, using an improved technical approach to make the results more significant. Their current findings are published in the journal Gastroenterology. The previous study explained that altered gut microbiota plays a role in promoting metabolic syndrome.
According to the experts, gut microbiota performs certain key functions and when it becomes dysregulated it can promote chronic inflammatory diseases such as Crohn's disease and ulcerative colitis. In addition, altered gut microbiota promotes inflammation that leads to metabolic syndrome.
Normally, the bacteria are in the mucous layer at a certain distance away from epithelial cells. Researchers showed that altered gut microbiota is more aggressive in infiltrating the host and gets very close to the epithelium. This altered population produces flagellin and lipopolysaccharide, which further promote inflammation.
"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 added.
The team carried out experiments on mice modules. 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 healthier microbiota can treat or prevent metabolic disease," Gewirtz said. Inputs From PTI