Manipulating levels and ratios of gut bacteria can help prevent obesity and diabetes — a common risk factor for developing cardiovascular diseases finds a new study.

The study with the rodent equivalent of metabolic syndrome showed evidence that the intestinal microbiome — a ‘garden’ of bacterial, viral and fungal genes — plays a substantial role in the development of obesity and insulin resistance in mammals, including humans.

“This study adds to our understanding of how bacteria may cause obesity, and we found particular types of bacteria in mice that were strongly linked to metabolic syndrome,” said David Hackam, a researcher at the Johns Hopkins Children’s Centre in Baltimore, the US.

“With this new knowledge we can look for ways to control the responsible bacteria or related genes and hopefully prevent obesity in children and adults,” he added, in a paper published in the journal Mucosal Immunology.

Metabolic syndrome is a cluster of conditions including obesity around the waist, high blood sugar, and increased blood pressure, and is a risk factor for heart disease, stroke, and diabetes.

The team ran a series of experiments on both normal mice and mice genetically modified to lack Toll-like receptor 4 (TLR4)– a protein that receives chemical signals to activate inflammation — in their intestinal epithelium.

They fed both groups of mice “standard chow,” or food with 22 percent fat calories, for 21 weeks.

Compared to normal mice, those lacking TLR4 showed a series of symptoms consistent with metabolic syndromes, such as significant weight gain, increased body and liver fat, and insulin resistance.

When administered antibiotics there was a significant reduction in the number of bacteria in the intestinal tract, which prevented all symptoms of metabolic syndrome in the mice that lacked TLR4.

This demonstrates that bacterial levels can be manipulated to prevent the development of metabolic syndrome.

“Our experiments imply that the bacterial sensor TLR4 regulates both host and bacterial genes that play previously unrecognized roles in energy metabolism leading to the development of metabolic syndrome in mice,” Hackam said.