The bugs that help digest food may also cause the body to pack on the pounds if they are not properly regulated, a new study has found.
That is because if the wrong kinds of bacteria take over they can cause a low-level inflammation that leads to a pre-diabetic condition and an elevated appetite, the study published Thursday in the journal Science found.
"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost, high-calorie foods," said senior author Andrew Gewirtz of Emory University School of Medicine.
"However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism."
Gewirtz and his colleagues studied mice that were genetically engineered to be deficient in a key immune system protein - TLR5 - which helps cells sense the presence of bacteria.
"This protein serves as the neighborhood cop of the intestinal community," Gewirtz told AFP.
"It knows which bacteria it has to keep in check and it knows not to apply too much force and doesn't harm the good bacteria."
The immune system can continue to regulate bacteria without TLR5, but it does a poorer job. The bacterial composition changes, a low level inflammation sets in and insulin receptors are desensitized.
The protein-deficient mice ate about 10 percent more food and ended up about 20 percent heavier than normal mice.
They also developed metabolic syndrome, a cluster of disorders that in humans increases the risk of developing heart disease and diabetes.
While it was possible to get the mice to keep the weight off by restricting their food intake, they continued to show a decreased sensitivity to insulin.
That suggests that "at least some portion of obesity may result from insulin resistance rather than the commonly held view that type 2 diabetes and insulin resistance is a consequence of obesity," Gewirtz said.
Another key discovery was that if these bacteria were transferred to the intestines of mice which were not deficient in the protein, they would also develop metabolic syndrome.
This only worked, however, in mice whose intestines had been cleared of all other bacteria.
Humans have relatively stable intestinal bacterial populations which are acquired at birth but can be influenced by diet and antibiotics.
However, other studies have found that this baseline bacterial population is changing as a result of improvements in sanitation and the widespread use of antibiotics.
"It suggests that a portion of the epidemic of obesity and metabolic symptoms may be resulting from early environmental conditions that affect one's gut microbiota," Gewirtz said in a telephone interview.
While the study suggests a possible genetic predisposition to obesity, a deficiency in the TLR5 only affects a small percentage of the population, he said.
Changes in intestinal bacterial compositions could be significantly more widespread and could potentially one day be resolved by giving babies the right kind of bacteria before the wrong kind settles in, he added.