In the study, researchers examined mice that were genetically engineered to be deficient in a key immune system protein, namely TLR5, which helps cells sense the presence of bacteria. Such protein plays an important role in the intestinal community, meaning it knows not to apply too much force and does not harm the good bacteria.
In the absence of TLR5, the immune system can still regulate bacteria but it just could not do it properly. When the bacterial composition changes, a low level inflammation sets in and insulin receptors are desensitized.
To justify the theory, a series of experiments were preformed on mice. The results showed that if the TLR5-deficient mice were given unrestricted diets, they ate 10 percent more and gained 20 percent more weight than the normal mice. Even if their food was limited, the TLR5-deficient mice were still less sensitive to insulin than the normal mice.
The TLR5-deficient mice also developed metabolic syndrome, which could cause weight gain, high blood pressure and high cholesterol levels, and it could raise the risk for developing diabetes and heart disease.
While the study was limited to mice, experts still believe they might applicable to humans as well. The findings suggested that excess caloric consumption is not only the result of undisciplined eating style but also changes in appetite and metabolism caused by the intestinal bacteria.