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The human intestinal microbes, and the branch of the immune system that regulates them, may be partly responsible for the metabolic syndrome, according to a study in mice by researchers at Emory University in Atlanta (USA).

Metabolic syndrome includes a group of metabolic problems associated with obesity that increase the risk of diabetes and heart disease. The work, published in the journal Science, is based on recent discoveries that link the composition of intestinal microbes with obesity.

The study, led by Matam Vijay-Kumar, suggests that the innate immune system that defends the body against microbial pathogens, could be the bridge between intestinal microbes and metabolism.

The authors found that mice lacking an important component of the innate immune system, a protein called TLR5, developed key features of the metabolic syndrome such as increased fat accumulation and insulin resistance, accompanied by changes in intestinal flora.

In addition, the mutant mice also ate more food than their normal peers. The transfer of gut microbes in the mutant mice to germ-free mice, which lack of microbes in the intestines but otherwise normal, caused recipient mice develop several features of metabolic syndrome. This suggests that changes in intestinal flora of the animals were probably a cause rather than a consequence of metabolic syndrome.

The authors also sequenced part of the microbes’ genetic material taken from the intestines of the mutant mice, and used the information to identify a specific set of bacterial species whose abundance was abnormal.

The researchers propose that deficiencies in the innate immune system may cause changes in intestinal flora that induce low-grade inflammatory signals. These signals may in turn influence the insulin-receptor signals, increasing the appetite and food intake, which ultimately leads to other aspects of metabolic syndrome.

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