In a study, published in the journal Nature, Yale scientists report that proteins that alter microbe population in the stomach can trigger obesity and chronic liver disease, suggesting that the condition may be contagious.

A team of researchers led by Richard Flavell, a professor of immunobiology at Yale School of Medicine, found that when fed a Western-style diet, mice engineered to have a particular immune deficiency developed fatty liver disease and got fatter.

Researchers also observed that when healthy mice were kept in the same cage with these engineered mice, the former gained weight and started showing the symptoms of liver disease, indicating that the altered intestinal environment that led to weight gain and liver disease was infectious among the community of mice.

Citing the findings of the research, Richard A. Flavell said, humans live in symbiosis with the bacteria in their gut; however in this case, the disease-associated bacteria increased 1,000 folds in immune-deficient mice.

Researchers blame deficiency in components of two particular inflammasomes in mice for the development of an altered microbial community. Emphasising the importance of more research, Flavell said that our next step would be to extend the research to humans to see whether findings apply to people or not.

The Yale team found that the microbial composition in mince was brought back to normal by targeted antibiotic treatment, indicating that addressing gut microorganisms can help develop more precise obesity treatment and fatty liver disease treatment for humans.

Read the original article here.