Obesity epidemic blamed on bacteria

Previous research has shown that intestinal bacteria populations differ between the obese and the lean in humans. A new study using mice shows that increased appetite and insulin resistance can be transferred by intestinal bacteria from one mouse to another. This indicates that the presence of the intestinal bacterial contributes to changes in both appetite and metabolism.

The team at Emory were studying mice with an altered immune system so that they lacked Toll-like receptor 5 (TLR5), a receptor that recognises flagellin, and therefore the presence of bacteria. The TLR5 deficient mice were heavier than their normal counterparts and also consumed more food. They had metabolic changes associated with obesity. When the TLR5 deficient mice were fed a restricted diet, they remained insulin resistant. When given a full-fat diet, they developed diabetes and fatty liver disease. When TLR5 deficient mice were given strong antibiotics, enough to kill most of their intestinal flora, their metabolic abnormalities decreased. Studying the gut flora of TLR5 deficient mice and normal mice showed differing compositions of bacterial families. Previous research has already shown that the components of gut flora can alter the ability of the intestines to extract calories from food...