Obesity epidemic blamed on bacteria

Scientists at the Emory University School of Medicine, Atlanta, Georgia have published a study that suggests that the obesity epidemic in the developed world may not be as a result of poor diet and lack of exercise alone, but may be helped along by 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.

Andrew Gewirtz, associate professor of pathology and laboratory medicine, said “our results suggest that excess calorific consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism”.

Georgina Lavender