Obesity is a pervasive and potentially lethal public health concern. The concept of energy balance is central to our understanding of obesity: excessive calorie intake combined with minimal physical activity creates a surplus of energy that is stored in the body as fat. This caloric algebra may be accurate, but it is an incomplete description of the obesity problem, leaving many questions unanswered. Why are some individuals more likely than others to become obese? Are factors other than consumption and activity involved? What can be done to prevent or reverse excessive weight gain?

Recently, much attention has been focused on the community of bacteria living in our intestines. Results of nutritional and pathological studies suggest that this intestinal microflora may be critically important to our health. For example, some of these bacteria help to provide important nutrients (e.g., vitamin B-12) to their hosts. Coupled with data showing that obese individuals tend to have different intestinal microbial communities than lean individuals, these observations have led scientists to consider the possibility that our gut microflora might directly affect our risk of becoming obese.

To investigate this possibility, researchers Frank Duca, Yassine Sakar and Mihai Covasa from the French National Institute for Agricultural Research (Paris) designed a study to test whether altering an animal's bacterial profile could influence its likelihood of developing obesity. They collected gut bacteria from two strains of rats with different incidences of obesity and then transferred the bacteria into the intestinal tracts of germ-free mice, which had no gut microflora of their own. The mice were fed either a regular diet or a high-fat diet, and food intake and weight gain were monitored for 8 weeks. Intestinal samples were then collected for metabolic analysis.

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Covasa presented the study results at the Experimental Biology 2012 conference in San Diego, CA, on 23 April. Mice that received intestinal bacteria from obesity-prone rats ate more food, gained more weight and became more obese than did mice that received bacteria from obesity-resistant rats and also showed changes in intestinal nutrient sensors and gut peptide levels, which could influence their responses to eating.

The researchers believe that gut microflora may influence behavior and food intake, possibly by interfering with the ability to sense and respond to a meal, and may promote excessive weight gain in obese individuals given the opportunity to overeat. They hope to eventually find ways to manipulate intestinal bacterial communities of at-risk individuals to reduce the likelihood of obesity.