Historically, medical research has focused on pathogenic bacteria when trying to understand the relationship between human health and microorganisms. This makes intuitive sense – since pathogens make us sick – but our bodies host way more nonpathogenic bacteria than pathogens and they function in keeping us healthy. Our gastrointestinal tract has trillions of bacteria in it and much recent work has been trying to understand these complex communities. Mice are a common model for understanding human gut microbes and health. Enter Obie, the obese mouse (Figure 1, left) and Lenny, the lean mouse (right).
Obie and Lenny are genetically different at a locus in their genomes that codes for leptin – a hormone that inhibits appetite. Mice that can’t make this hormone become very hungry and morbidly obese. These two mice also differ in the composition of their gut microbiota – obese individuals (both mice and human) have different amounts of the main bacterial phyla in their gut and as a result, are able to more efficiently extract calories from food. In other words, if you give both of them the exact same amount of food, Obie is going to get more calories from it than Lenny, contributing to Obie’s weight problem. In humans, where the status of our “leptin locus” is not normally known and probably not as straightforward as the case of Obie and Lenny– it’s been hard to tell whether this shift in gut microbiota is the CAUSE of obesity or the EFFECT of obesity. That brings me to today’s paper: a short communication in The ISME Journal (that’s open access!) by Fei and Zhao that addresses this exact problem.