Which came first: The obese chicken or its obese microbiota?

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).

Figure 1: Obie and Lenny

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.

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My gut microbiota made me do it!

Our bodies are teeming with bacteria: for every one human cell in your body, there are at least 10 microbial cells. That’s about 100,000,000,000,000 microbes – what are they all doing?

The communities of microorganisms that live on or in a particular host are called the microbiota, and are responsible for a lot of physiological and biochemical functions. It’s probably no surprise that the gut microbiota digest complex molecules we’ve eaten and they keep pathogens from colonizing our bodies (most of the time). They synthesize vitamins and amino acids that we can’t make ourselves. Recent studies have shown that variation in gut microbiota are associated with obesity, diabetes, normal brain development and insulin signaling (which has a downstream affects on body size and developmental rate). But there’s one effect that variation in microbiota can have on their host that is particularly fascinating to me: they can influence host mate choice.

In 1989, Diane Dodd reared fruit flies (Drosophila pseudoobscura) from a common stock on two different food sources: starch and maltose. She found that after multiple generations of isolation on their separate substrates, starch-flies preferred to mate with starch-flies and maltose-flies preferred to mate with maltose-flies. The result was robust and repeatable, but the reason why and its mechanism were unknown.

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