Blame it on the bacteria

The bacteria in human guts could be partially responsible for obesity, report US researchers. Jeffrey Gordon and his team from the Washington University School of Medicine, Missouri, think that changing these bacterial populations could offer another approach to treating a disease which causes hundreds of thousands of deaths every year. 

As the researchers explain, the human gut teems with trillions of microbes, far more than the number of cells in our body. These bacteria help us break down otherwise indigestible foods, receiving shelter and their own food supply in return. 

The gut bacterial community is dominated by two main divisions, the Firmicutes and the Bacteroides. Gordon’s team found that obese people had a higher proportion of Firmicutes in their guts than had lean people.1 Twelve obese people who were put on either fat-restricted or carbohydrate-restricted diets lost weight and the relative proportion of their gut Firmicutes decreased, becoming more like that of a leaner person. 

The researchers explained why this might happen by studying the gut microbes of mice that were genetically obese (they lacked genes for leptin, a hormone that monitors body fat and can limit food intake).2 As expected, the obese mice had more Firmicutes bacteria in their gut than their leaner relatives. A detailed analysis showed that obese mice gut microbes were better at harvesting calories from food - suggesting that the bacteria made the mice fatter. 

Gordon’s team went further: they transplanted the Firmicutes-rich ’obese microbes’ into germ-free mice, born without any gut microbes at all and kept in sterile bubbles. These mice increased their body fat by more than those colonised with a more reasonable mix of ’lean microbes’. 

All this suggests, says Gordon, that our gut microbes contribute in some way to our regulation of body weight, via their efficiency of harvesting energy from food. Manipulating our gut microbial community could offer a new therapeutic treatment for obesity. 

But many questions about how and why the microbes in our gut are regulated remain to be answered before any obesity treatment can be trialled, points out Randy Seeley, of the University of Cincinnati, US. ’The idea that microbes of our choice tossed into the gut would then survive is not at all clear,’ he said. 

Stephen Bloom, of Imperial College London, UK, similarly cautions against any simplistic conclusions. For example, it is not clear how a combination of gut microbes and food intake affect the release of so-called ’satiety’ hormones, like leptin, that help us feel full. He says this was not sufficiently considered by Gordon’s team. 

And, Bloom points out, we all have an inbuilt feedback system - based on hormones - that guides us unconsciously to take in more or less food. If microbes in our guts extracted more energy from food, wouldn’t we just eat less to compensate? Drugs used to treat obesity rely on diminishing our appetite, our food intake, or our fat storage. But, says Bloom, the current chemical treatments inevitably cause side effects to our general metabolism, the details of which are far from understood. The best advice for avoiding obesity is still as it always was: eat less, exercise more, and don’t rely on drugs or gut microbes to stop you piling on the flab. 

Richard Van Noorden