If the scale has tipped too far in the wrong direction, perhaps you should blame the bugs living in your gut. Some microbes are better at wringing calories out of those holiday meals than others, researchers report in two papers in today's Nature. Transferring such high-octane bugs into lean mice causes the rodents to plump up, suggesting a microbial contribution to obesity.
Genetics certainly play a role in obesity, which is on the rise in many countries. But there's more to the problem. In 2004, Jeffrey Gordon from Washington University in St. Louis, Missouri, and his colleagues demonstrated that intestinal bacteria could also contribute to weight gain in mice. A year later, microbial ecologist Ruth Ley, a postdoctoral fellow working in Gordon's lab, discovered that lean and obese mice have different microbial communities in their gut. Now Gordon and his colleagues have shown this difference exists in people as well, and that diets can shift the microbial balance.
Ley put a dozen obese volunteers on either a low-fat or a low-carbohydrate diet for a year. At regular intervals, she surveyed their intestinal microbial communities--which can contain hundreds of species--by sequencing part of a gene for ribosomal RNA that all species have. At the onset, Firmicutes, a type of gram-positive bacteria, represented more than 90% of the microbes present in the volunteers, while gram-negative Bacteroidetes species barely made up 3%. (By contrast, Ley found, Bacteroidetes account for some 30% of microbes in people of healthy weight.) After a year, the volunteers had lost 2% to 6% of their weight, the Firmicutes had dropped to 73%, and the Bacteroidetes increased to about 15%, irrespective of the diet followed, Ley and her colleagues report. It's not clear whether obese people had excess Firmicutes before they were obese, or if those bacteria became more common as the pounds piled on.
A second paper suggests the microbes themselves help determine weight. Gordon's graduate student Peter Turnbaugh analyzed the genomes of gut microbes in two pairs of mice. In each pair, one mouse was healthy, while the other, a sibling, carried two mutant copies of a gene called leptin,which made it obese. Microbes from the obese mice had more genes for processing starches and complex sugars and produced more simple sugars and fatty acids--that is, calories--for the gut to absorb. When the researchers transplanted microbes from the obese mice into germ-free mice, the recipients had a 47% increase in body fat over 2 weeks. In contrast, germ-free mice supplied with microbes from lean mice had only a 27% increase, says Gordon.
Microbiologist Jeremy Nicholson from Imperial College London believes the researchers are onto something of "exceptional interest and importance. ... The obesity epidemic cannot be explained in human genetic or even simple lifestyle change terms alone," Nicholson says. "There has to be another dynamic factor, and that is the gut microbes."