Bacteria living naturally within the gut provide a gateway to flab, according to a few reports this week. These bacteria may explain how antibiotics fatten farm animals and perhaps people too, and how certain genes predispose organisms to obesity.
In a study published 22 August in Nature, researchers mimicked what farmers have been doing for decades to fatten up their livestock: they fed young mice a steady low dose of antibiotics. The antibiotics altered the composition of bacteria in the guts of the mice and also changed how the bacteria broke down nutrients. The bacteria in treated mice activated more genes that turn carbohydrates into short-chain fatty acids, and they turned on genes related to lipid conversion in the liver. Presumably, these shifts in molecular pathway enable fat build-up. Just as farm animals get fat, the antibiotic-fed mice put on weight.
Martin Blaser, a microbiologist at New York University in New York, says that parents might unknowingly be promoting a similar phenomenon when they treat common ailments and ear infections in their children. To back that idea up, he points to another study he authored. The study, published on 21 August, found that a disproportionate number of 11,000 kids in the United Kingdom who were overweight by the time they were 3 years old had taken antibiotics within their first 6 months of life.
“Antibiotics are extremely important drugs,” Blaser says, “but especially when given early in life, I believe they come at a cost that parents, doctors and patients should be aware of.”
Microbes also seem to be an accomplice in genetically induced pudginess, according to a study published today in Nature Immunology. When researchers rid mice of a gene encoding a gut molecule called lymphotoxin, segmented filamentous bacteria overwhelmed the normal microbial community. These bacteria may gobble up excess fat like tapeworms — the mice remained thin no matter what they ate. What’s more, mice with lymphotoxin intact were able to keep their slim figures when the researchers implanted the segmented filamentous bacteria in their guts.
Although the papers provide tantalizing links, Peter Turnbaugh, a microbiologist at Harvard University in Cambridge, Massachusetts, says that there’s more work to be done before microbes enter the limelight in the fight against obesity. “These studies suggest mechanisms by which different bacteria promote adiposity, but they don’t fully define pathways,” he says. “What really excites me about these papers is that now we have two new mouse models to do the follow-up experiments.”