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Getting Fat? Blame Your Gut Bugs
4 November 2004 (All day)
If your weight has been creeping up lately, it may not be just your sweet tooth for Krispy Kremes that's at fault. New research finds that microbes living in the rodent gut control an enzyme that regulates fat uptake and storage. Drugs that target this protein may one day help fight obesity, says lead researcher Jeffrey Gordon, a molecular biologist at Washington University in St. Louis, Missouri.
Microbiologists have known for decades that the human digestive system is teeming with bacteria--indeed, bacterial cells outnumber our own 10 to 1. Some of these gut guests earn their keep by processing otherwise indigestible food, thereby providing the host with more calories per bite. That assistance was a great help in the millennia when food was scarce, but nowadays this efficiency can be a curse. Obesity rates are soaring, and excess weight gain increases the risk of diabetes, heart disease, high blood pressure, and liver malfunction.
Gordon, Washington University's Fredrik Bäckhed, and their colleagues have now discovered that certain bacteria do more than just aid digestion. They report in the 2 November Proceedings of the National Academy of Sciences that Bacteroides bacteria inhibit an enzyme that normally reduces fat uptake and storage. Bäckhed and colleagues started with mice raised in a germ-free environment and exposed some of them to a variety of microbes from the gut of another mouse. To the researchers' surprise, after 2 months, the newly infected mice were 42% fatter, even though they had eaten 29% less than the bacteria-free mice. And fast metabolism wasn't the answer, as the metabolism of the bacteria-free mice was 27% slower than that of their microbe-carrying counterparts.
The researchers discovered that these lean, bacteria-free rodents had more of an enzyme called fasting-induced adipocyte factor (FIAF), which is produced in the gut lining, liver, and fat cells. It lowers the amount of fat in these cells, but when Bacteroides is hard at work in the gut, FIAF is absent, and fat cells load up. When Bäckhed and Gordon bred mice lacking a functional FIAF gene, the mice were more than 50% flabbier than mice with the gene intact.
"This finding sheds light on the so-far-underestimated function of the gut microorganisms in constituting energy reserves," says Walter Wahli, a molecular biologist at the University of Lausanne, Switzerland. By unveiling the mechanisms by which the microbiota regulates fat storage, he says, the research helps identify pathways that are potential targets for antiobesity treatments.