Hear that little voice in your head telling you to skip a second slice of pumpkin pie? It might be coming not from your conscience, but from the masses of bacteria in your stomach.
Experiments in mice and rats suggest that certain microbes living in your body as part of the gut microbiome have ways of letting the brain know when they’ve received enough nutrients to reach their goal—creating a billion more of their kind. Those signals seem to turn hunger on and off in their hosts.
The findings build on a bounty of evidence that microbes play a key role in the physiology of appetite—and perhaps could help people with eating disorders.
“We have long known that after eating we get a feeling of fullness. Most have assumed that it is because our stomach or intestines are stretched,” says Martin Blaser, director of NYU’s Human Microbiome Program and author of Missing Microbes. “We never thought that the bacteria we were carrying could be part of that signal, but this new work provides evidence that that is what is occurring.”
In recent years scientists have been exploring the many ways the microbiome may affect its animal host’s feelings and behaviors. To test its influence over appetite, Serguei Fetissov and his team looked at proteins produced by the common intestinal bacteria Escherichia coli.
The team noticed that about 20 minutes after feeding and multiplying their numbers, E. coli switch from pumping out one set of proteins to another. So Fetissov, of Rouen University, and his team injected tiny doses of those post-meal proteins into rats and mice.
They found that the injected rodents reduced their food intake whether they’d previously been freely fed or kept hungry. Further analysis showed that one protein stimulated the release of a hormone associated with satiety. Another of the chemicals found in the animals’ bloodstream appears to increase the firing of brain neurons that diminish appetite, the team reports this week in Cell Metabolism.
Many studies suggest that our gut produces hormones that tell our brain to either grab some more grub or stop eating. Fetissov thinks that E. coli may be hijacking this molecular pathway to produce the signals that make animals feel full, and that doing so may be a way for the bacteria to self-regulate their populations.
“It looks like it’s not the host animal that regulates that number, but that once bacteria multiply to a certain number, they will stop growing,” Fetissov says. “We provide the nutrients to these bacteria, and they will produce, more or less, a billion more bacteria and then they will stop growing. Why they stop after producing about one billion, I have no idea. But in only 20 minutes they produce this new one billion bacteria and then they start producing new proteins that have some inhibiting effect on appetite.”
This isn’t the only line of research suggesting that bacteria can play a role in jump-starting or curbing their hosts’ appetites. Previous work by Blaser, for instance, provided evidence of a stomach bacterium, Helicobacter pylori, playing such a role.
And earlier this year, Sean Davies of Vanderbilt University engineered bacteria to produce a lipid that signaled feelings of fullness to mice. When mice drank water filled with those bacteria, they ate less and had lower body fat no matter the diet offered them, Davies explained at the American Chemical Society national meeting in March.
Last year a different group of researchers also explored the evolutionary reasons microbes might manipulate the way their hosts eat and the ways they might take action. Aside from producing satiety hormones, potential mechanisms include influencing reward pathways in the brain, producing mood-altering toxins and hijacking taste receptors.
Fetissov says his findings suggest some interesting avenues for future research that might help scientists better understand why we eat the way we do, including any potential chemical triggers behind some eating disorders.
“This is something that I think could possibly be important to help understand the problem of binge eating,” he says. “If people are constantly snacking so that there is no long interval between meals, it may be that the body doesn’t receive a good satiety signal. So that could help to explain why some people would eat continually.”
The results also speak to the fascinating possibility that the trillions of microbes we house inside our gut could be influencing our bodies and minds in many more unforeseen ways.
“Here we see a bacterial protein that appears to inhibit appetite by stimulation of neurons in the brain,” Fetissov notes. “But you can imagine that other bacteria can produce other proteins that can influence not only other appetite pathways but entirely different pathways. We may find out that human behavior is in some part very much influenced by gut bacteria.”
source: smithsonian.com By Brian Handwerk