Bacteria in our stomachs might be deciding when we have eaten enough and switch off appetite, according to new research. Rather than stopping eating because we have decided to, scientists suggest eating starts a population growth of more than a billion microbes in the gut which, after 20 minutes, reaches critical mass and puts on the brakes, making us feel full.
They looked at the proteins produced by Escherichia coli bacteria, common in the human gut. They found that after 20 minutes of feeding and a resulting growth in bacteria numbers, the bacteria switch from pumping out one set of proteins to pumping out another, one of which releases a hormone that acts to decrease appetite.
The findings build on evidence that bacteria play a key role in the regulation of appetite and ultimately could lead to a better understanding of treatments for eating disorders, such as obesity.
The researchers injected tiny doses of those post-meal proteins into rats and mice. The animals' appetites decreased and further experiments revealed that the bacterial proteins stimulated the release of an intestinal hormone known as Peptide YY (PPY) that acts in the brain to reduce appetite and produce satiety. In addition, the researchers found that another of the bacterial proteins called ClpB also acts within the brain to regulate food intake.
It is thought that Escherichia coli might be hijacking the signals that make animals feel full, and that doing so may be a way for the bacteria to control their own numbers.
Researchers believe that it is not the host animal who dictates the number of bacteria in their own gut, it is the bacteria themselves which multiply to a certain number then stop: "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," noted the research team.