Gut microbes signal brain when you are full

Don't have room for dessert? Your gut bacteria may be to blame!
The bacteria in your gut may help you control when and how much to eat by producing proteins 20 minutes after a meal that suppress food intake, according to a new study.
Researchers from the University of Rouen in France conducted the study on mice and rats to show how the proteins injected into the animals act on the brain reducing appetite.
The new evidence coexists with current models of appetite control, which involve hormones from the gut signalling to brain circuits when we are hungry or done eating.

The bacterial proteins - produced by mutualistic E coli after they have been satiated-were found for the first time to influence the release of gut - brain signals as well as activate appetite-regulated neurons in the brain.
"Our study shows that bacterial proteins from E coli can be involved in the same molecular pathways that are used by the body to signal satiety, and now we need to know how an altered gut microbiome can affect this physiology," said senior study author Serguei Fetissov, from Rouen University.

Mealtime brings an influx of nutrients to the bacteria in the gut and in response, they divide and replace any members lost in the development of stool.

The researchers found that after 20 minutes of consuming nutrients and expanding numbers, E coli bacteria from the gut produce different kinds of proteins than they did before their feeding.
The 20 minute mark seemed to coincide with the amount of time it takes for a person to begin feeling full or tired after a meal.
They saw that injection of small doses of the bacterial proteins produced after feeding reduced food intake in both hungry and free-fed rats and mice.
Further analysis showed that "full" bacterial proteins stimulated the release of peptide YY, a hormone associated with satiety, while "hungry" bacterial hormones did not.

The opposite was true for glucagon-like peptide-1 (GLP-1), a hormone known to simulate insulin release.
The researchers also found that ClpB, one of the "full" bacterial proteins, increased firing of neurons that reduce appetite.
"We now think bacteria physiologically participate in appetite regulation immediately after nutrient provision by multiplying and stimulating the release of satiety hormones from the gut," Fetissov said.
"In addition, we believe gut microbiota produce proteins that can be present in the blood longer term and modulate pathways in the brain," Fetissov added.
The findings were published in the journal Cell Metabolism.