Don't have room for dessert? The bacteria in your gut may
be telling you something. Twenty minutes after a meal, gut
microbes produce proteins that can suppress food intake in
animals, reports a study published in Cell Metabolism. The
researchers also show how these proteins injected into mice and
rats act on the brain reducing appetite, suggesting that gut
bacteria may help control when and how much we eat.
The new evidence coexists with current models of
appetite control, which involve hormones from the gut
signalling to brain circuits when we're hungry or done eating.
The bacterial proteins--produced by mutualistic E. coli after
they've been satiated--were found for the first time to influence
the release of gut-brain signals (e.g., GLP-1 and PYY) as well
as activate appetite-regulated neurons in the brain.
There are so many studies now that look at microbiota
composition in different pathological conditions but they do not
explore the mechanisms behind these associations," says senior
study author Sergueï Fetissov of Rouen University and
INSERM's Nutrition, Gut & Brain Laboratory in France. "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."
Mealtime brings an influx of nutrients to the bacteria in
your gut. In response, they divide and replace any members lost
in the development of stool. The study raises an interesting theory: since gut microbes depend on us for a place to live, it is
to their advantage for populations to remain stable. It would
make sense, then, if they had a way to communicate to the host
when they're not full, promoting host to ingest nutrients again.
In the laboratory, Fetissov and colleagues 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. Excited over this discovery, the
researcher began to profile the bacterial proteins pre- and postfeeding.
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 revealed 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 investigators next developed an assay that could detect
the presence of one of the "full" bacterial proteins, called ClpB in
animal blood. Although blood levels of the protein in mice and
rats detected 20 minutes after meal consumption did not change,
it correlated with ClpB DNA production in the gut, suggesting
that it may link gut bacterial composition with the host control of
appetite. The researchers also found that ClpB increased firing of
neurons that reduce appetite. The role of other E.coli proteins in
hunger and satiation, as well as how proteins from other species
of bacteria may contribute, is still unknown.
These are neurons (c-fos, green) in the rat central amygdala
activated by E. coli proteins in stationary phase and surrounded
by nerve terminals (calcitonin gene-related peptide, red)
originating from anorexigenic brainstem projections.
(Image Credit: J. Breton, N. Lucas & D. Schapman)
"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," Fetisov says. "In addition, we believe gut
microbiota produce proteins that can be present in the blood
longer term and modulate pathways in the brain.
Source: www.sciencedaily.com
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