As we approach Thanksgiving in the US – when eating in moderation tends to go out the window – there is new evidence that gut bacteria may play a role in appetite control, according to a study published in Cell Metabolism.
When people eat, nutrients flow toward the bacteria in the gut. These bacteria divide and replace any members lost in the development of stool.
Current models of appetite control propose that hormones from the gut signal to brain circuits when a person is hungry or has eaten enough. It has been suggested that gut microbiota control food intake through energy-harvesting activities or production of neuroactive transmitters and metabolites.
In the present study, Sergueï Fetissov, of Rouen University in France, and colleagues explored the possibility that bacterial proteins act directly on appetite-controlling pathways locally in the gut or through the circulation.
The team hypothesized that since gut microbes depend on people for a place to live, and survival depends on the host environment remaining stable, there must be a way to communicate to the host when more nutrients are needed.
The researchers studied the growth dynamics of E. coli K12, a model organism of commensal strains of gut E. coli bacteria, when exposed to regular nutrient supply, modeling two daily meals.
Then, they compared proteins extracted from E. coli and analyzed them for their relevance to energy metabolism.
After 20 minutes of consuming nutrients and expanding numbers, it was found that E. coli bacteria from the gut produce different kinds of proteins than they do before feeding.
The 20-minute mark coincides with the time taken for a person to begin feeling full or tired after a meal.
Excited by this discovery, the researchers began to profile the bacterial proteins before and after feeding. They injected small doses of the bacterial proteins produced after feeding, which reduced food intake in both hungry and free-fed rats and mice.
“Full” bacterial proteins were found to stimulate the release of peptide YY – a hormone associated with feeling full – while “hungry” bacterial hormones did not. The opposite was true for glucagon-like peptide-1 (GLP-1), a hormone known to stimulate insulin release.
The investigators next tested for the presence of one of the “full” bacterial proteins, called ClpB.
Levels of CLpB in mice and rats 20 minutes after eating remained unchanged in the blood, but the levels did correlate with ClpB DNA production in the gut, suggesting a mechanism linking gut bacterial composition with the host control of appetite. The researchers also found that ClpB increased production of appetite-reducing neurons.
Evidently, bacterial proteins produced by satiated E. coli influence the release of gut-brain signals, as well as activating appetite-regulated neurons in the brain. It seems they can participate in the same molecular pathways that are used by the body to indicate satiety.
More research is needed into how an altered gut microbiome might be affected.
“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. In addition, we believe gut microbiota produce proteins that can be present in the blood longer term and modulate pathways in the brain.”
It seems that gut bacteria may help control when and how much we eat. So if, after your Thanksgiving meal, you feel you do not have room for dessert, it is probably the bacteria in your gut telling you that you have had enough.
Medical News Today reported last month that gut microbiota composition may be linked to anorexia nervosa.