For the first time, researchers have shown in an experimental model that commensal bacteria may affect hunger and satiety through their influence on gut-brain signals and activation of appetite-regulated brain neurons.
The recent study involved monitoring the growth dynamics of commensal strains of the bacteria Escherichia coli, when exposed to the equivalent of two daily meals. Researchers then analysed proteins, and their resulting actions, introduced to and extracted from this bacteria during their exponential (Exp) and stationary (Stat) growth phases.
The researchers found that during the feeding time there was corresponding bacterial growth (Exp phase). But after twenty minutes of feeding, once the commensal E. coli were satisfied nutritionally, the growth stopped even when extra nutrients were provided. These results seemed to coincide with the time it takes for a person to begin feeling full or tired after a meal.
When proteins to stop bacterial growth (E. coli Stat proteins), equivalent to a satiated bacteria, were introduced there was an increased release of the satiety hormone peptide YY. The opposite effect was seen with the hormone that stimulates insulin release, (glucagon-like peptide 1 or GLP-1). It was stimulated during the feeding phase (Exp growth phase) only.
One of the bacterial proteins in the gut that is associated with being "full" is called ClpB (caseinolytic peptidase B protein). The researchers developed an assay to test the levels of this protein in animal blood. ClpB plasma levels did not alter twenty minutes after meal consumption but were correlated with ClpB DNA in gut microbiota and were found at higher levels once the bacteria were satisfied nutritionally, during the Stat growth phase.
They also found that ClpB, and other E. coli proteins, activated and increased the firing rate of anorexigenic neurons that reduce appetite.
Many studies have reviewed the effect of bacterial diversity on nutrient-induced bacterial growth and microbiota composition in obesity and other pathological conditions. However, no studies have looked at the mechanism underlying their effects on appetite.
"Our study reveals that bacterial proteins may physiologically link gut E. coli to host control of appetite involving both short-term effects on satiation, associated with nutrient-induced bacterial growth, acting locally in the gut, as well as long-term regulation of feeding pattern associated with plasmatic changes of bacterial proteins that may activate central anorexigenic circuitries."
These results suggest microbiota balance, with changes in high or low E. coli and possibly other bacteria, may physiologically influence meal patterns through the release of satiety hormones. Also, proteins released by these bacteria may modulate brain appetite pathways.
1. Breton J, Tennoune N, Lucas N, et al. Gut commensal E. coli proteins activate host satiety pathways following nutrient-induced bacterial growth. Cell Metab 2016;23:1-11. [Abstract]