Feeling hungry is one of the most clearly compelling reasons to eat. You normally stop short of eating an entire chocolate cake because, at some point, you feel satisfied. The hormones you release are key to this feeling of satiety, and recent science has raised the possibility that gut microbes may exert some influence over our appetite, too.
Can gut microbes generate cravings? Can they make you feel unsatisfied until you eat the food they need for their own survival? These were the questions covered by a scientific review published in BioEssays in 2014. Authors argued that gut microbes rely on human a ‘host’ for their survival, so if a certain species of bacteria needs a certain nutrient to grow stronger, it might evolve ways to make you want to eat that nutrient. At this stage the authors could not answer these questions because they had little evidence one way or the other, but they summarized some ways that microbes could theoretically control eating behavior in their host: for example, by changing taste receptors or by influencing appetite-related hormones.
A new study added preliminary evidence for the idea that gut microbiota could affect appetite through hormones. The researchers began by culturing normally benign bacteria, E. coli K12, in a Petri dish and adding nutrients twice a day, every 12 hours. The numbers of E. coli started to grow exponentially when these nutrients were added – researchers called this the ‘exponential’ growth phase. After about twenty minutes the growth levelled off – the ‘stationary’ phase.
The E. coli are like little factories, churning out different kinds of proteins in the exponential and stationary phases. During the stationary growth phase the bacteria made particularly high numbers of a protein called caseinolytic protease B (ClpB), which mimics a hormone that signals when you’ve had enough food.
In another part of the experiment, a group of rats received only the proteins produced in the exponential and stationary phases. The proteins from the exponential growth phase stimulated one satiety hormone (glucagon-like peptide-1) in the rats’ blood, while the proteins from the stationary growth phase stimulated an even more potent satiety hormone (peptide YY) and decreased the rats’ food intake. This showed that the bacteria, through their protein messengers, were stimulating hormones that curbed appetite. Furthermore, the protein abundant in the stationary phase, ClpB, also increased the firing rate of particular neurons in rats’ brains that are associated with reduced appetite.
This evidence from rodents hints that proteins made by the gut bacteria might be able to message you that your meal is over. But it’s not to say that, faced with a bag of potato chips, you’re completely at the mercy of your microbes. Much more evidence is needed to determine how these bacterial signals work in humans, and how they fit into everything we already know about appetite control.
Alcock J, Maley CC, Aktipis CA. Is eating behavior manipulated by thegastrointestinal microbiota? Evolutionary pressures and potential mechanisms. Bioessays. 2014; 36: 940-949. doi: 10.1002/bies.201400071
Breton J, Tennoune N, Lucas N, et al. Gut Commensal E. coli Proteins Activate Host Satiety Pathways following Nutrient-Induced Bacterial Growth. Cell Metabolism. 2016; 23(2): 324–334. doi: http://dx.doi.org/10.1016/j.cmet.2015.10.017
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