Could you ever imagine that the bacteria in your gut are in control of your hunger and therefore how much and when you eat, and ultimately your weight? Well, the science tells us that is indeed what is happening! Here’s the story:
The gut microbiota and its metabolites play a crucial role in the control of satiety signals and eating behaviors. Eating 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. Since gut microbes depend on us for a place to live, it is to their advantage for populations to remain stable so therefore they communicate to the host to ingest nutrients again, or to stop eating.
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 feeding. The 20-minute mark seemed to coincide with the amount of time it takes for a person to begin feeling full after a meal. “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.
So some people have microbiomes that make them more hungry, and therefore obese, and others have a “skinny” microbiome. In studies, fecal transplantation from obese mice who were too hungry and ate too much (“hyperphagic”) to germ-free mice was able to induce hyperphagic behavior and weight gain in the recipients. Mice who were able to have portion control before the fecal transplant started overeating after getting a new “hungry” microbiome!
Even more interesting are the changes that happen to your gut microbiome after bariatric surgery. Fecal transplantation from mice after bariatric surgery to fat mice was able to transmit the weight loss effects of bariatric surgery to a germ-free non-operated mouse, inducing weight loss and reduced food intake. It’s all about transferring that “skinny” microbiome.
So how do you get that “skinny” microbiome? One tip is fiber!
Short chain fatty acids, or SCFA are produced through fermentation of carbohydrates that escape digestion and absorption in the small intestine (AKA- FIBER! Especially resistant starch). The main SCFAs are acetate, propionate, and butyrate. Studies have demonstrated that fermentable fiber is associated with improved appetite regulation. Supplementation of fiber intake in the range 16 – 35 g/d is necessary to induce these effects. It is likely that high fiber intake elicits appetite-regulating effects via SCFAs and FFAR 2/3 signaling pathways. Evidence of the role of SCFA in appetite regulation was shown in a study using propionate which demonstrated that propionate appears to induce short-term appetite regulation though PYY and GLP-1 mediated mechanisms
It all comes back to your gut and microbiome in the end- they are in charge! Feed your gut!
Sources:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6047317/
Cell Press. “Gut microbes signal to the brain when they’re full.” ScienceDaily. ScienceDaily, 24 November 2015.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939913/[/vc_column_text][/vc_column][/vc_row]