Obesity has been known to be related to changes within our gut microbiome for some time. However, until now, the exact mechanism or cause as to this link was unknown.
A new study by Yale researchers has now identified the mechanism with which this occurs.
Earlier, researchers found that short-chain fatty acids (SCFAs) caused the release of insulin in mice. The team compared acetate to various SCFAs and found that those animals who consumed a diet high in fat were more likely to have high acetate levels.
In follow-up research, it was found that when acetate is injected directly into a part of the brain responsible for the parasympathetic nervous system, it triggers a release of high amounts of insulin. Supposedly, acetate stimulates the cells that produce insulin.
Next, the researchers examined whether acetate release by bacteria within the gut-microbiome could be responsible for increased insulin production. They found a strong correlation between certain gut microbioata, concentration of acetate and insulin release.
The researchers concluded that their study demonstrated a causal relationship between the gut microbioate in response to alteration of the diet. Increased acetate concentration was found to in turn lead to greater satiety (hunger) and food intake. This results in a feedback loop, where more acetate is now consumed, triggering further hunger, and thus the stage is set for obesity to present itself.
And thus, the link between acetate intake, increased satiety, the gut microbiome and obesity is now set out in a clear pathway thanks to the Yale researchers.
Study Source: Nature