Think it’s your inability to resist cheesecake that’s making it tough to fit into your skinny jeans? Well, your bacteria may share some of the blame. Because a new study in mice shows that the response of intestinal microbes to a high-fat diet ends up triggering the release of a hormone that makes mammals feel hungry, causing them to eat even more. The finding is served up in the journal Nature. [Rachel J. Perry et al., Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome]
Previous work has shown that the types of bacteria in the gut in diabetic or obese individuals are different from the bacteria in healthy people. But does this bacterial makeup contribute to these disorders? Or is it just a side effect?
To unravel this mystery, researchers put mice on a high-fat diet. The animals experienced a buildup of a chemical called acetate, particularly in the large intestine.
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That location points to gut bacteria, which can produce acetate, as a possible culprit. So the researchers wiped out the microbes using antibiotics or a simple saline wash. And acetate levels plummeted.
Okay, so the gut bacteria in fat-fed mice make acetate. What does acetate do? Well, it gets the involuntary part of the nervous system, the parasympathetic nervous system, to put out the call to produce more insulin. Unfortunately, in this case, acetate also gets the parasympathetic nervous system to stimulate production of a hunger hormone called ghrelin. And the more fats an animal consumes, the more acetate it makes—which means the more ghrelin it produces and, of course, the more it eats. And bacteria make the whole sequence happen.
The researchers are now investigating whether the same biochemical events happen in humans. If they do, it’s possible that obtaining a better assortments of gut bacteria could help us control our weight. Of course, the best way to get those good bacteria is from a fecal transplant—in which bacteria-rich feces come out of one person and into you. The very thought of which could help curb your appetite.
—Karen Hopkin
[The above text is a transcript of this podcast.]
[Scientific American is part of Springer Nature.]
