We might hate to admit it, but we aren’t in complete control of our own bodies; bacteria can sometimes reign supreme, even in our hankering for a cookie or a glass of sweet tea. A recent study in Nature Microbiology identifies a connection between the abundance of a common bacterium in a person’s gut and the amount of sugar the person consumes. The results could help researchers develop novel treatments for a variety of metabolic conditions.
Yong Q. Chen, a cancer biologist at China’s Jiangnan University, and his team had been investigating the role of a protein called free fatty acid receptor four (FFAR4) in mice’s fat-metabolism process. Initially they put the rodents on a high-fat diet. “One day I suggested using a high-carbohydrate [high-sugar] diet for comparison, and the results were surprising,” Chen says. “We expected that a fatty acid receptor may regulate fat preference. Surprisingly, it modulates sugar craving instead.”
Chen’s team found that less FFAR4 in mice correlated with a greater preference for the high-sugar diet. The researchers also compared FFAR4 levels in both mice and humans with diabetes with those in counterparts without the condition, and the levels turned out to be significantly lower in the diabetes groups. That’s where the gut microbiome comes in; the scientists also found that in mice, lower FFAR4 levels were tied to a decreased abundance of a gut microbe called Bacteroides vulgatus.
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The researchers investigated how this bacterium might be involved and found that a metabolite produced by B. vulgatus, pantothenate—better known as vitamin B5—triggers production of the hormone GLP-1, which regulates appetite. In other words, less FFAR4 means less B. vulgatus, less pantothenate and less GLP-1.
This newly identified interplay of receptors, hormones and appetite reveals just one of the stealthy ways our gut microbes work to keep us healthy.
“I was happy to find that the study further supports the existence of intrinsic interactions between host and microbiome,” says Sergueï O. Fetissov, a physiologist at the University of Rouen Normandy in France, who was not involved in the research. He says the identification of pantothenate from B. vulgatus as a molecule that stimulates GLP-1 secretion and reduces sugar preference is “a major finding” because it could open up new treatments for type 2 diabetes.
Elisa Caffrey, a microbiology and immunology doctoral candidate at Stanford University, agrees, noting the potential of vitamin B5 supplementation or even a drug to increase the amount of FFAR4, although more research, including clinical trials, is needed first. (Caffrey was also not involved in the study.)
But there are still unanswered questions. B. vulgatus isn’t the only microbe that influences GLP-1 production; Fetissov’s team previously found that Escherichia coli also stimulates its release. Comparing B. vulgatus with other GLP-1-regulating factors needs further exploration, Chen says.
