Craving Sugar Linked to Gut Bacteria



Photo Credit: Creative Commons CCO public domain, photo by Andres Ayrton

Source: Photo Credit: Creative Commons CCO public domain, photo by Andres Ayrton

We tend to think of craving as a psychological phenomenon triggered by habits, desires, and emotional swings, but new research shows that a wide range of psychological conditions are generated by the community of bacteria thriving in our gut. These microbes release substances that act as hormones or neurotransmitters to affect mental function. A new study finds that craving sugar is driven in part by particular gut microbes that release a substance that acts much like the new drug Ozempic and similar drugs, that lower blood sugar levels in people with diabetes.

In a new study, researchers in China analyzed the blood of 60 patients with type 2 diabetes and compared them with people having normal blood sugar levels and found a tell-tale clue. A protein called FFAR4 was present in much lower levels in the samples from diabetics. Studies in diabetic mice revealed the same thing. This protein is known to activate a hormone, GLP-1, which is a powerful regulator of blood sugar and appetite. It is this hormone that the new diabetic drugs act upon to lower blood sugar and increase the sensation of “feeling full” after eating (satiety). This appetite-suppressing effect is why the drug acting on GLP-1 is also widely used to reduce body weight in people with obesity. The lower levels of FFAR4 in the blood of diabetics could mean that they would have less GLP-1 and, therefore, have higher blood sugar and increased appetite.

To test whether lower levels of FFAR4 caused increased cravings for sugar, the researchers monitored sugar consumption in mice in which the FFAR4 protein had been deleted by genetic manipulation. They found that these mice had a much higher preference for consuming sugar than mice with normal levels of FFAR4, when they were offered the choice between a normal diet, a high-fat diet, and a high-sugar diet.

This finding raises the question of why FFAR4 levels are lower in diabetics. The emerging understanding of the importance of gut microflora (the microbiome) on brain function inspired them to suspect that bacteria in the gut might differ in mice craving sugar.

When they analyzed the community of microflora in the intestines of mice lacking this protein, one species stood out as being much less abundant, called Bacteroides vulgatus. They found the same thing when they analyzed fecal samples of 45 patients with diabetes compared to a control group. This raised the possibility that something B. vulgatus might be releasing in the small intestine could elevate levels of FFAR4 and, via a similar pathway as the new GLP-1 drugs, decrease the craving for sugar. Experimental animals and people with lower FFAR4 would then have an increased craving for sugar.

To track down this suspected substance, the researchers analyzed the metabolites released by B. vultatus grown in culture and found eleven compounds that piqued their interest. In particular, the metabolite pantothenate was the most abundant metabolite released. It was already known that FFAR4 levels are regulated by pantothenate in the liver. Connecting the dots, lower B. vultatus levels in the gut could be releasing less pantothenate which would cause the deficiency in FFAR4 that is detected in the blood of mice and people craving sugar. Supporting this, experiments showed that giving mice additional pantothenate or supplementing them with more B. vultatus lowered the animals’ craving for sugar. But to quell the craving for sugar, these molecules set into play in the small intestine and the liver by B. vultatus would somehow have to reach the brain to modify the craving.

Further research showed that the FFAR4-pantothenate-GLP-1 chain of events causes an increase in another factor that is released from the liver (FGF21). This hormone acts on the part of the brain controlling appetite and sugar craving, the hypothalamus. To sum up, the bacterium B. vultatus in the gut sets into play a chain reaction of signaling molecules that leave the gut to act on neurons in the brain that suppress sugar craving.

So you can’t entirely blame weak fortitude for the overindulgence of sugar. Psychology is not the only reason for an irresistible sweet tooth that puts people at risk for high blood sugar, obesity, and diabetes; biology, the community of bacteria in the gut, are also pressing on the hormone-activated buttons driving sugar craving in the brain.


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