Researchers have discovered a type of gut bacteria that may be associated with reduced sugar intake in the diet. These findings, based on the analysis of humans and mice, may help to develop treatments for obesity and metabolic diseases (such as type 2 diabetes).

Animals naturally crave sugar in biology, but uncontrolled sugar preference can lead to high sugar intake, resulting in increased risk of hyperglycemia and metabolic diseases. Previous studies have shown that our cravings for different foods stem from signals sent from the gut to the brain, which is a key organ for transmitting dietary preferences. However, regulating sugar cravings is a complex process, and the role of gut microbiota is not yet clear.

Experts analyzed the blood of 18 diabetes mice and 60 type 2 diabetes patients, and compared it with the healthy control group (including 24 human control groups). They found that the level of FFAR4, a protein that activates the secretion of GLP-1, a hormone regulating blood sugar and appetite, in the blood of diabetes mice and humans was reduced.

Researchers have observed that lower levels of FFAR4 in mice are associated with a higher preference for sugar. They also found that the decrease in FFAR4 levels reduced the abundance of gut microbiota such as Bacteroidetes and its metabolite pantothenic acid.

In a mouse model, experts found that pantothenic acid is responsible for the secretion of GLP-1 and subsequent secretion of FGF21, a liver hormone that directly acts on the hypothalamus, a brain region that controls eating behavior. They verified this complex gut liver brain connection by feeding diabetes mice pantothenic acid or colonizing them with B. vulgatus, and found that both methods could significantly reduce their sugar seeking behavior.

Experts point out that further clinical studies are needed to investigate this gut liver brain axis as a potential therapeutic target for managing metabolic diseases.

This article only introduces the progress of medical research,

Cannot be used as a reference for treatment plans.

Reference source:

DOI: 10.1038/s41564-024-01902-8