After a hearty meal, that little voice returns: a square of chocolate, a dessert, something very sweet. What if it was not only a question of will, but also the effect of a intestinal bacteria very specific hidden in your stomach?
A study published in the journal Nature Microbiology
suggests in fact that certain components of the
intestinal microbiota directly influence our food preferences. In the background, we find overconsumption of sugar, obesity and
type 2 diabetesfor which drugs like Ozempic mimic the hormone GLP-1
to regulate appetite and blood sugar. It remains to be understood how a bacteria can tip the scales towards sweetness.
A bacteria, a receptor and a changing sugar craving
A researcher at Jiangnan University, Yong Q. Chen was studying the FFAR4 receptor, also called GPR120, which detects certain fatty acids in the intestine. In both diabetic mice and humans, the quantity of this receptor decreases and the preference for sugar increases.
The researchers then linked the decrease in FFAR4 to a lesser presence of the bacteria. Bacteroides vulgatus in the intestine. This species produces pantothenate, or vitamin B5, which stimulates the secretion of
GLP-1a key appetite hormone. Less FFAR4 therefore means less Bacteroides vulgatusless vitamin B5, less GLP-1, and ultimately an increased attraction to sweet foods.
From vitamin B5 to GLP-1: when the gut speaks to the brain
GLP-1 participates in blood sugar control and the feeling of satiety. Certain treatments for type 2 diabetes (including the famous Ozempic) act precisely like this hormone, slowing down digestion and suppressing hunger. In animal models, the increase in Bacteroides vulgatus or pantothenate intake boosts GLP-1 production and improves blood sugar control, while reducing sugar cravings.
© Nature Microbiology
Excessive carbohydrate consumption is an important factor in the increased incidence of diabetes. This dietary preference involves complex signaling mechanisms between the gut and the brain, in which the gut microbiota could play a crucial regulatory role. The role of vitamin B5 produced by Bacteroides vulgatus in the secretion of GLP-1 and the preference for sugar represents an advance which could, ultimately, lead to new approaches against type 2 diabetes.
What concrete solutions for diabetes and sugar cravings?
This discovery reveals a new regulatory network of the gut-liver-brain axis, offering a potential therapeutic target for the treatment of metabolic diseases. The idea of a targeted probiotic, vitamin B5 supplements or drugs capable of increasing FFAR4 is therefore beginning to circulate. In France, where 92% of diabetics have type 2 diabetes, these avenues inevitably attract attention.
The authors, however, remain cautious. The main results come from mouse models, and other microorganisms, such as Escherichia coli, also influence the production of GLP-1. “Comparing B. vulgatus with other factors regulating the amount of GLP-1 will therefore require further research.“, concludes Yong Q. Chen.
This study reinforces the idea that type 2 diabetes does not only occur in the pancreas or the plate, but also at the heart of our microbiota. If the hope of targeted probiotics or new strategies inspired by GLP-1 is emerging, researchers call for caution: the dialogue between intestine and brain remains complex, and only the multiplication of clinical trials will tell if these discoveries can really transform the management of sugar cravings and diabetes.