Gut bacteria reduce sugar absorption in diabetic mice and humans

Gut bacteria reduce sugar absorption in diabetic mice and humans

Excessive sugar consumption is linked to several non-communicable diseases, including obesity, cardiovascular disease, metabolic syndrome and type 2 diabetes. Animals naturally crave sugar, and uncontrolled sugar preferences can lead to high sugar intake, increasing the risk of hyperglycemia and metabolic diseases.

Previous research suggests that food cravings in humans are driven by signals from the gut to the brain, highlighting the gut's crucial role in shaping dietary preferences. However, the regulation of sugar preference is complex and the specific influence of gut microbes remains unclear.

In a study published inNatural microbiologyA research team led by Prof. Liang

The researchers analyzed the blood of 18 mice with induced diabetes and 60 patients with type 2 diabetes. They identified low levels of free fatty acid receptor 4 (FFAR4) in the blood cells of both diabetic mice and humans, as well as increased sugar preference in individuals with FFAR4 mutations. They also found outbActeroidesVulgateand its important metabolite, pantothenic acid. Pantothenic acid activated the GLP-1-FGF21 hormonal axis.

These results revealed a novel mechanism of intestinal liver-brain interaction. The researchers validated this complex interaction in mouse models.bActeroidss vulgatusand pantothenic acid were administered to diabetic mice, showing their effects on sugar preference in mice.

The results revealed a novel regulatory mechanism underlying sugar preference and that intestinal fatty acid receptors play a critical role in regulating sugar intake behavior.

This study offers a promising strategy for the prevention of diabetes. The development of tissue-specific FFAR4 agonists or targetingbActeroidesVulgateOffers new approaches to preventing diabetes. Future clinical studies are important to validate the application of intestinal liver-brain interaction as a nutrient-sensing pathway for the treatment of metabolic diseases.

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