New Insights Uncover the Intrinsic Mechanism behind Sugar Cravings
Researchers identified an intestinal bacterium that can reduce dietary sugar intake. This discovery, published in Nature Microbiology, opens new avenues for the therapies of obesity and metabolic diseases.
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, raising 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.Recently, a research team led by Prof. LIANG Xinmiao from the Dalian Institute of Chemical Physics (DICP) of the Chinese Academy of Sciences (CAS), in collaboration with Prof. ZHU Shenglong and Prof. CHEN Yongquan from Jiangnan University, identified an intestinal bacterium that can reduce dietary sugar intake. This discovery, published in Nature Microbiology, opens new avenues for the therapies of obesity and metabolic diseases.FFAR4 deficiency or inactivation increases the host's sugar preference (Image by YE Xianlong and ZHANG Tingting)In this study, researchers identified low levels of free fatty acid receptor 4 (FFAR4) in the blood cells of both diabetic mice and humans, alongside an increased sugar preference in individuals with FFAR4 mutations. They also found that reduced gut FFAR4 levels significantlyaffected the abundance of the gut microbe Bacteroides vulgatus and its key metabolite, pantothenic acid. Furthermore, pantothenic acid produced by Bacteroides vulgatus activated the GLP-1-FGF21 hormone axis.The researchers validated this complex gut-liver-brain interaction by feeding pantothenic acid to diabetic mice or colonizing them with Bacteroides vulgatus, demonstrating its effects on sugar preference in mice.These findings reveal a novel regulatory mechanism underlying sugar preference. Intestinal fatty acid receptors play a crucial role in regulating sugar uptake behavior by modulating the levels of Bacteroides vulgatus and its metabolite pantothenic acid, which subsequently induces hormone secretion.This study provides a promising strategy for diabetes prevention. The development of tissue-specific FFAR4 agonists or targeting Bacteroides vulgatus present new approaches for preventing diabetes. Future clinical studies are essential to validate the application of the gut-hepatic-brain axis as a nutrient-sensing pathway for managing metabolic diseases.