Lu Jiaxin, Huang Yanting, Zhang Yujing, Xie Jiayu, Guo Qingjun, Yang Huifan, Yang Yunyan, Chen Jing, Su Lijie
Department of Nutrition and Food Hygiene, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
Sino-French Hoffmann Institute, School of Basic Medical Science, Guangzhou Medical University, Guangzhou, Guangdong, China.
Front Nutr. 2025 Apr 16;12:1574792. doi: 10.3389/fnut.2025.1574792. eCollection 2025.
Obesity is a chronic metabolic disease, mainly caused by excessive/abnormal fat accumulation, as well as accompanied by endotoxemia and chronic inflammation. Quercetin, a natural flavonoid, may alleviate obesity by regulating gut microbiota and metabolites, but its exact mechanism for improving obesity is unknown.
The aim of this study was to investigate the effects of quercetin on high-fat diet (HFD)-induced obesity in mice. In particular, we focused on the regulatory effects of quercetin on gut microbiota and the tryptophan metabolite indole-3-propionic acid (IPA).
The C57BL/6J mice were subjected to a 20-week HFD feeding regimen with concurrent daily oral administration of quercetin or IPA. The body weight, fat accumulation, gut barrier function, and chronic inflammation were determined. Gut microbiota composition was analyzed by 16S rRNA sequencing and IPA levels were measured in serum and feces. experiments, Caco-2 cells were used to evaluate the effects of IPA and fecal dilutions from quercetin-treated mice on tight junction protein expression and aryl hydrocarbon receptor (AhR) activation.
Our results revealed that quercetin supplementation significantly mitigated obesity and chronic inflammation, and improved the disrupted gut barrier function through the actvation of AhR/interleukin 22 (IL-22) pathway. 16S rRNA sequencing revealed that quercetin treatment increased the abundance of . Quercetin intervention increased the levels of IPA in the serum and feces of mice. IPA supplementation alleviated obesity and chronic inflammation, and enhanced intestinal barrier function through AhR activation. The findings were further corroborated by Caco-2 cell experiment, which indicated that the modulation of the dysregulated gut microbiota to change microbial metabolite IPA coordinated the improvement effect of quercetin on gut barrier disruption.
Quercetin supplementation alleviates obesity by restoring high-fat diet induced gut microbiota disorder, which elevates IPA level to activate AhR/IL-22 pathway, thereby enhancing intestinal barrier integrity and suppressing chronic inflammation.
肥胖是一种慢性代谢性疾病，主要由脂肪过度/异常堆积引起，同时伴有内毒素血症和慢性炎症。槲皮素是一种天然黄酮类化合物，可能通过调节肠道微生物群和代谢产物来减轻肥胖，但其改善肥胖的确切机制尚不清楚。
本研究旨在探讨槲皮素对高脂饮食（HFD）诱导的小鼠肥胖的影响。特别地，我们重点研究了槲皮素对肠道微生物群和色氨酸代谢产物吲哚-3-丙酸（IPA）的调节作用。
将C57BL/6J小鼠进行为期20周的高脂饮食喂养方案，同时每日口服给予槲皮素或IPA。测定体重、脂肪堆积、肠道屏障功能和慢性炎症。通过16S rRNA测序分析肠道微生物群组成，并测定血清和粪便中的IPA水平。在实验中，使用Caco-2细胞评估IPA和槲皮素处理小鼠的粪便稀释液对紧密连接蛋白表达和芳烃受体（AhR）激活的影响。
我们的结果显示，补充槲皮素可显著减轻肥胖和慢性炎症，并通过激活AhR/白细胞介素22（IL-22）途径改善受损的肠道屏障功能。16S rRNA测序显示，槲皮素处理增加了……的丰度。槲皮素干预增加了小鼠血清和粪便中IPA的水平。补充IPA可减轻肥胖和慢性炎症，并通过激活AhR增强肠道屏障功能。Caco-2细胞实验进一步证实了这一发现，表明调节失调的肠道微生物群以改变微生物代谢产物IPA可协同槲皮素对肠道屏障破坏的改善作用。
补充槲皮素可通过恢复高脂饮食诱导的肠道微生物群紊乱来减轻肥胖，这会提高IPA水平以激活AhR/IL-22途径，从而增强肠道屏障完整性并抑制慢性炎症。
