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Regulatory Roles of Quercetin in Alleviating Fructose-Induced Hepatic Steatosis: Targeting Gut Microbiota and Inflammatory Metabolites

文献类型： 外文期刊

作者： Li, Jinjun 1 ; Zhao, Zhiqi 2 ; Deng, Yixuan 4 ; Li, Xinxin 2 ; Zhu, Liying 2 ; Wang, Xin 2 ; Li, Li 5 ; Li, Xiaoqiong 1 ;

作者机构： 1.Zhejiang Acad Agr Sci, State Key Lab Managing Biot & Chem Threats Qual &, Hangzhou, Peoples R China

2.Zhejiang Acad Agr Sci, Inst Food Sci, Hangzhou, Peoples R China

3.Minist Agr & Rural Affairs, Coconstruct Minist & Prov, Key Lab Postharvest Preservat & Proc Vegetables, Hangzhou, Peoples R China

4.Wenzhou Med Univ, Chashan Univ Town, Sch Med, Wenzhou, Zhejiang, Peoples R China

5.Hangzhou Normal Univ, Clin Med Coll, Hangzhou, Peoples R China

关键词： fructose; gut microbiota; hepatic steatosis; quercetin

期刊名称：FOOD SCIENCE & NUTRITION （ 影响因子：3.8； 五年影响因子：4.5 ）

ISSN： 2048-7177

年卷期： 2025 年 13 卷 1 期

页码：

收录情况： SCI

摘要： While fructose is a key dietary component, concerns have been raised about its potential risks to the liver. This study aimed to assess quercetin's protective effects against fructose-induced mouse hepatic steatosis. Thirty-two male C57BL/6J mice were randomly allocated into four groups: control, high fructose diet (HFrD), HFrD supplemented with low-dose quercetin (HFrD+LQ), and HFrD supplemented with high-dose quercetin (HFrD+HQ). Biochemical, pathological, immune, and metabolic parameters were assessed. Quercetin treatment significantly reduced liver fat percentages in mice on a high fructose diet, with the most notable reduction observed in the HFrD+HQ group. Histological examination confirmed this reduction, revealing diminished lipid droplets and decreased inflammation and steatosis in hepatocytes. Compared to the high fructose group, interleukin-1 beta and tumor necrosis factor alpha were significantly decreased, serum aspartate aminotransferase concentrations were markedly reduced, and blood high-density lipoprotein concentrations were substantially elevated after quercetin intervention (p < 0.05). Total bilirubin and triglyceride levels, which were significantly altered following high fructose intervention and reversed after quercetin intervention. Following the administration of 100 mg/kg quercetin, the Firmicutes/Bacteroidetes ratio was significantly reduced compared to the high fructose group. At the genus level, Erysipelotrichaceae_uncultured, Faecalibaculum, Odoribacter, and Allobaculum were significantly decreased (p < 0.05), Lacnospiraceae NK4A136 group, Parabacteroides, and Alloprevotella significantly increased (p < 0.05). However, the 50 mg/kg quercetin treatment only decreased the abundance of Erysipelotrichaceae_uncultured (p < 0.05). In addition, quercetin significantly enhanced the content of propionic acid and total acid (p < 0.05). Moreover, the intestinal flora showed a significant correlation with the hepatic health-related phenotype in mice. Both 50 and 100 mg/kg quercetin treatments significantly mitigated liver fat deposition in mice with fructose-induced hepatic steatosis. However, the higher dose of quercetin (100 mg/kg) demonstrated a more pronounced effect in reducing liver inflammation, likely due to its impact on gut microbiota regulation. This suggests quercetin's potential as a therapeutic agent for fructose-related hepatic steatosis, emphasizing the importance of dose considerations.

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