The Key Laboratory of Geriatrics, Beijing Institute of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, PR China.
The Key Laboratory of Geriatrics, Beijing Institute of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, PR China.
Food Res Int. 2021 May;143:110240. doi: 10.1016/j.foodres.2021.110240. Epub 2021 Feb 25.
Caffeic acid (CA) is derived from many plants and may have the ability to reduce hepatic lipid accumulation. The gut microbiota produces lipopolysaccharides and further influences hepatic lipid metabolism, and thus plays an important role in the development of nonalcoholic fatty liver disease (NAFLD). However, whether the beneficial effects of CA are associated with the gut microbiota remains unclear. The present study aimed to investigate the benefits of experimental treatment with CA on the gut microbiota and metabolic functions in a mouse model of NAFLD. In this study, C57BL/6J mice received a high-fat diet (HFD) for 8 weeks and were then fed a HFD supplemented with or without CA for another 8 weeks. HFD induced obesity and increased accumulation of intrahepatic lipids, serum biochemical parameters and gene expression related to lipid metabolism. Microbiota composition was determined via 16S rRNA sequencing, and analysis revealed that HFD led to dysbiosis, accompanied by endotoxemia and low-grade inflammation. CA reverted the imbalance in the gut microbiota and related lipopolysaccharide-mediated inflammation, thus inhibiting deregulation of lipid metabolism-related gene expression. Our results support the possibility that CA can be used as a therapeutic approach for obesity-associated NAFLD via its anti-inflammatory and prebiotic integrative response.
咖啡酸（CA）来源于多种植物，可能具有减少肝脂质积累的能力。肠道微生物群产生脂多糖，并进一步影响肝脏脂质代谢，因此在非酒精性脂肪性肝病（NAFLD）的发展中起着重要作用。然而，CA 的有益作用是否与肠道微生物群有关尚不清楚。本研究旨在探讨实验性 CA 治疗对 NAFLD 小鼠模型肠道微生物群和代谢功能的益处。在这项研究中，C57BL/6J 小鼠接受高脂肪饮食（HFD）8 周，然后再用 HFD 补充或不补充 CA 喂养 8 周。HFD 诱导肥胖和肝内脂质堆积增加，血清生化参数和与脂质代谢相关的基因表达增加。通过 16S rRNA 测序确定微生物群落组成，分析表明 HFD 导致肠道微生物群落失调，伴有内毒素血症和低度炎症。CA 逆转了肠道微生物群的失衡和相关脂多糖介导的炎症，从而抑制脂质代谢相关基因表达的失调。我们的结果支持 CA 可以通过其抗炎和益生菌综合反应被用作肥胖相关 NAFLD 的治疗方法的可能性。
