Shi Liping, Li Zhuoyuan, Ma Xiaojun, Wang Junru, Wu Yueping, Zhu Yongbin, Wang Yanrong, Yang Yue, Luo Minxiu, Li Jiangping, Sun Xian, He Shulan
Department of Epidemiology and Health Statistics, School of Public Health, Ningxia Medical University, Yinchuan, China.
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Front Nutr. 2025 Jan 22;11:1503879. doi: 10.3389/fnut.2024.1503879. eCollection 2024.
High consumption of Ultra-processed foods (UPF) have been identified as a potential risk factor for Non-alcoholic fatty liver disease (NAFLD). Nevertheless, there is limited empirical evidence regarding the impact of UPF, which are typical combination of processed foods, on liver health through alterations in gut microbiota and metabolic processes. We aim to examine the potential impact of UPF on liver health and to explore the role of gut microbiota and metabolites.
This study used Sprague-Dawley rats to mimic modern UPF diets for 90 days. Some serum biochemical indices, inflammatory factors, oxidative stress markers, hematoxylin-eosin (HE) staining of the liver, 16S ribosomal RNA (rRNA) and Liquid chromatography-mass spectrometry (LC-MS) of rat feces were detected.
The UPF diet-induced simple steatosis of the liver in rats without affecting the levels of IL-6, GSH, MDA, and SOD. Additionally, it modified the gut microbiota, increasing potentially harmful bacteria, such as and , while also elevating the relative abundance of potentially beneficial bacteria, including and . Furthermore, the consumption of UPF led to a metabolomic disorder characterized by disruptions in the sphingolipid signaling pathway, sulfur relay system, and arachidonic acid metabolism.
In conclusion, the findings of this study indicate that the consumption of UPF influences the development of simple hepatic steatosis, potentially through alterations in gut microbiota and metabolomics.
超加工食品(UPF)的高摄入量已被确定为非酒精性脂肪性肝病(NAFLD)的潜在危险因素。然而,关于作为加工食品典型组合的UPF通过改变肠道微生物群和代谢过程对肝脏健康的影响,实证证据有限。我们旨在研究UPF对肝脏健康的潜在影响,并探讨肠道微生物群和代谢物的作用。
本研究使用Sprague-Dawley大鼠模拟现代UPF饮食90天。检测了一些血清生化指标、炎症因子、氧化应激标志物、肝脏苏木精-伊红(HE)染色、大鼠粪便的16S核糖体RNA(rRNA)和液相色谱-质谱(LC-MS)。
UPF饮食诱导大鼠肝脏单纯性脂肪变性,而不影响白细胞介素-6、谷胱甘肽、丙二醛和超氧化物歧化酶水平。此外,它改变了肠道微生物群,增加了潜在有害细菌,如[具体细菌名称1]和[具体细菌名称2],同时也提高了潜在有益细菌的相对丰度,包括[具体细菌名称3]和[具体细菌名称4]。此外,食用UPF导致代谢组学紊乱,其特征是鞘脂信号通路、硫传递系统和花生四烯酸代谢受到破坏。
总之,本研究结果表明,食用UPF可能通过改变肠道微生物群和代谢组学影响单纯性肝脂肪变性的发展。