Saarinen Markku T, Forssten Sofia D, Evans Kara, Airaksinen Kaisa, Telving Rasmus, Hornshøj Bettina Høj, Jensen Henrik Max, Jokkala Jenna, Hanhineva Kati, Tiihonen Kirsti
IFF, Health & Biosciences, Sokeritehtaantie 20, 02460 Kantvik, Finland.
IFF, Health & Biosciences, 3329 Agriculture Drive, Madison, WI 53716, USA.
Nutrients. 2024 Dec 30;17(1):109. doi: 10.3390/nu17010109.
BACKGROUND/OBJECTIVES: Ergothioneine (EGT) is an effective antioxidant that animals cannot produce and has an important anti-inflammatory role in cell protection, which can help lower the risk of various diseases. In this study, we investigated the potential role of gut microbiota in the production of EGT, which was found to increase in the mouse liver after dietary supplementation with betaine (BET) or polydextrose (PDX).
The effects of BET and PDX on the gut microbiota and tissue EGT content were investigated using a diet-induced obese mouse model and simulated fermentation in the human colon. Male C57BL/6J mice were fed a high-fat diet (HFD) for 8 weeks to induce obesity and related metabolic disorders, and for the last 4 weeks of this study, the mice continued on the same diet, supplemented with BET, PDX, or their combination. The potential function of BET and PDX in microbial EGT production was further studied in an in vitro human colon model.
The quantity of spp. and Bacteroidota were significantly higher in the feces of mice on diets supplemented with PDX or BET + PDX, and Enterobacteriaceae levels were significantly higher in PDX-supplemented mice than in HFD-fed mice. Untargeted metabolomic analysis of the liver revealed a significant increase in EGT in mice fed HFDs with BET or BET + PDX. Microbial analysis from samples collected from the human in vitro model showed significant changes in , , , , and species, along with an increase in microbial metabolites, namely, acetic, propionic and butyric acids, and a decrease in 2-methylbutyric acid.
Although PDX and BET or their combination affected microbial composition and metabolites in the human colon simulation model, the model used was not able to detect a significant change in microbiota-based EGT production and, therefore, could not explain the increase in EGT in the liver of betaine-fed mice.
背景/目的：麦角硫因（EGT）是一种动物无法自行产生的有效抗氧化剂，在细胞保护中具有重要的抗炎作用，有助于降低患各种疾病的风险。在本研究中，我们调查了肠道微生物群在EGT产生中的潜在作用，发现在用甜菜碱（BET）或聚葡萄糖（PDX）进行饮食补充后，小鼠肝脏中的EGT含量会增加。
使用饮食诱导的肥胖小鼠模型和人结肠模拟发酵来研究BET和PDX对肠道微生物群和组织EGT含量的影响。雄性C57BL/6J小鼠喂食高脂饮食（HFD）8周以诱导肥胖和相关代谢紊乱，在本研究的最后4周，小鼠继续食用相同饮食，并补充BET、PDX或它们的组合。在体外人结肠模型中进一步研究了BET和PDX在微生物产生EGT中的潜在功能。
补充PDX或BET+PDX饮食的小鼠粪便中 菌属和拟杆菌门的数量显著更高，补充PDX的小鼠中肠杆菌科水平显著高于喂食HFD的小鼠。对肝脏的非靶向代谢组学分析显示，喂食含BET或BET+PDX的HFD的小鼠中EGT显著增加。从人体外模型收集的样本进行的微生物分析显示， 、 、 、 和 物种有显著变化，同时微生物代谢产物（即乙酸、丙酸和丁酸）增加，2-甲基丁酸减少。
尽管PDX和BET或它们的组合影响了人结肠模拟模型中的微生物组成和代谢产物，但所使用的模型无法检测到基于微生物群的EGT产生的显著变化，因此无法解释喂食甜菜碱的小鼠肝脏中EGT增加的原因。
