Moon Heewon, Kang Keunsoo, Kim Misook
Department of Food Science and Nutrition, Dankook University, Cheonan 31116, Republic of Korea.
Department of Microbiology, Dankook University, Cheonan 31116, Republic of Korea.
Foods. 2024 Oct 14;13(20):3267. doi: 10.3390/foods13203267.
This study investigated the impact of a transglycosylated product (ACOD) catalyzed by MKSR dextransucrase using sucrose as a glucosyl donor and both maltose and as acceptors on gut microbiota through fecal fermentation. ACOD promoted the growth of probiotics such as , , GG, and MKSR, while inhibiting the growth of pathogenic bacteria such as , O157:H7, , , , , , , and during independent cultivation. Fecal fermentation for 24 h revealed that ACOD significantly increased the production of short-chain fatty acids (SCFAs) compared to the blank and fructoooligosaccharide (FOS) groups. Specifically, ACOD led to a 4.5-fold increase in acetic acid production compared to FOSs and a 3.3-fold increase in propionic acid production. Both the ACOD and FOS groups exhibited higher levels of butyric acid than the blank. Notably, ACOD significantly modulated the composition of the gut microbiota by increasing the relative abundances of and decreasing and In contrast, FOSs remarkably promoted the growth of . These findings suggest that ACOD is a potential candidate for prebiotics that improve the intestinal environment by being actively used by beneficial bacteria.
本研究通过粪便发酵，调查了以蔗糖作为葡萄糖基供体、麦芽糖和[此处原文缺失物质名称]作为受体，由MKSR葡聚糖蔗糖酶催化产生的转糖基化产物（ACOD）对肠道微生物群的影响。在独立培养过程中，ACOD促进了诸如[此处原文缺失益生菌名称]、[此处原文缺失益生菌名称]、GG和MKSR等益生菌的生长，同时抑制了诸如[此处原文缺失病原菌名称]、O157:H7、[此处原文缺失病原菌名称]、[此处原文缺失病原菌名称]、[此处原文缺失病原菌名称]、[此处原文缺失病原菌名称]、[此处原文缺失病原菌名称]、[此处原文缺失病原菌名称]和[此处原文缺失病原菌名称]等病原菌的生长。24小时的粪便发酵显示，与空白组和低聚果糖（FOS）组相比，ACOD显著增加了短链脂肪酸（SCFA）的产生。具体而言，与FOS相比，ACOD使乙酸产量增加了4.5倍，丙酸产量增加了3.3倍。ACOD组和FOS组的丁酸水平均高于空白组。值得注意的是，ACOD通过增加[此处原文缺失菌属名称]的相对丰度和降低[此处原文缺失菌属名称]和[此处原文缺失菌属名称]的相对丰度，显著调节了肠道微生物群的组成。相比之下，FOS显著促进了[此处原文缺失菌属名称]的生长。这些发现表明，ACOD是一种潜在的益生元候选物，可通过被有益细菌积极利用来改善肠道环境。
