Abstract：
Acesulfame potassium (ACK) was generally regarded as innocuous and extensively ingested. Nevertheless, ACK has recently gained attention as a burgeoning pollutant that has the potential to induce a range of health hazards, particularly to the digestive system. Herein, we uncover that ACK initiates inflammatory bowel disease (IBD) in mice and zebrafish, as indicated by the aggregation of macrophages in the intestine and the inhibition of intestinal mucus secretion. Transcriptome analysis of mice and zebrafish guts revealed that exposure to ACK typically impacts the cell cycle, focal adhesion, and PI3K-Akt signaling pathways. Using pharmacological approaches, we demonstrate that the PI3K-Akt signaling pathway and the generation of reactive oxygen species (ROS) triggered by cell division are not significant factors in the initiation of IBD caused by ACK. Remarkably, inhibition of the focal adhesion pathway is responsible for the IBD onset induced by ACK. Our results indicate the detrimental impacts and possible underlying mechanisms of ACK on the gastrointestinal system and provide insights for making informed choices about everyday dietary habits.
摘要：
乙酰磺胺酸钾（ACK）通常被认为是无害且广泛摄入的。然而，作为一种新兴的污染物，它有可能引起一系列健康危害，尤其是消化系统。在这里，我们发现ACK在小鼠和斑马鱼中引发炎症性肠病（IBD），如肠中巨噬细胞的聚集和肠粘液分泌的抑制所示。对小鼠和斑马鱼肠道的转录组分析显示，暴露于ACK通常会影响细胞周期，病灶粘连,和PI3K-Akt信号通路。使用药理学方法，我们证明，PI3K-Akt信号通路和细胞分裂触发的活性氧（ROS）的产生不是由ACK引起的IBD启动的重要因素。值得注意的是,局灶性粘附途径的抑制是由ACK诱导的IBD发作的原因。我们的结果表明了ACK对胃肠系统的有害影响和可能的潜在机制，并为做出有关日常饮食习惯的明智选择提供了见解。
