School of Environmental and Municipal Engineering, Qingdao University of Technology, Qingdao 266520, China.
School of Environmental and Municipal Engineering, Qingdao University of Technology, Qingdao 266520, China.
Sci Total Environ. 2024 Aug 15;938:173417. doi: 10.1016/j.scitotenv.2024.173417. Epub 2024 May 24.
Florfenicol, a widely used veterinary antibiotic, has now been frequently detected in various water environments and human urines, with high concentrations. Accordingly, the ecological risks and health hazards of florfenicol are attracting increasing attention. In recent years, antibiotic exposure has been implicated in the disruption of animal glucose metabolism. However, the specific effects of florfenicol on the glucose metabolism system and the underlying mechanisms are largely unknown. Herein, zebrafish as an animal model were exposed to environmentally relevant concentrations of florfenicol for 28 days. Using biochemical and molecular analyses, we found that exposure to florfenicol disturbed glucose homeostasis, as evidenced by the abnormal levels of blood glucose and hepatic/muscular glycogen, and the altered expression of genes involved in glycogenolysis, gluconeogenesis, glycogenesis, and glycolysis. Considering the efficient antibacterial activity of florfenicol and the crucial role of intestinal flora in host glucose metabolism, we then analyzed changes in the gut microbiome and its key metabolite short-chain fatty acids (SCFAs). Results indicated that exposure to florfenicol caused gut microbiota dysbiosis, inhibited the production of intestinal SCFAs, and ultimately affected the downstream signaling pathways of SCFA involved in glucose metabolism. Moreover, non-targeted metabolomics revealed that arachidonic acid and linoleic acid metabolic pathways may be associated with insulin sensitivity changes in florfenicol-exposed livers. Overall, this study highlighted a crucial aspect of the environmental risks of florfenicol to both non-target organisms and humans, and presented novel insights into the mechanistic elucidation of metabolic toxicity of antibiotics.
氟苯尼考是一种广泛应用于兽医的抗生素,现已在各种水环境和人类尿液中频繁检出,且浓度较高。因此,氟苯尼考的生态风险和健康危害正引起越来越多的关注。近年来,抗生素暴露被认为会扰乱动物的葡萄糖代谢。然而,氟苯尼考对葡萄糖代谢系统的具体影响及其潜在机制在很大程度上尚不清楚。在此,我们以斑马鱼为动物模型,用环境相关浓度的氟苯尼考暴露 28 天。通过生化和分子分析,我们发现氟苯尼考暴露扰乱了葡萄糖稳态,表现为血糖和肝/肌肉糖原水平异常,以及参与糖异生、糖生成和糖酵解的基因表达改变。鉴于氟苯尼考具有高效的抗菌活性,以及肠道菌群在宿主葡萄糖代谢中的关键作用,我们随后分析了肠道微生物组及其关键代谢物短链脂肪酸 (SCFAs) 的变化。结果表明,氟苯尼考暴露导致肠道微生物群失调,抑制了肠道 SCFAs 的产生,最终影响了涉及葡萄糖代谢的 SCFA 下游信号通路。此外,非靶向代谢组学表明,花生四烯酸和亚油酸代谢途径可能与氟苯尼考暴露肝脏中胰岛素敏感性的变化有关。总的来说,本研究强调了氟苯尼考对非靶标生物和人类的环境风险的重要方面,并为阐明抗生素代谢毒性的机制提供了新的见解。