Abstract：
T-2 toxin is one of trichothecene mycotoxins, which can impair appetite and decrease food intake. However, the specific mechanisms for T-2 toxin-induced anorexia are not fully clarified. Multiple research results had shown that gut microbiota have a significant effect on appetite regulation. Hence, this study purposed to explore the potential interactions of the gut microbiota and appetite regulate factors in anorexia induced by T-2 toxin. The study divided the mice into control group (CG, 0 mg/kg BW T-2 toxin) and T-2 toxin-treated group (TG, 1 mg/kg BW T-2 toxin), which oral gavage for 4 weeks, to construct a subacute T-2 toxin poisoning mouse model. This data proved that T-2 toxin was able to induce an anorexia in mice by increased the contents of gastrointestinal hormones (CCK, GIP, GLP-1 and PYY), neurotransmitters (5-HT and SP), as well as pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) in serum of mice. T-2 toxin disturbed the composition of gut microbiota, especially, Faecalibaculum and Allobaculum, which was positively correlated with CCK, GLP-1, 5-HT, IL-1β, IL-6 and TNF-α, which played a certain role in regulating host appetite. In conclusion, gut microbiota changes (especially an increase in the abundance of Faecalibaculum and Allobaculum) promote the upregulation of gastrointestinal hormones, neurotransmitters, and pro-inflammatory cytokines, which may be a potential mechanism of T-2 toxin-induced anorexia.
摘要：
T-2毒素是一种单端孢菌毒素,这会损害食欲并减少食物摄入量。然而,T-2毒素诱导厌食症的具体机制尚未完全阐明.多项研究结果表明，肠道菌群对食欲调节有显著影响。因此，本研究旨在探讨肠道菌群与食欲调节因子在T-2毒素致厌食症中的潜在相互作用。研究将小鼠分为对照组(CG，0mg/kgBWT-2毒素）和T-2毒素治疗组（TG，1mg/kgBWT-2毒素），其中口服灌胃4周，构建亚急性T-2毒素中毒小鼠模型。该数据证明，T-2毒素能够通过增加胃肠激素的含量来诱导小鼠厌食症（CCK，GIP,GLP-1和PYY），神经递质（5-HT和SP），以及促炎细胞因子(IL-1β，小鼠血清中的IL-6和TNF-α）。T-2毒素扰乱了肠道微生物群的组成，尤其是,FaecalibaculumandAllobaculum,与CCK呈正相关，GLP-1,5-HT,IL-1β,IL-6和TNF-α,对调节宿主食欲起到一定的作用。总之,肠道微生物群的变化（尤其是粪杆菌和Allobaculum的丰度增加）促进胃肠激素的上调，神经递质,和促炎细胞因子，这可能是T-2毒素诱导厌食症的潜在机制。
