Environmental cadmium, with a high dietary intake and long biological half-life, is a severe health risk by harming physiological function directly or through gut microbiota. However, the toxicity mechanisms of environmental cadmium on microbes and host systems remain unclear. Herein, we established three C. elegans and E. coli cultivated systems to investigate the vital role of microorganisms in cadmium-induced lipid toxicity and depict the interaction between environmental cadmium, bacteria, and the host. We found that only nematodes in the system with live bacteria, rather than UV-killed bacteria or no bacteria, could be induced to fat accumulation by cadmium exposure, suggesting that bacteria mediated the effect of environmental cadmium on body fat. Cadmium caused perturbation of metabolite in bacteria, most notably oleic acid, elevated the synthesis genes expression, and enhanced the bacterial oleic acid production, which further promoted the expression of lipid metabolism-related genes and fat deposition in C. elegans regardless of the cultivated system. Finally, we showed the potential protective effect of Vitamin D3 which prevented cadmium- or oleic acid-induced fat storage significantly. In conclusion, this study illustrates the mechanism underlying cadmium-induced lipid accumulation in body through bacterial metabolites and reveals the interplay between environmental cadmium, microorganisms, and the host.

环境镉具有高膳食摄入量和长生物半衰期，直接或通过肠道微生物群损害生理功能，对健康构成严重威胁。然而，环境镉对微生物和宿主系统的毒性机制仍不清楚。在此，我们建立了三个秀丽隐杆线虫和大肠杆菌培养系统研究微生物在镉诱导的脂质毒性中的重要作用，并描述环境镉、细菌和宿主之间的相互作用。我们发现只有具有活细菌的系统中的线虫，而不是紫外线杀死的细菌或没有细菌的线虫，才能通过镉暴露诱导脂肪积累，这表明细菌介导了环境镉对身体脂肪的影响。镉引起细菌代谢物的扰动，最显着的是油酸，提高合成基因的表达，并增强细菌油酸的产生，进一步促进了线虫脂质代谢相关基因的表达和脂肪沉积与栽培系统无关。最后，我们展示了维生素 D3 的潜在保护作用，可显着防止镉或油酸诱导的脂肪储存。总之，本研究通过细菌代谢物阐明了镉诱导体内脂质积累的机制，并揭示了环境镉、微生物和宿主之间的相互作用。