Hermetia illucens can digest toxic castor meal and tolerate ricinine stress. However, the underlying mechanisms of ricinine degradation and detoxification within the larval gut microbiome remain largely unknown. Here, the enhanced degradation kinetic process, and the roles of the gut bacterial community and metabolomics were investigated. When the ricinine content was 1000 mg kg−1 in feeding substrate, larval development was not significantly affected. The ricinine degradation kinetics, facilitated by larval digestion, were significantly enhanced, reducing the degradation half-life to 5.13 days. The gut bacterial community structure adjusted in response to ricinine stress, suggesting that genera such as Dysgonomonas, Actinomyces, Phascolarctobacterium, Lachnoclostridium and Sedimentibacter might play key roles in ricinine resistance and degradation. Furthermore, the gut microbial metabolism responded to toxin stress, reflected by variations in metabolite expression and the enrichment of key metabolic pathways involved in amino acid and vitamin metabolism. This emphasizes the potential role of microbial metabolism in ricinine degradation and detoxification. The close association between gut bacteria and metabolites suggests a cooperative metabolic network within the gut microbiota, where bacteria may participate in ricinine degradation and detoxification either directly or through metabolic cooperation. These findings provide insights into host–microbe interactions and ricinine resistance, highlighting the need for further exploration into the microbiota’s role in host metabolism and the development of new therapeutic strategies.
Li et al. (Fri,) studied this question.