Foodborne
carbon dots (CDs), an emerging food nanocontaminant, are an increasing risk factor for metabolic toxicity in mammals. Here, we report that chronic CD exposure induced
glucose metabolism disorders via disruption of the gut-liver axis in mice.
16s rRNA analysis demonstrated that CD exposure decreased the abundance of beneficial bacteria (Bacteroides, Coprococcus, and S24-7) and increased the abundance of harmful bacteria (Proteobacteria, Oscillospira, Desulfovibrionaceae, and Ruminococcaceae), as well as increased the Firmicutes/Bacteroidetes ratio. Mechanistically, the increased pro-inflammatory bacteria release the
endotoxin lipopolysaccharide, which induces an intestinal
inflammation and disruption of the intestinal mucus layer, activating systemic
inflammation and inducing hepatic
insulin resistance in mice via the TLR4/NFκB/MAPK signaling pathway. Furthermore, these changes were almost completely reversed by probiotics.
Fecal microbiota transplantation from CD-exposed mice induced
glucose intolerance, damaged liver function, intestinal mucus layer injury, hepatic
inflammation, and
insulin resistance in the recipient mice. However, microbiota-depleted mice exposed to CDs had normal levels of these
biomarkers consistent with microbiota-depleted control mice, which revealed that gut microbiota
dysbiosis contributes to CD-induced
inflammation-mediated
insulin resistance. Together, our findings revealed that gut microbiota
dysbiosis contributes to CD-induced
inflammation-mediated
insulin resistance and attempted to elucidate the specific underlying mechanism. Furthermore, we emphasized the importance of assessing the hazards associated with foodborne CDs.