Foodborne
carbon dots (CDs) are generally produced during cooking and exist in food items. Generally, CDs are regarded as nontoxic materials, but several studies have gradually confirmed the cytotoxicity of CDs, such as oxidative stress, reduced cellular activity, apoptosis, etc. However, studies focusing on the health effects of long-term intake of food-borne CDs are scarce, especially in populations susceptible to
metabolic disease. In this study, we reported that CDs in self-brewing beer had no effect on
glucose metabolism in CHOW-fed mice but exacerbated high-fat-diet (HFD)-induced
glucose metabolism disorders via the gut-liver axis. Chronic exposure to foodborne CDs increased fasting
glucose levels and exacerbated liver and intestinal barrier damage in HFD-fed mice. The
16s rRNA sequencing analysis revealed that CDs significantly altered the gut microbiota composition and promoted
lipopolysaccharide (LPS) synthesis-related KEGG pathways (superpathway of (Kdo)2-
lipid A, Kdo transfer to
lipid IVA Ill (Chlamydia),
lipid IVA biosynthesis, and so on) in HFD-fed mice. Mechanically, CD exposure increased the abundance of Gram-negative bacteria (Proteobacteria and Desulfovibrionaceae), thus producing excessive
endotoxin-LPS, and then LPS was transferred by the blood circulation to the liver due to the damaged intestinal barrier. In the liver, LPS promoted TLR4/NF-κB/
P38 MAPK signaling, thus enhancing systemic
inflammation and exacerbating HFD-induced
insulin resistance. However, pretreating mice with
antibiotics eliminated these effects, indicating a key role for gut microbiota in CDs exacerbating
glucose metabolism disorders in HFD-fed mice. The finding herein provides new insight into the potential health risk of foodborne nanoparticles in susceptible populations by disturbing the gut-liver axis.