Chronic oral exposure to food-grade SiO2 nanoparticles for 8 weeks in mice caused colonic barrier injury, elevated circulating LPS, microbiota changes at high dose, reduced intestinal and hepatic FXR-related markers, altered bile acid synthesis and transport genes, and liver injury, suggesting disturbance of intestinal and hepatic homeostasis potentially involving FXR-related bile acid dysregulation along the gut-liver axis.
Key Findings
Results
Dietary SiO2NP exposure for 8 weeks induced colonic barrier injury in male C57BL/6J mice.
Male C57BL/6J mice were fed control or SiO2NP-containing diets providing 225, 1000, or 5000 mg/kg bw/day for 8 weeks.
The abstract reports colonic barrier injury following SiO2NP exposure.
Specific barrier-marker values are not given in the abstract.
Elevated circulating LPS was observed alongside colonic barrier injury.
This is consistent with impaired gut barrier function and translocation of microbial products.
Exact LPS concentrations and dose-specific effects are not given in the abstract.
Results
High-dose SiO2NP exposure altered fecal microbiota composition compared with controls.
Fecal microbiota profiling was performed on the normal control (NC) and high-dose groups only.
Compositional alterations were associated with high-dose exposure (5000 mg/kg bw/day).
Low and medium doses were not profiled for microbiota.
Results
Intestinal and hepatic FXR-related marker expression was reduced after SiO2NP exposure.
Reduced expression was seen in both intestine and liver.
This suggests disrupted FXR signaling along the gut-liver axis.
Specific markers and fold changes are not given in the abstract.
Results
SiO2NP exposure altered expression of genes involved in bile acid synthesis and transport.
Changes were observed in genes controlling bile acid synthesis and transport in parallel with reduced FXR-related markers.
The abstract does not specify the direction of change for individual genes.
Results
Exposed mice showed elevated serum total bile acid levels.
Serum total bile acids were increased in SiO2NP-exposed mice.
This was reported alongside altered bile acid synthesis and transport gene expression.
Results
SiO2NP exposure caused liver injury with inflammatory, lipid metabolic, and fibrotic responses.
Liver injury was accompanied by inflammatory, lipid metabolic, and fibrotic responses.
Exposure doses were 225, 1000, or 5000 mg/kg bw/day for 8 weeks.
Conclusions
The authors conclude that chronic oral SiO2NP exposure disturbs intestinal and hepatic homeostasis, potentially involving FXR-related bile acid dysregulation.
The interpretation is framed as potential involvement of FXR-related bile acid dysregulation along the gut-liver axis.
The study was motivated by concern over repeated exposure to nanoscale fractions of food-grade silica (E551), an anticaking additive.
What This Means
This study asked whether tiny silica particles, like those found in the common food additive E551 (used to keep powders from clumping), could harm the gut and liver when eaten over a long time. Male mice were fed diets containing silica nanoparticles at three dose levels for 8 weeks, and were compared with mice on a normal diet.
The exposed mice showed damage to the colon's barrier and higher levels of a bacterial toxin (LPS) in the blood. In the highest-dose group, the gut bacteria community differed from that of control mice. Signals tied to FXR, a receptor that helps regulate bile acids, were reduced in the gut and liver, and genes for making and moving bile acids were changed. The mice also had higher bile acid levels in the blood and signs of liver injury, including inflammation, altered fat metabolism, and scarring-related changes.
This research suggests that long-term, high-level exposure to silica nanoparticles may disturb the communication between the gut and liver in mice, possibly through bile acid regulation. The doses were given to mice in an animal study, and the abstract does not show how these results would translate to typical human dietary exposure, so the findings point to a need for further research rather than direct conclusions about human health.
Qu Z, Wang P, Zhang S, Wang J, Wang Y, Wu Y, et al.. (2026). Food-Grade Silicon Dioxide Nanoparticles Disrupt the Microbiota-Associated Gut-Liver Axis and FXR-Related Bile Acid Homeostasis in Mice.. Journal of agricultural and food chemistry. https://doi.org/10.1021/acs.jafc.6c06989