Corncob-Derived Xylo-Oligosaccharides Attenuate Acrylamide-Induced Gut–Liver Toxicity in Mice, Associated with Modulation of Gut Microbiota and SCFA Metabolism

Acrylamide (AA) is a common foodborne toxicant formed during the thermal processing of starch-rich foods and poses significant risks to the gut–liver axis. Although corncob-derived xylo-oligosaccharides (XOS) have emerged as promising prebiotics with multiple bioactivities, their protective effects against foodborne toxicants have not been explored. This study investigated the ameliorative effects of dietary corncob-derived XOS on AA-induced gut–liver toxicity and the underlying mechanisms in mice. Female C57BL/6J mice were gavaged with AA and concurrently fed diets with or without 7.0% XOS for 7 weeks. The results showed that XOS effectively alleviated AA-induced gut–liver toxicity, as evidenced by attenuated intestinal and hepatic inflammation (decreased pro-inflammatory cytokines IL-6 in colon, TNF-α, and IL1-β in liver; increased anti-inflammatory IL-10 in colon and liver), restored intestinal barrier integrity (upregulated Zo-1, Occludin, and Claudin-1 mRNA, along with increased goblet cell numbers and mucus secretion), and ameliorated hepatic oxidative stress (upregulated Nrf2/Nqo1/Ho1 mRNA expression, restored CAT activity, and reduced H2O2 accumulation). 16S sequencing revealed that XOS supplementation significantly increased the Shannon index in AA-exposed mice compared with the AA group, suggesting enhanced cecal microbial diversity, although AA exposure did not significantly reduce α-diversity. Further analysis showed that XOS reshaped the community composition, particularly by reducing pro-inflammatory genera (Dubosiella, Desulfovibrio, Faecalibaculum, and Faecalimonas) and enriching short chain fatty acid (SCFA)-producing bacteria (Bifidobacterium, norank_f__Muribaculaceae, and Akkermansia). Furthermore, XOS significantly elevated SCFA levels in AA-treated mice, including acetic, propionic, butyric, valeric, and isovaleric acids. Collectively, these findings demonstrate that dietary XOS ameliorates AA-induced gut–liver toxicity in mice when co-administered with AA. This protective effect was associated with modulation of the gut microbiota and SCFA metabolism, providing a basis for future studies exploring the potential of XOS against foodborne contaminant toxicity.