Research Paper

D-allulose alleviates DSS-induced colitis via regulating gut microbiota and bile acid metabolism

G, N, G· Food Research International

Summary

D-allulose is a rare monosaccharide with established safety and documented biological functions, whereas its potential effects on ulcerative colitis remains controversial. This study aimed to evaluate the impact of D-allulose on DSS-induced colitis and explore the underlying mechanisms. The results demonstrated that D-allulose supplementation (125, 250 and 500 mg/kg/day) significantly alleviated DSS-induced colitis symptoms, including body weight loss, colon shortening, diarrhea, and mucosal injury. D-allulose restored intestinal barrier integrity by upregulating tight junction proteins and mucins.

Key Findings

  • The results demonstrated that D-allulose supplementation (125, 250 and 500 mg/kg/day) significantly alleviated DSS-induced colitis symptoms, including body weight loss, colon shortening, diarrhea, and mucosal injury.
  • Notably, D-allulose reduced neutrophil and macrophage infiltration and downregulated proinflammatory cytokines expression.
  • Both untargeted and targeted metabolomic analyses demonstrated that D-allulose supplementation modulated bile acid metabolism, particularly by promoting the production of secondary bile acids (DCA and LCA) through the TGR5-PKA-NF-κB signaling pathway.
  • Collectively, these results provided novel insights into the gut microbiota-metabolite-host crosstalk mediated by D-allulose and highlighted its potential as a functional food component for the management of colitis.

Industry Relevance

This study provides important insights into how allulose interacts with the gut microbiome, supporting its safety profile as a low-digestible sweetener. For manufacturers, this research helps address consumer and regulatory questions about digestive tolerance and prebiotic potential.

Read the full paper: Food Research International | DOI: 10.1016/j.foodres.2025.117923

View Full Paper →DOI: 10.1016/j.foodres.2025.117923

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