Allulose enhances epithelial barrier function by tight junction regulation via the TLR4/MyD88/NF-κB immune signaling pathway in an intestinal Caco-2 cell model

Abstract

d-allulose, a fructose isomer with almost zero calories, has been widely used as a food ingredient that is generally recognized as safe. In recent studies, d-allulose has been shown to alleviate some diseases via restoration of the intestinal barrier. To better understand the role of d-allulose in intestinal epithelial barrier function, we conducted experiments to demonstrate its effects. Our results demonstrated that d-allulose increased transepithelial electrical resistance and decreased intestinal barrier function–associated permeability toward 4 kDa FITC–dextran flux in the damaged intestinal epithelial barrier. It also repaired the disruption pattern of tight junction proteins (ZO-1, occludin, and claudin-1) and inhibited the inflammatory response by inhibiting the TLR4/MyD88/NF-κB pathway. Overall, these findings suggest that d-allulose has the potential to be a beneficial food supplement for improving intestinal epithelial barrier dysfunction.

Keywords

• d-allulose
• TLR4/MyD88/NF-κB signaling
• Tight junction
• Immune regulation