Fructose Promotes Oxidative Stress, Sphingolipid Remodelling and Transient Intestinal Barrier Dysfunction in Differentiated Caco-2 Cells

Background/Objectives: High dietary fructose consumption has been linked to impaired intestinal barrier function and several metabolic disorders. Although oxidative stress has been proposed as a mediator of fructose-related epithelial injury, the involvement of tight-junction (TJ) proteins and sphingolipid metabolism is still not fully defined. Here, differentiated Caco-2 monolayers were exposed to fructose (1–50 mM) to examine changes in epithelial barrier integrity and associated molecular responses.