The effect of tumor necrosis factor-alpha on the expression of glucose transporters SGLT1 and GLUT2 in differentiated CACO-2 cells

Abstract

Inflammatory bowel disease is characterized by chronic ulcerations of the bowel, manifested as diarrhea, rectal bleeding, and weight loss. Disease progression is often accompanied by the production of different cytokines, such as Tumor Necrosis Factor-α (TNF-α) and interleukins. Studies in our lab have demonstrated an alteration in jejunal glucose absorption after experimental colitis. In this study, we examined the potential role of the pro-inflammatory cytokine TNF-α as a mediator of the observed change in glucose absorption. We treated differentiated Caco-2 cells with 10 ng/mL of TNF-α for different time-points. Subsequently, RT-PCR was performed to measure SGLT1 mRNA levels, while western blot analyses determined SGLT1 and GLUT2 protein expression. TNF-α was shown to significantly decrease GLUT2 protein levels 18 hours post-treatment, but had no effect on SGLT1 mRNA or protein levels at any of the time-points. These results suggest a possible role for TNF-α in glucose absorption alterations in experimental colitisand in IBD, providing an insight on what is clinically needed to improve the treatment of IBD patients.