Altered peripheral taste function in a mouse model of inflammatory bowel disease

Abstract

Increased sugar intake and taste dysfunction have been reported in patients with inflammatory bowel disease (IBD), a chronic disorder characterized by diarrhea, pain, weight loss and fatigue. It was previously unknown whether taste function changes in mouse models of IBD. Mice consumed dextran sodium sulfate (DSS) during three 7-day cycles to induce chronic colitis. DSS-treated mice displayed signs of disease, including significant weight loss, diarrhea, loss of colon architecture, and inflammation of the colon. After the last DSS cycle we assessed taste function by recording electrophysiological responses from the chorda tympani (CT) nerve, which transmits activity from lingual taste buds to the brain. DSS treatment significantly reduced neural taste responses to natural and artificial sweeteners. Responses to carbohydrate, salt, sour or bitter tastants were unaffected in mice with colitis, but umami responses were modestly elevated. DSS treatment modulated the expression of receptor subunits that transduce sweet and umami stimuli in oral taste buds as a substrate for functional changes. Dysregulated systemic cytokine responses, or dysbiosis that occurs during chronic colitis may be upstream from changes in oral taste buds. We demonstrate for the first time that colitis alters taste input to the brain, which could exacerbate malnutrition in IBD patients.

Intestinal Taste Receptor Expression and Its Implications for Health: An Integrative Analysis in Female Rats after Chronic Insect Supplementation

“…Goblet cells, specialized in producing mucus, play a crucial role in maintaining intestinal health and initiating immunological responses, 57 reinforcing the idea of Tas1r1 involvement in immune function. 58 Moreover, this connection between goblet cells and Tas1r1 may be produced by the presence of this receptor in colonic tuft cells, which are involved in the immune response that can activate goblet cells. 59 , 60 However, an additional explanation for this negative correlation could be attributed to the influence of insect compounds on the composition of intestinal cells.…”