Sweet taste perception changes due to an increase GLP-1 in inflammatory bowel disease

Taste-sensing mechanisms in the taste buds of the tongue has triggered by chemosensory cells in the intestinal. Indeed, the intestinal is the key interface between food and the human body and can sense tastes in much the same way as the tongue, through the glucagon-like peptide-1 (GLP-1). The inflammatory bowel disease (IBD) has manifestation both oralmucosal and intestinal mucosal as ulceration. The IBD patients has taste alteration especially in sweet taste because the increased the TNF-a and IL-6 production. These cytokine will increased the GLP-1 secretion in EEC and act as endocrine to stimulate secretion GLP-1 in taste bud. The increase in GLP-1 by taste buds on the tongue is caused by GPCR activation and resulted in the increased the sweet taste. The objective of this review is to describe the mechanism of changes in taste sensation, especially sweet taste due to an increase in GLP-1 in IBD patient.