Taste-sensing mechanisms in the taste buds of the tongue have triggered by chemosensory cells in the intestinal. Intestinal is the crucial interface between food and the human body and can sense tastes in much the same way as the tongue. Chrons disease (CD) patients show an increase in glucose consumption, due to an increase in the production of pro-inflammatory cytokines such as TNF-α in both the blood and intestinal mucosa, which can cause changes in appetite, taste and olfactory function. The presence of ulcers in the oral mucosa, causing pain and disrupting the eating process so that it can cause malnutrition.
Eating activity is a process carried out as a way to eliminate hunger. However, the important thing from the eating process is to obtain nutrients that are important for life and health. Therefore, the taste and digestive system contain a variety of receptors that help to regulate the digestive system which includes the assimilation of nutrients, avoiding or neutralizing toxins, endocrine and neural responses that affect metabolism. G protein coupled receptor (GPCR) can identify toxins and nutrients that act as taste receptors in the oral mucosa and intestinal mucosa, regulate glucose balance, homeostasis and bone regeneration. Sweetness is a taste that arises due to the stimulation of molecules such as monosaccharides, disaccharides, and polysaccharides. This molecule plays a role in increasing sweet taste sensation through signaling in GPCR by glucagon like peptide-1 (GLP-1) both in taste buds on the tongue, and enteroendocrine cells (EEC) in the intestinal mucosa.
Physiological functions in the digestive tract are regulated by enteroendocrine cells (EEC). EEC functions as signalling in the transepithelial layer by releasing mediators such as cholecystokinin (CCK) from duodenal cells, GLP-1 and polypeptide YY (PYY) from L cells in the intestine. In patients with IBD, there is a condition of increased expression of PYY and GLP-1 in L cells due to the release of inflammatory mediators, namely pro-inflammatory cytokines such as TNF-alpha and IL-6. Increased expression of GLP-1 will cause an increase in the perception of sweetness in the intestinal mucosa. The same thing will increase GLP-1 in the tongue because GLP-1 can enter the blood circulation and has an endocrine role by activating GPCR. Therefore, patients with IBD, especially CD consume sweet food products, such as pudding, honey and jam, chocolate, and cakes 40% more than ordinary people. This process explains why patients with inflammatory bowel disease experience a change in the perception of sweet taste and an increase in the consumption of sweet foods.
Author: Meircurius Dwi Condro Surboyo, drg., M.Kes
Meircurius Dwi Condro Surboyo, Ida Bagus Pramana Putra Manuabaand Jenny Sunariani (2020). SWEET TASTE PERCEPTION CHANGES DUE TO AN INCREASE GLP-1 IN INFLAMMATORY BOWEL DISEASE. Biochemical and Cellular Archives; 20(Supp 1): 3039-3043