<b>Expression patterns of T1R3 in duodenal epithelial cells with some gastrointestinal hormone</b>

Abstract

may regulate the secretion of serotonin by stimuli other than a mechanical one. IntroductionThe taste system, which is made up of taste receptor cells clustered in taste buds at the surface of the tongue and the soft palate, plays a key role in the decision to ingest or reject food. Its function is therefore, essential to protect organisms against harmful toxins and select the most appropriate nutrients. Ingested nutrients stimulate the secretion of gastrointestinal hormones necessary for the coordinated processes of food digestion.The T1Rs, G-protein-coupled receptors (GPCRs) that form two novel seven-transmembrane domains, are expressed in topographically distinct subpopulations of taste receptor cells and taste buds (Hoon et al., 1999). The functional expression of T1Rs is influenced by sweet and umami taste stimuli. A T1R2/T1R3 heterodimer serves as a chemical receptor for sweet tastes (diverse natural and synthetic sweeteners). T1R1/T1R3 heterodimers are receptors for the umami compound l-glutamate, a response enhanced by 5'-ribonucleotides (Nelson et al., 2001;Li et al., 2002).Recent studies have demonstrated that solitary cells expressing taste cell signal transduction proteins exist in hollow organs. It has been previously shown that T1Rs are expressed in the gastrointestinal tract (GI) (Hofer et al., 1996;Wu et al., 2002; Dyer et al., 2005;Grundy, 2005). They are additionally expressed in the stomach, small intestine -including the duodenum, and colon in mice and humans, with the exception of T1R2, which has not been detected in the mouse or human stomach or in the mouse colon (Bezençon et al., 2007

A Randomized Placebo-controlled Trial of an Oral Preparation of High Molecular Weight Fucoidan in Patients with Type 2 Diabetes with Evaluation of Taste Sensitivity

“…A relationship between diabetes and the gustatory system has attracted lots of attention since the discovery of taste receptors on the intestinal epithelium where augmentation of insulin secretion is provoked through the incretin pathway. [33][34][35][36][37] Accordingly, this randomized, double-blind, placebo-controlled, cross-over study investigated the effects of long-term intake of high molecular weight fucoidan on clinical parameters, the intestinal environment, and the gustatory system controlling taste sensation in patients with type 2 diabetes.…”

“…The subgroup with an above average increase in the number of bowel movements showed a decrease of the baseline GLP-1 level, an increase of leptin and increased sensitivity to 4 tastes (except sourness) after intake of fucoidan. Recently, it was demonstrated that taste receptors are expressed throughout the entire gastrointestinal tract epithelium, [33][34][35][36][37] and that sweetness receptors in the small and large intestines are involved in the secretion of GLP-1. [44][45][46][47] In this context, it is possible that the changes of GLP-1 and the taste threshold could be due to modulation of the intestinal environment by fucoidan intake.…”