Intestinal STC-1 cells respond to five basic taste stimuli

Saitoh, Osamu; Hirano, Atsushi; Nishimura, Yui

doi:10.1097/wnr.0b013e3282f242d3

Cited by 21 publications

(15 citation statements)

References 17 publications

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“…The T1R1 protein is specific to the umami taste receptor, which is activated by L-AAs, including MSG. Our group and others have also demonstrated the presence of T1R3, ␣-gustducin, and transient receptor potential cation channel, subfamily M, member 5 (TRPM5) in gut tissues, as well as in the STC-1 mouse EEC line (3,13,38,48). Although these signaling components are necessary for the complete functional receptor, they are not specific to the umami receptor and do not specifically identify the capacity for chemosensation of L-AAs.…”

Section: Discussionmentioning

confidence: 93%

Activation of the umami taste receptor (T1R1/T1R3) initiates the peristaltic reflex and pellet propulsion in the distal colon

Kendig

Hurst

Bradley

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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Kendig DM, Hurst NR, Bradley ZL, Mahavadi S, Kuemmerle JF, Lyall V, DeSimone J, Murthy KS, Grider JR. Activation of the umami taste receptor (T1R1/T1R3) initiates the peristaltic reflex and pellet propulsion in the distal colon. Am J Physiol Gastrointest Liver Physiol 307: G1100 -G1107, 2014. First published October 16, 2014; doi:10.1152/ajpgi.00251.2014.-Intraluminal nutrients in the gut affect the peristaltic reflex, although the mechanism is not well defined. Recent evidence supports the presence of taste receptors and their signaling components in enteroendocrine cells, although their function is unclear. This study aimed to determine if nutrients modify colonic motility through activation of taste receptors. Colonic sections were immunostained for the umami taste receptor T1R1/T1R3, which mediates the response to umami ligands, such as monosodium glutamate (MSG), in taste cells. Ascending contraction, descending relaxation, and calcitonin gene-related peptide release were measured in three-chamber flat-sheet preparations of rat colon in response to MSG alone or with inosine 5=-monophosphate (IMP). Velocity of artificial fecal pellet propulsion was measured by video recording in guinea pig distal colon. T1R1/T1R3 receptors were present in enteroendocrine cells of colonic sections from human, rat, mouse, and guinea pig. MSG initiated ascending contraction and descending relaxation components of the peristaltic reflex and calcitonin gene-related peptide release in flat-sheet preparations. IMP augmented the MSG-induced effects, suggesting activation of T1R1/T1R3 receptors. In T1R1 Ϫ/Ϫ mice, mucosal stroking, but not MSG, elicited a peristaltic reflex. Intraluminal perfusion of MSG enhanced the velocity of artificial fecal pellet propulsion, which was also augmented by IMP. Propulsion was also increased by L-cysteine, but not L-tryptophan, supporting a role of T1R1/T1R3 receptors. We conclude that T1R1/T1R3 activation by luminal MSG or L-cysteine elicits a peristaltic reflex and CGRP release and increases the velocity of pellet propulsion in distal colon. This mechanism may explain how nutrients regulate colonic propulsion. monosodium glutamate, T1R1/T1R3; motility; human colon; chemosensation THE ABILITY OF INTRALUMINAL nutrients to affect motility of the gastrointestinal (GI) tract has been known for decades (14). However, some of the receptors responsible for sensing intraluminal nutrients have only been discovered very recently. These receptors are the same as those responsible for the detection of taste qualities in the lingual epithelium. Multiple studies show the presence of taste receptors and the associated intracellular signaling molecules in the upper GI tract; however, there is less evidence for the existence of these receptors in the distal gut, specifically, the distal colon (13,37,48). While absorption of nutrients occurs almost completely in the small intestine, amino acids from the diet, dead mucosal cells, digested luminal enzymes, and amino acids generated by bacteria are present in the lumin...

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Section: Discussionmentioning

confidence: 93%

Activation of the umami taste receptor (T1R1/T1R3) initiates the peristaltic reflex and pellet propulsion in the distal colon

Kendig

Hurst

Bradley

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In addition to bitter tastants, compounds of four other basic tastants also stimulated STC-1 cells. Therefore, it was suggested that the gastrointestinal system can sense all five of the basic taste stimuli, and that it might contain a taste receptor signaling system similar to the oral taste system (17). The expression of T1R taste receptors in mouse enteroendocrine cells has also been reported by Dyer et al (6) and Margolskee et al (12).…”

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confidence: 77%

“…Stimulation with sweet, umami, or salty compound does not induce the CCK release from STC-1 cells. It was previously reported that STC-1 cells can respond to five basic tastants by using the Ca 2+ -imaging technique (17). First, STC-1 cells were treated with each of three taste ligands of saccharin, Glu-Na (Na-glutamate), and NaCl for 1 h and the incubated buffer (Hank's balanced salt solution, HBSS) of STC-1 cells was applied to CCKAR/HEK cells.…”

Section: +mentioning

confidence: 99%

“…When CCK is released from STC-1 cells to culture medium with taste stimulation, Ca 2+ activation of CCKAR/HEK should be observed. When monitor- The Fluo8 fluorescence was recorded every 3 sec and the relative fluorescence change (ΔF/F) was determined as previously described (17). At 6 sec, the ligand was applied to the bath (indicated by an arrow).…”

Section: +mentioning

confidence: 99%

“…Next, we examined effect of other two taste lingands out of five basic tastes on the release of CCK from STC-1 cells. STC-1 cells were treated with denatonium benzoate (DB, bitter compound) or HCl for 1 h, and that the release of CCK from STC-1 cells is stimulated by dibutyryl cAMP, forskolin, KCl, phenylalanine, sodium oleate, bitter tastants, and allyl isothiocyanate (AITC) (1-3, 8, 15 -imaging analysis was performed as previously described (17). As shown in Fig.…”

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confidence: 99%

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Effect of five taste ligands on the release of CCK from an enteroendocrinecell line, STC-1

Miyata

Kurogi

et al. 2014

Biomed. Res.

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Here, we investigated which taste ligand induces the CCK (cholecystokinin) release from intestinal STC-1 cells. We first developed a new assay to measure the release of CCK. The expression vector for CCK type A receptor (CCKAR) was permanently introduced into HEK293T cells and a cell line was established (CCKAR/HEK). Then, STC-1 cells were treated with taste ligands and the incubated buffer of STC-1 cells containing released CCK was applied to CCKAR/HEK cells. Since CCKAR couples to Gq-signaling, the CCK-induced receptor activation can be monitored by the method of Ca 2+ -imaging. Therefore, when CCK is released from STC-1 cells to culture medium with taste stimulation, Ca 2+ activation of CCKAR/HEK should be observed. Among five different taste ligands (saccharin, Na-glutamate, NaCl, denatonium benzoate, HCl), only denatonium benzoate and HCl induced the release of CCK in STC-1 cells. Thus, we found that only specific taste ligands induce the CCK release, and that other three taste ligands cannot induce the release of CCK despite of their ability to elevate the intracellular Ca 2+ level in STC-1 cells.

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A novel functional screening assay to monitor sweet taste receptor activation in vitro

Bastiaan‐Net

Berg-Somhorst

Ariëns

et al. 2017

Flavour & Fragrance J

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The human sweet taste receptor is a heterodimer comprised of the class C G protein‐coupled receptor (GPCR) subunits TAS1R2 and TAS1R3. A wide collection of sweet tasting compounds and modulators of sweet taste interact with this receptor. Although TAS1R2/TAS1R3‐mediated signaling is well‐studied, the molecular basis for its desensitization remains unclear while such knowledge would signify a profound step forward in understanding the mechanism behind sweet taste perception and taste modulation. In this work, the possible involvement of β‐arrestin in downstream signaling was investigated. A stable clonal Human Embryonic Kidney (HEK)‐derived cell line containing the PathHunter™ GPCR technology was developed, in which β‐arrestin‐mediated endosomal receptor internalization can be monitored by ligand‐induced enzyme complementation of β‐galactosidase (β‐gal). Stimulatory responses and antibody‐specific receptor detection indicated that the TAS1R2/TAS1R3 receptor is endogenously expressed in this clonal cell line. Natural sugars (including fructose, glucose, sucrose, maltose, maltitol and mannitol) and artificial sweeteners (acesulfame‐K and sucralose) stimulated enzyme complementation activity in a concentration dependent manner. Besides, we observed that the assay detected modification of sugar induced cell responses by sweetness enhancers. These results combined implicate that TAS1R2/TAS1R3 receptor desensitization by internalization is most likely mediated by β‐arrestin‐induced endocytosis. This assay approach, making use of naturally expressed TAS1R2/TAS1R3 receptors and required co‐factors, further allows effective screening for and development of novel high potency non‐caloric sweeteners, sweet taste modulators or optimal blends with enhanced sweet taste.

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Intestinal STC-1 cells respond to five basic taste stimuli

Cited by 21 publications

References 17 publications

Activation of the umami taste receptor (T1R1/T1R3) initiates the peristaltic reflex and pellet propulsion in the distal colon

Activation of the umami taste receptor (T1R1/T1R3) initiates the peristaltic reflex and pellet propulsion in the distal colon

Effect of five taste ligands on the release of CCK from an enteroendocrinecell line, STC-1

A novel functional screening assay to monitor sweet taste receptor activation in vitro

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