TAS2R43

Last update 08 May 2025

Basic Info

Synonyms

T2R43, T2R52, TAS2R43

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Introduction

Gustducin-coupled receptor immplicated in the perception of bitter compounds in the oral cavity and the gastrointestinal tract. Signals through PLCB2 and the calcium-regulated cation channel TRPM5. Activated by the sulfonyl amide sweeteners saccharin and acesulfame K. In airway epithelial cells, binding of bitter compounds increases the intracellular calcium ion concentration and stimulates ciliary beat frequency. May act as chemosensory receptors in airway epithelial cells to detect and eliminate potential noxious agents from the airways (By similarity).

100 Clinical Results associated with TAS2R43

100 Translational Medicine associated with TAS2R43

0 Patents (Medical) associated with TAS2R43

Literatures (Medical) associated with TAS2R43

01 Aug 2025·Food Chemistry

Bitter peptides formed during in-vitro gastric digestion induce mechanisms of gastric acid secretion and release satiating serotonin via bitter taste receptors TAS2R4 and TAS2R43 in human parietal cells in culture

Article

Author: Richter, Phil ; Gradl, Katrin ; Somoza, Veronika

A key barrier in transitioning to plant-based, more satiating diets, is the bitter taste of plant proteins. We hypothesize that both, a more bitter tasting (MBT) and a less bitter tasting (LBT) pea protein hydrolysate (PPH) can be digested in the stomach into bitter tasting peptides that stimulate proton secretion (PS) and serotonin release, as two of the key gastric satiety signals, via the functional involvement of bitter taste receptors (TAS2Rs). Using a sensory-guided LC-MS approach, we identified six bitter peptides that were released from LBT-PPH and MBT-PPH during gastric digestion in vitro. TAS2R4 and TAS2R43 involvement in PS and serotonin release was confirmed via CRISPR-Cas9 knockout experiments. Our hypothesis was proven with all six peptides equally stimulating PS in immortalized human gastric HGT-1 cells, and LBT-PPH-derived peptides eliciting a higher serotonin release in HGT-1 cells than MBT-PPH peptides, indicating a satiating potential of less bitter tasting protein hydrolysates.

01 Mar 2025·Food Chemistry

Contribution of mozambioside roasting products to coffee's bitter taste

Article

Author: Fröhlich, Sonja Maria ; Brychcy, Valeria ; Graßl, Angelika ; Bichlmaier, Coline ; Behrens, Maik ; Lang, Roman

Roasting degrades the coffee compound mozambioside (1) into several products, including 17-O-β-D-glucosyl-11-hydroxycafestol-2-one (2), 11-O-β-D-glucosyl-16-desoxycafestol-2-one (3), 11-O-β-D-glucosyl-(S)-16-desoxy-17-oxocafestol-2-one (4), 11-O-β-D-glucosyl-15,16-dehydrocafestol-2-one (5), 11-O-β-D-glucosyl-(R)-16-desoxy-17-oxocafestol-2-one (6), bengalensol (7), and 11-hydroxycafestol-2-one (8). A UHPLC-MS/MS method was established to quantify 1-8 and monitor their formation during authentic coffee roasting. Concentrations of 1 and the dominant roasting products 4, 5, and 7 ranged from 21.0 to 170.4 nmol/g in coffee powders, with ∼41-128 % extracted into the brew. Human bitter taste thresholds of 1, 2, and 4-8 were determined. The major roasting products exhibited lower thresholds (27-80 μM) than 1 (132 μM). Genotyping of panelists revealed a correlation between sensitivity for mozambioside-derivatives and the presence of intact TAS2R43 gene loci. The combination of 1-8 in coffee concentrations elicited a bitter taste recognized in 80 % of the panelists, suggesting this compound class contributes to coffee's taste profile.

01 Oct 2024·Molecular Metabolism

Bitter-tasting drugs tune GDF15 and GLP-1 expression via bitter taste or motilin receptors in the intestine of patients with obesity

Article

Author: Van der Schueren, Bart ; Farhadipour, Mona ; Wang, Qian ; Tack, Jan ; Sosoranga, Emily Ruilova ; Depoortere, Inge ; Lannoo, Matthias ; Ceulemans, Laurens J ; Deleus, Ellen ; Thijs, Theo

OBJECTIVEGrowth differentiation factor 15 (GDF15), a stress related cytokine, was recently identified as a novel satiety signal acting via the GFRAL receptor located in the hindbrain. Bitter compounds are known to induce satiety via the release of glucagon-like peptide 1 (GLP-1) through activation of bitter taste receptors (TAS2Rs, 25 subtypes) on enteroendocrine cells in the gut. This study aimed to investigate whether and how bitter compounds induce a stress response in intestinal epithelial cells to affect GDF15 expression in patients with obesity, thereby facilitating satiety signaling from the gut.METHODSThe acute effect of oral intake of the bitter-containing medication Plaquenil (hydroxychloroquine sulfate) on plasma GDF15 levels was evaluated in a placebo-controlled, double-blind, randomized, two-visit crossover study in healthy volunteers. Primary crypts isolated from the jejunal mucosa from patients with obesity were stimulated with vehicle or bitter compounds, and the effect on GDF15 expression was evaluated using RT-qPCR or ELISA. Immunofluorescence colocalization studies were performed between GDF15, epithelial cell type markers and TAS2Rs. The role of TAS2Rs was tested by 1) pretreatment with a TAS2R antagonist, GIV3727; 2) determining TAS2R4/43 polymorphisms that affect taste sensitivity to TAS2R4/43 agonists.RESULTSAcute intake of hydroxychloroquine sulfate increased GDF15 plasma levels, which correlated with reduced hunger scores and plasma ghrelin levels in healthy volunteers. This effect was mimicked in primary jejunal cultures from patients with obesity. GDF15 was expressed in enteroendocrine and goblet cells with higher expression levels in patients with obesity. Various bitter-tasting compounds (medicinal, plant extracts, bacterial) either increased or decreased GDF15 expression, with some also affecting GLP-1. The effect was mediated by specific intestinal TAS2R subtypes and the unfolded protein response pathway. The bitter-induced effect on GDF15/GLP-1 expression was influenced by the existence of TAS2R4 amino acid polymorphisms and TAS2R43 deletion polymorphisms that may predict patient's therapeutic responsiveness. However, the effect of the bitter-tasting antibiotic azithromycin on GDF15 release was mediated via the motilin receptor, possibly explaining some of its aversive side effects.CONCLUSIONSBitter chemosensory and pharmacological receptors regulate the release of GDF15 from human gut epithelial cells and represent potential targets for modulating metabolic disorders or cachexia.

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TAS2R43

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