BitterDB: a database of bitter compounds

Wiener, Ayana; Shudler, Marina; Levit, Anat; Niv, Masha Y.

doi:10.1093/nar/gkr755

Cited by 227 publications

(215 citation statements)

References 47 publications

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“…Two other agonists that activate β-defensin secretion are parthenolide, which activates T2R10 and 46, and amarogentin, which activates T2R46 and 47 (60). A role for T2R47 in this response is in agreement with its localization to solitary nonciliated cells (Figure 2 and Supplemental Figure 7).…”

Section: Figuresupporting

confidence: 55%

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Bitter and sweet taste receptors regulate human upper respiratory innate immunity

Lee¹,

Kofonow²,

Rosen³

et al. 2014

J. Clin. Invest.

353

639

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Bitter taste receptors (T2Rs) in the human airway detect harmful compounds, including secreted bacterial products. Here, using human primary sinonasal air-liquid interface cultures and tissue explants, we determined that activation of a subset of airway T2Rs expressed in nasal solitary chemosensory cells activates a calcium wave that propagates through gap junctions to the surrounding respiratory epithelial cells. The T2R-dependent calcium wave stimulated robust secretion of antimicrobial peptides into the mucus that was capable of killing a variety of respiratory pathogens. Furthermore, sweet taste receptor (T1R2/3) activation suppressed T2R-mediated antimicrobial peptide secretion, suggesting that T1R2/3-mediated inhibition of T2Rs prevents full antimicrobial peptide release during times of relative health. In contrast, during acute bacterial infection, T1R2/3 is likely deactivated in response to bacterial consumption of airway surface liquid glucose, alleviating T2R inhibition and resulting in antimicrobial peptide secretion. We found that patients with chronic rhinosinusitis have elevated glucose concentrations in their nasal secretions, and other reports have shown that patients with hyperglycemia likewise have elevated nasal glucose levels. These data suggest that increased glucose in respiratory secretions in pathologic states, such as chronic rhinosinusitis or hyperglycemia, promotes tonic activation of T1R2/3 and suppresses T2R-mediated innate defense. Furthermore, targeting T1R2/3-dependent suppression of T2Rs may have therapeutic potential for upper respiratory tract infections.

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Section: Figuresupporting

confidence: 55%

“…Based on heterologous expression data, the receptors T2R10, T2R46, and T2R47 are activated by both denatonium and absinthin (16,60). Two other agonists that activate β-defensin secretion are parthenolide, which activates T2R10 and 46, and amarogentin, which activates T2R46 and 47 (60).…”

Section: Figurementioning

confidence: 99%

Bitter and sweet taste receptors regulate human upper respiratory innate immunity

Lee¹,

Kofonow²,

Rosen³

et al. 2014

J. Clin. Invest.

353

639

View full text Add to dashboard Cite

show abstract

“…We used quinine, an anti-malarial drug extracted from the bark of the cinchona tree, able to trigger bitter taste by the activation of several members of T2R family receptors. 29 The drug was administered by an acid-resistant capsule for 2 main reasons: (1) in order to prevent the activation of the taste receptors of the oral cavity and (2) to prevent the release of ghrelin, produced by the X/A-like cells of the oxyntic glands of the stomach and to allow its release into the duodenum where CCK-releasing EECs are located. 19 The role of bitter taste in the control of digestive functions is controversial: bitter compounds are naturally unpleasant.…”

Section: Discussionmentioning

confidence: 99%

The Bitter Taste Receptor Agonist Quinine Reduces Calorie Intake and Increases the Postprandial Release of Cholecystokinin in Healthy Subjects

Andreozzi

Sarnelli

Pesce

et al. 2015

J Neurogastroenterol Motil

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Background/AimsBitter taste receptors are expressed throughout the digestive tract. Data on animals have suggested these receptors are involved in the gut hormone release, but no data are available in humans. Our aim is to assess whether bitter agonists influence food intake and gut hormone release in healthy subjects. MethodsTwenty healthy volunteers were enrolled in a double-blind cross-over study. On 2 different days, each subject randomly received an acid-resistant capsule containing either placebo or 18 mg of hydrochloride (HCl) quinine. After 60 minutes, all subjects were allowed to eat an ad libitum meal until satiated. Plasma samples were obtained during the experiment in order to evaluate cholecystokinin (CCK) and ghrelin levels. Each subject was screened to determine phenylthiocarbamide (PTC) tasting status. ResultsCalorie intake was significantly lower when subjects received HCl quinine than placebo (514 ± 248 vs 596 ± 286 kcal; P = 0.007). Significantly higher CCK ΔT90 vs T0 and ΔT90 vs T60 were found when subjects received HCl quinine than placebo (0.70 ± 0.69 vs 0.10 ± 0.86 ng/mL, P = 0.026; 0.92 ± 0.75 vs 0.50 ± 0.55 ng/mL, P = 0.033, respectively). PTC tasters ingested a significantly lower amount of calories when they received HCl quinine compared to placebo (526 ± 275 vs 659 ± 320 kcal; P = 0.005), whereas no significant differences were found for PTC non-tasters (499 ± 227 vs 519 ± 231 kcal; P = 0.525).Paolo Andreozzi, et al Journal of Neurogastroenterology and Motility 512 ConclusionsThis study showed that intra-duodenal release of a bitter compound is able to significantly affect calorie intake and CCK release after a standardized meal. Our results suggest that bitter taste receptor signaling may have a crucial role in the control of food intake. (J Neurogastroenterol Motil 2015;21:511-519)

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“…3,4,6) Meyerhof et al have systematically investigated the molecular receptive ranges of bitter taste receptors using natural or synthetic bitter chemicals to challenge all 25 human TAS2Rs in transfected cells. 3) Correlation between Taste Sensor and hTAS2Rs…”

Section: Response Profiles Of Htas2rs Stimulated With Drugs By In Vitmentioning

confidence: 99%

The Utility of the Artificial Taste Sensor in Evaluating the Bitterness of Drugs: Correlation with Responses of Human TASTE2 Receptors (hTAS2Rs)

et al. 2018

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The purpose of this study was to examine the ability of the artificial taste sensor to evaluate the bitterness of drugs by comparing the responses of the taste sensor with documented responses of human TASTE2 receptors (hTAS2Rs). For this purpose 22 bitter compounds, used as ingredients of pharmaceutical medicines in Japan and known ligands of hTAS2Rs, were selected for testing. Their solutions (0.01, 0.03, 0.1 mM) were evaluated by five different taste sensors (AC0, AN0, BT0, C00, AE1). Correlations between physicochemical parameters of the compounds and the responses of the taste sensors and hTAS2Rs were evaluated. From taste sensor measurements, diphenidol, haloperidol, diphenhydramine, dextromethorphan and papaverine, all ligands of hTAS2R 10 and/or hTAS2R14, were predicted to express strong bitterness, surpassing that of quinine. Responses of taste sensors BT0 were found to be significantly correlated with responses of hTAS2R14. High log P values (≧2.73) and responses of hTAS2R14 were also significantly correlated (** p<0.01, chi-square test). In conclusion, taste sensor BT0 is highly sensitive to bitterness and correlates significantly with hTAS2R14, making it useful for evaluating the bitterness of hydrophobic compounds which respond to hTAS2R14 and their inhibitors.

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BitterDB: a database of bitter compounds

Cited by 227 publications

References 47 publications

Bitter and sweet taste receptors regulate human upper respiratory innate immunity

Bitter and sweet taste receptors regulate human upper respiratory innate immunity

The Bitter Taste Receptor Agonist Quinine Reduces Calorie Intake and Increases the Postprandial Release of Cholecystokinin in Healthy Subjects

The Utility of the Artificial Taste Sensor in Evaluating the Bitterness of Drugs: Correlation with Responses of Human TASTE2 Receptors (hTAS2Rs)

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