Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “bitterness”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1995

A novel psychophysical procedure for bitter taste assessment in rats.

A persistent problem with attempts to examine bitter taste mechanisms has been the lack of adequate behavioral methodology providing data which parallels that obtained from physiological investigations. We developed a brief contact procedure to assess the ability of rats to detect the presence of a weak bitter compound dissolved in a strong sucrose solution. Male Fischer 344 rats were trained to drink immediately to multiple 10-s presentations of acetaminophen (2, 8, 32, 128 mM), chlorpheniramine maleate (1, 3, 9, 27 mM) L-tryptophan (13.5, 27, 54, 108 mM), pseudoephedrine hydrochloride (1, 4, 16, 64 mM) and quinine hydrochloride (0.008, 0.04, 0.2, 1.0 mM) dissolved in 0.8 M sucrose. The number of licks to sucrose and water were also measured. A microcomputer controlled stimulus presentations and measured the animal's licks of each solution during each 10-s presentation. The responses to the bitter+sucrose mixture were significantly decreased at most concentrations with increasing levels of the bitter component. This was true for all five bitter-tasting compounds, but over different concentration ranges relatively unique to each compound. The present study is the first to characterize the sensory effects of acetaminophen, pseudoephedrine, and chlorpheniramine maleate, all purported to taste bitter to humans. These results demonstrate rats' acute ability to discriminate by taste not only the presence but the concentration of a dilute bitter compound dissolved in a strong sucrose solution.

Acetaminophen↗
PubMed2006

Response of CEDIA amphetamines assay after a single dose of bitter orange.

Bitter orange has recently been substituted as an ingredient in many "ephedra-free" dietary supplements used for weight loss. The primary active ingredient in bitter orange is synephrine. Previous reports have documented false-positive results from ephedrine with urine amphetamine assays. Because of the similarity in chemical structure of ephedrine and synephrine, it is hypothesized that ingestion of a bitter orange supplement may have the potential to cause false-positive results with urine amphetamine assays. The purpose of this study was to determine the response of the CEDIA Amphetamines Assay after ingestion of bitter orange. Six healthy adult male volunteers were administered a single oral dose of Nature's Way Bitter Orange, a 900-mg dietary supplement extract standardized to 6% synephrine. Urine specimens were collected at baseline and 3 and 6 hours post-administration. Additional urine specimens were collected from 1 subject at 9, 12, and 15 hours after administration. All specimens were analyzed by the CEDIA Amphetamines Assay. Urine specific gravity and pH also were measured. All urine specimens demonstrated a negative response to the CEDIA Amphetamines Assay. Urine specific gravity ranged from 1.007 to 1.028, and pH ranged from 5.0 to 7.0; thus, reducing the possibility that the negative results were caused by diluted specimens or reduced excretion of synephrine into alkaline urine. This information will be of value when health care providers or those who interpret drug screens are asked to provide consultation regarding the interference of bitter orange supplements with the CEDIA Amphetamines Assay. A single-dose of Nature's Way Bitter Orange was not found to cause a false-positive response to the CEDIA Amphetamines Assay in 6 healthy adult male volunteers.

Administration, Oral↗
PubMed1998

Electrophysiological responses to bitter stimuli in primate cortex.

Studies investigating fine details of gustatory coding in the domain of each basic taste quality have been completed for sweet, salt, and sour stimuli. In the present experiment, we used chemicals that humans describe as predominantly bitter. We recorded the activity of 50 taste neurons in insular cortex of two cynomolgus macaques. Stimuli were water, fruit juice, glucose, NaCl, HCl, and 16 bitter solutions. In a multidimensional taste space the 16 bitter stimuli formed a coherent cluster composed of three main subgroups: (1) QHCl, phenylalanine, theophylline, caffeine, propyl-thiouracil (PROP), and phenylthiocarbamide (PTC), all of which humans describe as rather purely bitter, (2) MgCl2, CaCl2, NH4Cl, and arginine, which humans describe as salty-bitter, and (3) urea, cysteine, and vitamin B1, which are described as sour-bitter. Vitamin B2, histidine and nicotine were in the center of the bitter cluster. Human descriptions of taste qualities conformed well to the presumed quality of each stimulus as inferred from its position in the multidimensional space (MDS), reinforcing the use of the macaque as a neural model for human gustation.

Animals↗
PubMed1999

IP(3)-Independent release of Ca(2+) from intracellular stores: A novel mechanism for transduction of bitter stimuli.

A variety of substances with different chemical structures elicits a bitter taste. Several different transduction mechanisms underlie detection of bitter tastants; however, these have been described in detail for only a few compounds. In addition, most studies have focused on mammalian taste cells, of which only a small subset is responsive to any particular bitter compound. In contrast, approximately 80% of the taste cells in the mudpuppy, Necturus maculosus, are bitter-responsive. In this study, we used Ca(2+) imaging and giga-seal whole cell recording to compare the transduction of dextromethorphan (DEX), a bitter antitussive, with transduction of the well-studied bitter compound denatonium. Bath perfusion of DEX (2.5 mM) increased the intracellular Ca(2+) level in most taste cells. The DEX-induced Ca(2+) increase was inhibited by thapsigargin, an inhibitor of Ca(2+) transport into intracellular stores, but not by U73122, an inhibitor of phospholipase C, or by ryanodine, an inhibitor of ryanodine-sensitive Ca(2+) stores. Increasing intracellular cAMP levels with a cell-permeant cAMP analogue and a phosphodiesterase inhibitor enhanced the DEX-induced Ca(2+) increase, which was inhibited partially by H89, a protein kinase A inhibitor. Electrophysiological measurements showed that DEX depolarized the membrane potential and inhibited voltage-gated Na(+) and K(+) currents in the presence of GDP-beta-S, a blocker of G-protein activation. DEX also inhibited voltage-gated Ca(2+) channels. We suggest that DEX, like quinine, depolarizes taste cells by block of voltage-gated K channels, which are localized to the apical membrane in mudpuppy. In addition, DEX causes release of Ca(2+) from intracellular stores by a phospholipase C-independent mechanism. We speculate that the membrane-permeant DEX may enter taste cells and interact directly with Ca(2+) stores. Comparing transduction of DEX with that of denatonium, both compounds release Ca(2+) from intracellular stores. However, denatonium requires activation of phospholipase C, and the mechanism results in a hyperpolarization rather than a depolarization of the membrane potential. These data support the hypothesis that single taste receptor cells can use multiple mechanisms for transducing the same bitter compound.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Biochemical and partial molecular characterization of bitter and sweet forms of Lupinus angustifolius, an experimental model for study of molecular regulation of quinolizidine alkaloid biosynthesis.

The bitter and sweet forms of a plant species differing with alkaloid contents may provide a model system for investigation of alkaloid biosynthesis at a molecular level. The pattern and concentration of quinolizidine alkaloids were determined by capillary GC-MS in bitter and sweet plants of Lupinus angustifolius. Bitter plant contained lupanine, 13alpha-hydroxylupanine, angustifoline, alpha-isolupanine, tetrahydrorhombifoline, and ester-derivatives of 13alpha-hydroxylupanine. In contrast, no alkaloid was detected in sweet plant. The enzymatic activity of acyltransferase for formation of 13alpha-tigloyloxylupanine was similar or even higher in the cell-free extracts of sweet plant than that in bitter plant. These results suggest that the biosynthetic step(s) of ring closure forming the initial cyclic alkaloid, lupanine, from cadaverine is presumably blocked in sweet plant, and that the later steps for modification of the cyclized alkaloids are not altered. We hypothesized that the gene(s) encoding enzyme(s) for ring-closure step might be repressed in sweet plant, and that the expression might take place only in bitter plant. To isolate the genes specifically expressed in bitter plant, cDNA-amplified fragment length polymorphism (cDNA-AFLP) analysis was carried out. However, no bitter-specific gene was isolated, suggesting that alkaloid biosynthesis in sweet plant may be down-regulated at a post-transcriptional level.

Alkaloids↗
PubMed2002

Method of evaluation of the bitterness of clarithromycin dry syrup.

The degree of bitterness of clarithromycin (CAM) dry syrup was evaluated using several methods. Using the inversion method, shaking method, and paddle method, a reasonable correlation between the bitter taste and the amount dissolved was not observed. A mini-column with inner diameter of 0.76 cm and height of 5 cm packed with CAM dry syrup was used for the release test. The release rate of CAM in test solution, which passed through the mini-column, was then measured to evaluate bitterness. The release rate of CAM in the release test using the mini-column correlated well with the results of a sensory test for the bitterness of CAM dry syrup. The dissolution rate constant, defined as the percentage of CAM dissolved from the unit void surface multiplied by the void volume, was inversely proportional to the linear velocity of the test solution. The critical factors affecting evaluation of bitterness were the void volume of the column and linear velocity of the test solution. The optimum linear velocity and void volume were 0.048-0.021 cm/min and 0.27-0.12 cm3, respectively. In addition, the threshold of bitterness of CAM dry syrup was defined as the concentration at which half of the volunteers recognized bitterness in the sensory test. This threshold was found to be 135 microg/ml using the mini-column.

Anti-Bacterial Agents↗
PubMed2003

The bitterness intensity of clarithromycin evaluated by a taste sensor.

The purpose of this study was to evaluate the ability of a quantitative prediction method using a taste sensor to determine the bitterness of clarithromycin powder suspensions of various concentrations and of a commercial clarithromycin dry syrup product (Clarith dry syrup, Taisho Pharmaceutical Co., Ltd., Tokyo) containing aminoalkyl methacrylate polymer as a taste-masker. The bitterness of the clarithromycin dry syrup product dissolved in various beverages was also evaluated in gustatory sensation tests and using the taste sensor. In the sensor measurements, three variables were used to predict bitterness in single and multiple regression analysis: relative sensor output (R), the change of membrane potential caused by adsorption (CPA), and CPA/R ratio. The CPA values for channel 3 of the sensor predicted well the bitterness of clarithromycin powder suspensions and their filtered solutions. For Clarith dry syrup, the sensor output was small, suggesting that aminoalkyl methacrylate polymer was successful in almost complete masking of the bitter taste of the dry syrup product. When the bitterness intensities of mixtures of 1 g of Clarith dry syrup with 25 ml of water, coffee, tea, green tea, cocoa, milk, and a sports drink were examined, a good correlation was obtained between the results from human taste tests and the predicted values calculated on the basis of multiple regression analysis using CPA data from channel 4, and the CPA/R ratio from channel 3 of the taste sensor (r(2)=0.963, p<0.005). Co-administration of 1 g of Clarith dry syrup with an acidic sports drink was found to be the most bitter using either method.

Adsorption↗
PubMed2004

Bitterness evaluation of medicines for pediatric use by a taste sensor.

The purpose of this study was to evaluate the bitterness of 18 different antibiotic and antiviral drug formulations, widely used to treat infectious diseases in children and infants, in human gustatory sensation tests and using an artificial taste sensor. Seven of the formulations were found to have a bitterness intensity exceeding 1.0 in gustatory sensation tests (evaluated against quinine as a standard) and were therefore assumed to have an unpleasant taste to children. The bitterness intensity scores of the medicines were examined using suspensions in water or an acidic sports drink. In the case of three macrolide antibiotic formulations containing erythromycin (ERYTHROCIN dry syrup), clarithromycin (CLARITH dry syrup for pediatric), and azithromycin (ZITHROMAC fine granules for pediatric use), the bitterness intensities of suspensions in acidic sports drinks were dramatically enhanced compared with the corresponding scores of suspensions in water. This enhancement could be predicted using the taste sensor. On the other hand, a reduction of bitterness intensity was observed for an acidic sports drink suspension of an amantadine product (SYMMETREL fine granules) compared with an aqueous suspension. This reduction in bitterness could also be predicted using the taste sensor output value. Thus, the taste sensor could predict whether or not suspension in an acidic sports drink would enhance or reduce the bitterness intensity of pediatric drug formulations, compared with suspensions in water.

Amantadine↗
PubMed2006

Evaluation of bitterness suppression of macrolide dry syrups by jellies.

The purpose of this study was to evaluate the bitterness-suppressing effect of three jellies, all commercially available on the Japanese market as swallowing aids, on two dry syrups containing the macrolides clarithromycin (CAM) or azithromycin (AZM). The bitterness intensities of mixtures of the dry syrups and acidic jellies were significantly greater than those of water suspensions of the dry syrups in human gustatory sensation tests. On the other hand, the mixture with a chocolate jelly, which has a neutral pH, was less bitter than water suspensions of the dry syrups. The bitterness intensities predicted by the taste sensor output values correlated well with the observed bitterness intensities in human gustatory sensation tests. When the concentrations of CAM and AZM in solutions extracted from physical mixtures of dry syrup and jelly were determined by HPLC, concentrations in the solutions extracted from mixtures with acidic jellies were higher than those from mixtures with a neutral jelly (almost 90 times higher for CAM, and almost 7-10 times higher for AZM). Thus, bitterness suppression is correlated with the pH of the jelly. Finally, a drug dissolution test for dry syrup with and without jelly was performed using the paddle method. There was no significance difference in dissolution profile. It was concluded the appropriate choice of jelly with the right pH is essential for taste masking. Suitable jellies might be used to improve patient compliance, especially in children. The taste sensor may be used to predict the bitterness-suppressing effect of the jelly.

Adult↗
PubMed2026

Mechanistic insights into flavor deterioration in bitter sturgeon caviar: Evidence from lipidomics and metagenomics.

This study systematically compared the flavor and multi-omics differences between normal caviar and bitter caviar based on quantitative descriptive analysis (QDA), volatile compounds (VOCs) analysis, untargeted lipidomics, and metagenomics. The results showed that bitter caviar was characterized not only by increased bitterness, but also by decreased positive sensory attributes, including buttery, nutty, and marine fresh. VOCs analysis indicated that the volatile profile of bitter caviar was reorganized. Compounds such as 3-hydroxy-2-butanone, 1-octen-3-ol, and (E, Z)-2,6-nonadienal showed higher relative odor activity values (rOAVs); however, these changes did not improve its overall sensory experience. Untargeted lipidomics identified 492 differential lipids. These changes were mainly characterized by decreased PC and increased DG and LPC in bitter caviar. KEGG pathways analysis showed that these differential lipids were mainly associated with glycerophospholipid metabolism, choline metabolism in cancer, and retrograde endocannabinoid signaling. Metagenomic analysis showed that bacteria dominated the microbial community of caviar. Among them, Bacillus and Micromonospora showed relatively high abundance in the caviar microbiota. They were also closely associated with lipid metabolic changes involving PC, DG, and LPC, suggesting their potential as candidate targets for future microbiota-directed regulation of caviar quality. These findings provide new insights into the mechanisms underlying sensory deterioration and flavor formation in bitter caviar, and offer a theoretical basis for improving caviar quality in industrial production.

Animals↗
PubMed2026

Genome-Wide Association Analyses of Bitter Food Preferences Link Genetic Loci to Sensory and Metabolic Pathways.

BACKGROUND: Genetic variation is implicated in individual preferences for bitter-tasting foods. However, previous studies have focused on candidate genes and limited varieties of bitter-tasting foods and have treated food preference scale responses as continuous data. OBJECTIVES: The present investigation aimed to identify genetic variants associated with preferences for bitter-tasting foods using ordinal multinomial regression models in genome-wide association studies (GWAS). In addition, post-GWAS functional annotation and mapping, genetic correlations, and associations with dietary intake were examined. METHODS: Food preference and genome-wide genotyping data were used from the UK Biobank (n = 125,578). Preference data from Likert scale rankings (from 1 to 9) for 12 individual foods were analyzed using ordinal multinomial regression GWAS. In addition, 1 composite continuous variable was created for preference for cruciferous vegetables as a group and analyzed using a linear mixed-model GWAS to enable the calculation of a polygenic score (PGS) for cruciferous vegetable preference. Convergent validity of GWAS results was assessed with dietary intake data for the same food items in the CARTaGENE cohort (n = 8176). Post-GWAS gene-level and pathway-level association analyses were conducted in MAGMA (Multimarker Analysis of GenoMic Annotation). RESULTS: Forty-six single-nucleotide polymorphisms (SNPs) were identified for preferences for 11 bitter-tasting foods at a genome-wide significance level (P < 7.14 &#xd7; 10-9). Gene-set analysis for enrichment identified pathways related to caffeine metabolism and bitter taste perception for preference of coffee without sugar and grapefruit, respectively. Genes with higher expression in brain tissues showed stronger genetic associations with cruciferous vegetable preference. The PGS for cruciferous vegetable preference was weakly correlated with intake (r = 0.05, P < 0.0001), but individual SNPs were not associated with intake in a consistent manner. CONCLUSIONS: Genetic variation contributes to preferences for bitter-tasting foods among adults, and some links with food intake are detectable. Nevertheless, effect sizes are small and inconsistent, reflecting the multifactorial complexity of food intake.

bitter taste↗
PubMed2005

Bitter gourd (Momordica charantia) modulates activities of intestinal and renal disaccharidases in streptozotocin-induced diabetic rats.

During diabetes, structural and functional changes in the alimentary tract are known to take place resulting in increased absorption of intestinal glucose and alterations in the activities of brush border disaccharidases. Similar observations are also reported in the renal cortex. In the present investigation, we examined the effect of feeding bitter gourd fruit devoid of seeds on activities of intestinal and renal disaccharidases, viz., maltase, sucrase, and lactase in streptozotocin-induced diabetic rats. Normal and diabetic rats were fed either with basal diet or a diet containing 10% bitter gourd powder. Specific activities of intestinal disaccharidases were significantly increased during diabetes, and supplementing bitter gourd in the diet clearly indicated amelioration in the activities of maltase and lactase during diabetes. However, a significant change was not observed with sucrase activity by feeding of bitter gourd. During diabetes, renal disaccharidase activities were significantly lower than those in the control rats. Bitter gourd supplementation was beneficial in alleviating the reduction in maltase activity during diabetes. However, not much change in the activities of sucrase and lactase was observed upon feeding. This positive influence of feeding bitter gourd on intestinal and renal disaccharidases clearly indicates their beneficial role in the management of diabetes, thus making diabetic animals more tolerant to hyperglycemia.

Animals↗
PubMed2005

Bitterness and toxicity in wild yam (Dioscorea spp.) tubers of Nepal.

Wild yams make a significant contribution to diets of tribal people in Nepal. However, these wild tubers are unpalatable, taste bitter, produce inflammation and show occasional toxicity. Four wild yam species, which are eaten after primary treatment by Nepali aborigines, were analyzed for bitter and toxic principles. Bitter components were identified as furanoid norditerpenes (diosbulbins A and B). Diosbulbins A and B were found in the range of 0.023-0.046 and 0.151-0.442 g kg(-1), respectively. Results demonstrated that diosbulbin B, with an average value of 0.314 g kg(-1), was the principal bitter compound as compared to diosbulbin A (0.037 g kg(-1)). The toxic alkaloid, dioscorine and histamine (an allergen) were not detected in these tubers, whereas cyanogens (as HCN equivalent) content were found ranging from 3.2 to 6.0 ppm. Our results revealed that Nepali wild yam tubers are not toxic varieties, as they do not contain either toxic dioscorine or histamine and cyanogens contents were satisfactorily below the safety limits. The inflammation and occasional toxicity observed could possibly be due to the presence of high level of oxalate in these tubers. Domestic cooking methods were found to be very efficient in removing bitterness, thus making the bitter yams palatable.

Consumer Product Safety↗
PubMed1985

Neuroblastoma cell as a model for a taste cell: mechanism of depolarization in response to various bitter substances.

The mouse neuroblastoma cell (N-18 clone) was used as a model for a taste cell. The N-18 cell was found to be reversibly depolarized by various bitter substances. The minimum concentrations of bitter substances which induced depolarization (threshold concentration) varied greatly with the type of the substance. There was a good correlation between the threshold concentrations for various bitter substances in the N-18 cell and those in the human taste responses. The input membrane resistance was little changed during the depolarization induced by the bitter substances. Replacement of Na+ and Cl- with impermeable ions had practically no effect on the depolarization response to the bitter substances and reduction of calcium concentration from 1.8 to 0.2 mM led to a slight increase in the responses. It was suggested that the depolarization of the N-18 cell by bitter substances mainly stems from changes in the phase-boundary potential at the outer surface of the cell.

Animals↗
PubMed2006

Potential applications of immobilized bitter gourd (Momordica charantia) peroxidase in the removal of phenols from polluted water.

The potential applications of immobilized bitter gourd peroxidase in the treatment of model wastewater contaminated with phenols have been investigated. The synthetic water was treated with soluble and immobilized enzyme preparations under various experimental conditions. Maximum removal of phenols was found in the buffers of pH values 5.0-6.0 and at 40 degrees C in the presence of 0.75 mM H(2)O(2). Fourteen different phenols were independently treated with soluble and immobilized bitter gourd peroxidase in the buffer of pH 5.6 at 37 degrees C. Chlorinated phenols and native phenol were significantly removed while other substituted phenols were marginally removed by the treatment. Phloroglucinol and pyrogallol were recalcitrant to the action of bitter gourd peroxidase. Immobilized bitter gourd peroxidase preparation was capable of removing remarkably high percentage of phenols from the phenolic mixtures. Significantly higher level of total organic carbon was removed from the model wastewater containing individual phenol or complex mixture of phenols by immobilized bitter gourd peroxidase as compared to the soluble enzyme. 2,4-dichlorophenol and a phenolic mixture were also treated in a stirred batch reactor with fixed quantity of enzyme for longer duration. The soluble bitter gourd peroxidase ceased to function after 3h while the immobilized enzyme was active even after 6h of incubation with phenolic solutions.

Carbon↗
PubMed1997

Behavioral specificity of the bitter taste gene Soa.

In mice, aversion to the bitter acetylated sugar sucrose octaacetate (SOA) is determined by a single genetic locus with three alleles. SWR/J (SW) inbred mice are SOA tasters: They avoid many compounds characterized as bitter-tasting by humans, at concentrations to which C3HeB/FeJ (C3:SOA demitasters) mice are less sensitive. C3.SW-Soa(a) congenic taster mice contain the taster allele transposed to a 99% C3 bitter-insensitive genetic background. SW, C3, C3.SW-Soa(a) congenic taster, and C3.SW demitaster mice were behaviorally tested with a series of 48-h two-bottle preference tests to determine the influence of the Soa(a) taster allele on sensitivity to a variety of bitter-tasting compounds. Soa allelic variation had a major effect on sensitivity to 0.003-1.0 mM SOA and several concentrations of the bitter-tasting alkaloids brucine, strychnine, and quinine. Effects were also found for 0.1 mM denatonium and 1 mM propylthiouracil. For caffeine, cycloheximide, thiamine, and two nonbitter compounds (NaCl and calcium hydroxide), the SW mice avoided lower concentrations than the other strains, but this avoidance was not due to the Soa(a) allele because both the C3 inbred and C3.SW-Soa(a) congenics were less sensitive. These results suggest the Soa gene product influences sensitivity to a subset of bitter-tasting compounds.

Alleles↗
PubMed2003

Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways.

Mammals can taste a wide repertoire of chemosensory stimuli. Two unrelated families of receptors (T1Rs and T2Rs) mediate responses to sweet, amino acids, and bitter compounds. Here, we demonstrate that knockouts of TRPM5, a taste TRP ion channel, or PLCbeta2, a phospholipase C selectively expressed in taste tissue, abolish sweet, amino acid, and bitter taste reception, but do not impact sour or salty tastes. Therefore, despite relying on different receptors, sweet, amino acid, and bitter transduction converge on common signaling molecules. Using PLCbeta2 taste-blind animals, we then examined a fundamental question in taste perception: how taste modalities are encoded at the cellular level. Mice engineered to rescue PLCbeta2 function exclusively in bitter-receptor expressing cells respond normally to bitter tastants but do not taste sweet or amino acid stimuli. Thus, bitter is encoded independently of sweet and amino acids, and taste receptor cells are not broadly tuned across these modalities.

Action Potentials↗
PubMed2001

Characterization of an intense bitter-tasting 1H,4H-quinolizinium-7-olate by application of the taste dilution analysis, a novel bioassay for the screening and identification of taste-active compounds in foods.

Thermal treatment of aqueous solutions of xylose and primary amino acids led to rapid development of a bitter taste of the reaction mixture. To characterize the key compound causing this bitter taste, a novel bioassay, which is based on the determination of the taste threshold of reaction products in serial dilutions of HPLC fractions, was developed to select the most intense taste compounds in the complex mixture of Maillard reaction products. By application of this so-called taste dilution analysis (TDA) 21 fractions were obtained, among which 1 fraction was evaluated with by far the highest taste impact. Carefully planned LC-MS as well as 1D and 2D NMR experiments were, therefore, focused on the compound contributing the most to the intense bitter taste of the Maillard mixture and led to its unequivocal identification as the previously unknown 3-(2-furyl)-8-[(2-furyl)methyl]-4-hydroxymethyl-1-oxo-1H,4H-quinolizinium-7-olate. This novel compound, which we name quinizolate, exhibited an intense bitter taste at an extraordinarily low detection threshold of 0.00025 mmol/kg of water. As this novel taste compound was found to have 2000- and 28-fold lower threshold concentrations than the standard bitter compounds caffeine and quinine hydrochloride, respectively, quinizolate might be one of the most intense bitter compounds reported so far.

Caffeine↗