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At least 325 records · Page 18Linked to original sources
PubMed1995

Coupling of bitter receptor to phosphodiesterase through transducin in taste receptor cells.

The rod and cone transducins are specific G proteins originally thought to be present only in photoreceptor cells of the vertebrate retina. Transducins convert light stimulation of photoreceptor opsins into activation of cyclic GMP phosphodiesterase (reviewed in refs. 5-7). A transducin-like G protein, gustducin, has been identified and cloned from rat taste cells. We report here that rod transducin is also present in vertebrate taste cells, where it specifically activates a phosphodiesterase isolated from taste tissue. Furthermore, the bitter compound denatonium in the presence of taste-cell membranes activates transducin but not Gi. A peptide that competitively inhibits rhodopsin activation of transducin also blocks taste-cell membrane activation of transducin, arguing for the involvement of a seven-transmembrane-helix G-protein-coupled receptor. These results suggest that rod transducin transduces bitter taste by coupling taste receptor(s) to taste-cell phosphodiesterase. Phosphodieterase-mediated degradation of cyclic nucleotides may lead to taste-cell depolarization through the recently identified cyclic-nucleotide-suppressible conductance.

Animals↗
PubMed2006

Independent evolution of bitter-taste sensitivity in humans and chimpanzees.

It was reported over 65 years ago that chimpanzees, like humans, vary in taste sensitivity to the bitter compound phenylthiocarbamide (PTC). This was suggested to be the result of a shared balanced polymorphism, defining the first, and now classic, example of the effects of balancing selection in great apes. In humans, variable PTC sensitivity is largely controlled by the segregation of two common alleles at the TAS2R38 locus, which encode receptor variants with different ligand affinities. Here we show that PTC taste sensitivity in chimpanzees is also controlled by two common alleles of TAS2R38; however, neither of these alleles is shared with humans. Instead, a mutation of the initiation codon results in the use of an alternative downstream start codon and production of a truncated receptor variant that fails to respond to PTC in vitro. Association testing of PTC sensitivity in a cohort of captive chimpanzees confirmed that chimpanzee TAS2R38 genotype accurately predicts taster status in vivo. Therefore, although Fisher et al.'s observations were accurate, their explanation was wrong. Humans and chimpanzees share variable taste sensitivity to bitter compounds mediated by PTC receptor variants, but the molecular basis of this variation has arisen twice, independently, in the two species.

Alleles↗
PubMed2006

Lipid lowering effects of Momordica charantia (Bitter Melon) in HIV-1-protease inhibitor-treated human hepatoma cells, HepG2.

1. Hyperlipidemic effects of HIV-1-protease inhibitors (PI) are associated with increased hepatic production of triglyceride (TG)-rich lipoproteins, rather than lipoprotein clearance. PI are known to increase apolipoprotein B (apoB) secretion, apoC-III mRNA expression and decrease apoA-1 secretion. Nutritional therapy remains an important strategy to manage PI-associated hyperlipidemia. 2. This study investigated the in vitro efficacy of Asian vegetable, Momordica charantia or bitter melon (BM) to ameliorate PI-associated apoB and lipid abnormalities in HepG2 cells. 3. Our study demonstrates that bitter melon juice (BMJ) significantly reduced apoB secretion and apoC-III mRNA expression and normalized apoA-I expression in PI-treated HepG2 cells. BMJ also significantly reduced cellular TG and microsomal TG transfer protein, suggesting that lipid bioavailability and lipidation of apoB assembly may play a role in decreased apoB secretion. 4. Identifying molecular targets of BM may offer alternative dietary strategies to decrease PI-associated hyperlipidemia and improve quality of life among HIV-1-infected patients.

Apolipoprotein A-I↗
PubMed2004

Worms taste bitter: ASH neurons, QUI-1, GPA-3 and ODR-3 mediate quinine avoidance in Caenorhabditis elegans.

An animal's ability to detect and avoid toxic compounds in the environment is crucial for survival. We show that the nematode Caenorhabditis elegans avoids many water-soluble substances that are toxic and that taste bitter to humans. We have used laser ablation and a genetic cell rescue strategy to identify sensory neurons involved in the avoidance of the bitter substance quinine, and found that ASH, a polymodal nociceptive neuron that senses many aversive stimuli, is the principal player in this response. Two G protein alpha subunits GPA-3 and ODR-3, expressed in ASH and in different, nonoverlapping sets of sensory neurons, are necessary for the response to quinine, although the effect of odr-3 can only be appreciated in the absence of gpa-3. We identified and cloned a new gene, qui-1, necessary for quinine and SDS avoidance. qui-1 codes for a novel protein with WD-40 domains and which is expressed in the avoidance sensory neurons ASH and ADL.

Amino Acid Sequence↗
PubMed1999

Biosynthesis of bitter acids in hops. A (13)C-NMR and (2)H-NMR study on the building blocks of humulone.

The biosynthesis of humulone, an antibacterial bitter acid from hops, was studied by isotope-incorporation experiments using (13)C-labelled glucose or (2)H(2)O. (13)C enrichments, (2)H enrichments and (13)C(13)C coupling patterns identify isovaleryl-CoA, malonyl-CoA and dimethylallyl pyrophosphate as precursors for humulone. Dimethylallyl pyrophosphate, which serves as a building block for the bitter acid, is generated via the deoxyxylulose pathway of terpenoid biosynthesis. The data confirm that a symmetrical intermediate is involved in humulone formation.

Acyl Coenzyme A↗
PubMed2006

Members of RTP and REEP gene families influence functional bitter taste receptor expression.

Functional characterization of chemosensory receptors is usually achieved by heterologous expression in mammalian cell lines. However, many chemoreceptor genes, including bitter taste receptors (TAS2Rs), show only marginal cell surface expression. Usually, these problems are circumvented by using chimeric receptors consisting of "export tags" and the receptor sequence itself. It seems likely that chemoreceptor cells express factors for cell surface targeting of native receptor molecules in vivo. For TAS2Rs, however, such factors are still unknown. The present study investigates the influence of RTP and REEP proteins on the functional expression of human TAS2Rs in heterologous cells. We expressed hTAS2Rs in HEK 293T cells and observed dramatic differences in responsiveness to agonist stimulation. By immunocytochemistry we show accumulation of the bitter beta-glucopyranoside receptor hTAS2R16 in the Golgi compartment. Coexpression of RTP and REEP proteins changed the responses of some hTAS2Rs upon agonist stimulation, which is likely due to efficient cell surface localization as demonstrated by cell surface biotinylation experiments. The coimmunoprecipitation of hTAS2R16 and RTP3 or RTP4 suggests that the mechanism by which these cofactors influence hTAS2R16 function might involve direct protein-protein interaction. Finally, expression analyses demonstrate RTP and REEP gene expression in human circumvallate papillae and testis, both of which are sites of TAS2R gene expression.

Animals↗
PubMed1997

Bitter taste of monosaccharide pentaacetate esters.

The pentaacetate esters of several, but not all, monosaccharides were recently found to stimulate insulin release from rat pancreatic islets. We have now compared the taste of solutions of either these esters or the corresponding unesterified monosaccharides. The sweet taste of the latter monosaccharides (0.22 M) ranged as follows: D-glucose approximately or = D-galactose approximately or = D-mannoheptulose > L-glucose. None of the esters (1.7 mM) displayed a sweet taste. However, the alpha- and beta-anomer of D-glucose pentaacetate, the alpha-anomer of D-mannose pentaacetate and the beta-anomer of L-glucose pentaacetate all displayed a bitter taste, whilst both alpha- and beta-D-galactose pentaacetate yielded doubtful results. Since such a situation is comparable to that characterizing the islet B-cell response to these esters, it is proposed that the intracellular interaction between the esters or their hydrolytic products and a protein involved in the recognition of bitter taste in taste buds may participate in their insulinotropic action.

Acetates↗
PubMed2005

Functional variant in a bitter-taste receptor (hTAS2R16) influences risk of alcohol dependence.

A coding single-nucleotide polymorphism (cSNP), K172N, in hTAS2R16, a gene encoding a taste receptor for bitter beta -glucopyranosides, shows significant association with alcohol dependence (P = .00018). This gene is located on chromosome 7q in a region reported elsewhere to exhibit linkage with alcohol dependence. The SNP is located in the putative ligand-binding domain and is associated with an increased sensitivity to many bitter beta -glucopyranosides in the presence of the N172 allele. Individuals with the ancestral allele K172 are at increased risk of alcohol dependence, regardless of ethnicity. However, this risk allele is uncommon in European Americans (minor-allele frequency [MAF] 0.6%), whereas 45% of African Americans carry the allele (MAF 26%), which makes it a much more significant risk factor in the African American population.

Black or African American↗
PubMed2000

Bitter taste, phytonutrients, and the consumer: a review.

Dietary phytonutrients found in vegetables and fruit appear to lower the risk of cancer and cardiovascular disease. Studies on the mechanisms of chemoprotection have focused on the biological activity of plant-based phenols and polyphenols, flavonoids, isoflavones, terpenes, and glucosinolates. Enhancing the phytonutrient content of plant foods through selective breeding or genetic improvement is a potent dietary option for disease prevention. However, most, if not all, of these bioactive compounds are bitter, acrid, or astringent and therefore aversive to the consumer. Some have long been viewed as plant-based toxins. As a result, the food industry routinely removes these compounds from plant foods through selective breeding and a variety of debittering processes. This poses a dilemma for the designers of functional foods because increasing the content of bitter phytonutrients for health may be wholly incompatible with consumer acceptance. Studies on phytonutrients and health ought to take sensory factors and food preferences into account.

Cardiovascular Diseases↗
PubMed1996

SW.B6-Soa(b) nontaster congenic strains completed and a sucrose octaacetate congenic quartet tested with other bitters.

Ten SW.B6 SOA nontaster strains congenic with the SWR/J SOA taster inbred strain were bred via repeated backcross-intercross cycles, with selection for nontasting in each cycle. Preference ratio distributions and phenotypic proportions across cycles at 0.1 mM SOA were consistent with monogenic predictions. The SW.B6 mice completed a congenic quartet with the SWR/J, B6.SW SOA taster and C57BL/6J SOA nontaster strains. The Soa locus controlled avoidance differences within the quartet for SOA, raffinose undecaacetate, glucose pentaacetate and brucine. Background genes not linked to Soa controlled avoidance differences for L-phenylalanine and ethanol. Avoidance of bitter picric acid was influenced by the Soa locus, but avoidance of acetic acid was not. The quartet pattern for quinine HCl was unclear, with indications of both Soa and background effects. Two forms of ribose tetraacetate yielded different patterns. Avoidance differences controlled by the Soa locus were found for the pyranose form; however, all four strains avoided the furanose form. The pleiotropic effects of Soa allele substitution within the quartet were limited to a subset of bitter compounds.

Acids↗
PubMed1998

Responses of cultured rat trigeminal ganglion neurons to bitter tastants.

The initial steps in taste and olfaction result from the activation by chemical stimuli of taste receptor cells (TRCs) and olfactory receptor neurons (ORNs). In parallel with these two pathways is the chemosensitive trigeminal pathway whose neurons terminate in the oral and nasal cavities and which are activated by many of the same chemical stimuli that activate TRCs and ORNs. In a recent single unit study we investigated the responses of rat chorda tympani and glossopharnygeal neurons to a variety of bitter-tasting alkaloids, including nicotine, yohimbine, quinine, strychnine and caffeine, as well as capsaicin, the pungent ingredient in hot pepper. Here we apply many of these same compounds to cultured rat trigeminal ganglion (TG) neurons and measure changes in intracellular calcium [Ca2+]i to determine whether TG neurons will respond to these same compounds. Of the 89 neurons tested, 34% responded to 1 mM nicotine, 7% to 1 mM caffeine, 5% to 1 mM denatonium benzoate, 22% to 1 mM quinine hydrochloride, 18% to 1 mM strychnine and 55% to 1 microM capsaicin. These data suggest that neurons from the TG respond to the same bitter-tasting chemical stimuli as do TRCs and are likely to contribute information sent to the higher CNS regarding the perception of bitter/irritating chemical stimuli.

Animals↗
PubMed2000

G protein betagamma complexes in circumvallate taste cells involved in bitter transduction.

G protein betagamma (Gbetagamma) complexes are considered to play an important role in second messenger signaling of phospholipase C (PLC). Monitoring the inositol 1,4,5-trisphosphate (IP(3)) response in circumvallate tissue homogenates upon stimulation with denatonium benzoate, it was demonstrated that a glutathione S-transferase-GRK3ct fusion protein-a Gbetagamma scavenger-attenuates the bitter tastant-induced second messenger reaction. Towards an identification of the Gbetagamma complex involved in rat bitter taste transduction, it was found that the G protein beta(3) subtype is specifically expressed in taste receptor cells of circumvallate papillae. Gbeta(3)-specific antibodies blocked the denatonium benzoate-induced IP(3) formation in a dose-dependent manner; the inhibitory effect was reversed by preincubation with the antigenic peptide. A less pronounced inhibition was observed using Gbeta(1)-specific antibodies. Analyzing individual taste cells by single cell reverse transcriptase-polymerase chain reaction approaches, overlapping expression patterns for PLCbeta(2), Galpha(gust), Gbeta(3) and Ggamma(3) could be demonstrated. Furthermore, the co-expression of all profiled signal transduction components in individual taste receptor cells could be detected. These data support the concept that the denatonium benzoate-induced IP(3) response is mediated by an activation of PLCbeta(2) via a Gbetagamma complex, possibly composed of Gbeta(3) as the predominant beta subunit and Ggamma(3), and imply that multiple second messenger pathways may exist in individual taste receptor cells.

Animals↗
PubMed2005

Characterization of bitter taste responses of intestinal STC-1 cells.

Cellular responses of STC-1 cells to two bitter tastants (denatonium and caffeine) were investigated using a calcium-imaging technique and compared with the response to bombesin. Caffeine is known to stimulate taste receptor cells, but the properties of its signaling have not been well studied. STC-1 cells responded to all three molecules in a dose-dependent manner, and when a reverse transcriptase-polymerase chain reaction (RT-PCR) for denatonium receptor was performed, the product of predicted size was detected in STC-1 cells. Furthermore, all three signaling pathways were blocked by a phospholipase C (PLC) inhibitor, demonstrating the essential involvement of PLC in cellular responses. To study the regulatory system of G protein signaling in STC-1 cells, we searched G protein-coupled receptor kinases (GRKs) by the degenerate-primer PCR method and found that GRK2 is expressed. We also demonstrated that three GRKs (GRK2, GRK3 and GRK5) are differentially distributed in the circumvallate papilla while only GRK2 is present in taste bud cells. Finally, we overexpressed GRK2 in SCT-1 cells and found that bombesin-induced response was strongly inhibited by GRK2 but denatonium-activated signaling was not affected. In the case of caffeine, response was decreased by expression of GRK2 only when cells were activated by 1 mM caffeine. Thus, we showed that STC-1 cells emerge as a cell model for studying the molecular mechanism of bitter taste signaling, and could indicate properties of caffeine-induced signaling in comparison with other signaling.

Animals↗
PubMed2006

Linoleic and oleic acids alter the licking responses to sweet, salt, sour, and bitter tastants in rats.

The free fatty acids (FFAs), linoleic and oleic acids, commonly found in dietary fats can be detected by rats on the basis of gustatory cues following conditioned taste aversion pairings. FFAs depolarize the membrane potential of isolated rat taste receptor cells by inhibiting delayed rectifying potassium channels. This study examined the licking response of rats to sweet, salt, sour, and bitter taste solutions when 88 muM linoleic acid, 88 muM oleic acid, or an 88 muM linoleic-oleic acid mixture was added to the solutions. The presence of linoleic, oleic, and the linoleic-oleic acid mixture in sweet solutions produced increases in the licking responses, whereas adding linoleic, oleic, and the linoleic-oleic acid mixture to salt, sour, or bitter taste solutions produced decreases in licking responses when compared with the licking responses to the solutions in the absence of the FFAs. We conclude that FFAs may act in the oral cavity to depolarize taste receptor cells and therefore to increase the perceived intensity of concomitant tastants, thus contributing to the enhanced palatability associated with foods containing high dietary fat.

Animals↗
PubMed1992

Fractionation by SFE and microcolumn analysis of the essential oil and the bitter principles of hops.

Supercritical fluid extraction (SFE) is evaluated and optimized for the enrichment and fractionation of the essential oil and the bitter principles of hops (Humulus lupulus), both of which contribute to the flavor of beer. Profiles of the essential oil of different hop varieties are compared. The bitter principles, the humulones and lupulones, are analyzed by miniaturized liquid chromatography (micro-LC) and by micellar electrokinetic chromatography (MEKC).

Chromatography↗
PubMed2005

Contrasting modes of evolution between vertebrate sweet/umami receptor genes and bitter receptor genes.

Taste reception is fundamental to diet selection in many animals. The genetic basis underlying the evolution and diversity of taste reception, however, is not well understood. Recent discoveries of T1R sweet/umami receptor genes and T2R bitter receptor genes in humans and mice provided an opportunity to address this question. Here, we report the identification of 20 putatively functional T1R genes and 167 T2R genes from the genome sequences of nine vertebrates, including three fishes, one amphibian, one bird, and four mammals. Our comparative genomic analysis shows that orthologous T1R sequences are relatively conserved in evolution and that the T1R gene repertoire remains virtually constant in size across most vertebrates, except for the loss of the T1R2 sweet receptor gene in the sweet-insensitive chicken and the absence of all T1R genes in the tongueless western clawed frog. In contrast, orthologous T2R sequences are more variable, and the T2R repertoire diverges tremendously among species, from only three functional genes in the chicken to 49 in the frog. These evolutionary patterns suggest the relative constancy in the number and type of sweet and umami tastants encountered by various vertebrates or low binding specificities of T1Rs but a large variation in the number and type of bitter compounds detected by different species. Although the rate of gene duplication is much lower in T1Rs than in T2Rs, signals of positive selection are detected during the functional divergences of paralogous T1Rs, as was previously found among paralogous T2Rs. Thus, functional divergence and specialization of taste receptors generally occurred via adaptive evolution.

Animals↗
PubMedDate not supplied

The Taste of Health: Nature's Bitter Gifts.

A plant-based diet is said to protect against aging, heart disease, and cancer. Yet, the given advice to eat more vegetables and fruit often goes unheeded. Some consumers have turned instead to dietary supplements that provide plant-based antioxidants in a more concentrated form. Although these supplements are beneficial to human health in small doses, such compounds can sometimes be toxic. Biologically active phytochemicals also tend to be bitter, acrid, or astringent. The food industry has been removing them from plant foods through selective breeding and debittering processes, in response to consumer demand. Concerning bitter phytonutrients, the consumer faces competing demands of taste, health, and food safety.

Journal Article↗
PubMed1996

Oil of bitter orange: new topical antifungal agent.

BACKGROUND: Superficial dermatophyte infection is one of the most common dermatologic diseases. Some of these infections are extremely resistant to therapy. METHODS AND PATIENTS: Sixty patients participated in this study; they were classified into three groups (20 patients in each). All groups had comparable numbers of patients with tinea corporis, cruris, and pedis. Group 1 was treated with a 25% emulsion of oil of bitter orange (OBO) three times daily; group 2 was treated with 20% OBO in alcohol three times daily and group 3 was treated with pure OBO, once daily. Clinical and mycologic examinations were performed before therapy and every week until a complete cure had occurred. RESULTS: In group 1, 80% of patients were cured in 1 to 2 weeks and 20% in 2 to 3 weeks. In group 2, 50% were cured in 1 to 2 weeks, 30% in 2 to 3 weeks and 20% in 3 to 4 weeks. In group 3, 25% of patients did not continue the trial. Of the remaining patients, 33.3% were cured in one week, 60% in 1 to 2 weeks, and 6.7% in 2 to 3 weeks. Oil of bitter orange produced no side effects except mild irritation seen with the use of the pure form. CONCLUSIONS: An in vitro study showed that OBO (natural product) exerts fungistatic and fungicidal activity against a variety of pathogenic dermatophyte species. It is a promising, cheap, and available topical antifungal therapeutic agent.

Administration, Topical↗