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PubMed2000

Bitter taste perception and severe vomiting in pregnancy.

Hyperemesis gravidarum or severe vomiting during pregnancy is a condition of elusive etiology that can harm both mother and fetus. This study examined the association between increased bitter-taste perception and history of hyperemesis gravidarum. Bitter-taste perception varies genetically and can be altered with conditions that damage taste-related cranial nerves. Sixty women were divided into high- (n = 21) and low-vomit (n = 39) groups based on vomiting exposure across all pregnancies and were screened for genetic variation in taste with bitterness of saturated 6-n-propylthiouracil (PROP) delivered on filter paper. Supertasters perceive PROP as intensely bitter; nontasters, as only weakly. Each reported their history of dysgeusia (persistent taste) and taste-related pathology (otitis media and head trauma). The vomit groups did not differ in the frequency of supertasters, but the high-vomit group had fewest nontasters. The high-vomit group also reported dysgeusia most frequently. A subsample (13 high-vomit and 18 low-vomit women) rated the taste intensity of sodium chloride (1 mol), sucrose (1 mol), citric acid (0.0032 mol), and quinine hydrochloride (0.001 mol) applied to areas innervated by cranial nerves VII and IX. The groups only varied significantly in bitterness of quinine hydrochloride. High-vomit women tasted least bitterness on the anterior tongue (chorda tympani branch of VII) and highest bitterness on the posterior tongue (cranial nerve IX) and palate (superficial petrosal branch of VII). In high-vomit women, elevated bitterness on the posterior tongue and palate does not appear related to hydrochloric acid exposure in vomitus; it may explain the occurrence of dysgeusia. This pattern of spatial taste perception may indicate altered oral sensations that if present during pregnancy, could increase the risk of hyperemesis.

Adult↗
PubMed1998

Effects of neem flowers, Thai and Chinese bitter gourd fruits and sweet basil leaves on hepatic monooxygenases and glutathione S-transferase activities, and in vitro metabolic activation of chemical carcinogens in rats.

The objectives of this study were to determine the effects of feeding of four vegetables commonly consumed in Thailand, namely, flowers of the neem tree (Azadirachta indica var. siamensis), fruits of Thai and the Chinese bitter gourd (Momordica charantia Linn.) and leaves of sweet basil (Ocimum basilicum Linn) on the levels of phase I enzymes, which include cytochrome P450 (P450), aniline hydroxylase (ANH) and aminopyrine-N-demethylase (AMD) as well as the capacity to activate the mutagenicities of aflatoxin B1 (AFB1) and benzo[a]pyrene (BaP), and to induce the phase II enzymes [i.e. glutathione S-transferase (GST)] in rat liver. It was found that feeding of the diets containing 12.5% neem flowers and Thai bitter gourd fruits for 2 weeks strongly enhanced GST activity, 2.7- and 1.6- fold of the pair-fed control values, respectively, while resulting in a marked reduction of the levels of most phase I reactions. Fruits of the Chinese bitter gourd, which is in the same species as Thai bitter gourd, had no effect on GST activity but decreased AMD activity and the in vitro metabolic activation of AFB1 and BaP. On the other hand, however, dietary sweet basil leaves caused a significant increase in the levels of both GST and all phase I enzymes. Results in the present study clearly demonstrate that neem flowers and Thai bitter gourd fruits contain monofunctional phase II enzyme inducers and compounds capable of repressing some monooxygenases, especially those involved in the metabolic activation of chemical carcinogens, while sweet basil leaves contain compounds, probably bifunctional inducers, capable of inducing both phase I and phase II enzymes and Chinese bitter gourd fruits contain only compounds capable of repressing some monooxygenases. These results therefore suggest that neem flowers and Thai bitter gourd fruits may possess chemopreventive potential, while those of Chinese bitter gourd fruits and sweet basil leaves are uncertain.

Aflatoxin B1↗
PubMed1990

Synthetic chemoreceptive membranes. Sensing bitter or odorous substances on a synthetic lipid multibilayer film by using quartz-crystal microbalances and electric responses.

Specific adsorptions of bitter or odorous substances on a synthetic lipid multibilayer matrix (2C18N+2C1/PSS-) were detected by observing frequency changes of a multibilayer-coated quartz-crystal microbalance (QCM). Partition coefficient (P) and diffusion constants (D) of these substances in the lipid matrix could be obtained quantitatively by using the QCM method. There were good correlations between partition coefficients of various bitter or odor substances to the synthetic multibilayer film on the QCM and the intensity of bitter tastes or olfactory receptions in humans: the stronger the intensity of a bitter substance or odorant, the greater the adsorption on the lipid matrix. This indicates that the lipid-coated QCM acts as a sensitive and selective sensor for bitter taste and odor. Electric responses (changes of membrane potential and membrane resistance) of the 2C18N+2C1/PSS-film occurred consecutively by the adsorption of these substances. The bitter or odor substance showing the stronger intensity induced membrane potential change in lower concentrations. It was found that bitter substances having sterically bulky molecular structures adsorb on the surface of the lipid matrix, and the phase-boundary potential of the membrane is thereby changed. On the contrary, odor substances with relatively small or slender structures can penetrate into the lipid matrix and cause reduction of the membrane resistance (the increase of ion permeability). The selective adsorption behavior of bitter and odor substances by molecular shapes was confirmed by adsorption studies of simple C9-10 hydrophobic alcohols having various molecular structures.

Adsorption↗
PubMed2005

The receptors and coding logic for bitter taste.

The sense of taste provides animals with valuable information about the nature and quality of food. Bitter taste detection functions as an important sensory input to warn against the ingestion of toxic and noxious substances. T2Rs are a family of approximately 30 highly divergent G-protein-coupled receptors (GPCRs) that are selectively expressed in the tongue and palate epithelium and are implicated in bitter taste sensing. Here we demonstrate, using a combination of genetic, behavioural and physiological studies, that T2R receptors are necessary and sufficient for the detection and perception of bitter compounds, and show that differences in T2Rs between species (human and mouse) can determine the selectivity of bitter taste responses. In addition, we show that mice engineered to express a bitter taste receptor in 'sweet cells' become strongly attracted to its cognate bitter tastants, whereas expression of the same receptor (or even a novel GPCR) in T2R-expressing cells resulted in mice that are averse to the respective compounds. Together these results illustrate the fundamental principle of bitter taste coding at the periphery: dedicated cells act as broadly tuned bitter sensors that are wired to mediate behavioural aversion.

Animals↗
PubMed2006

Short-term vegetable intake by young children classified by 6-n-propylthoiuracil bitter-taste phenotype.

BACKGROUND: Genetic variation in sensitivity to the bitterness of 6-n-propylthiouracil (PROP) is thought to play a role in the acceptance and rejection of bitter-tasting vegetables by young children. OBJECTIVES: We investigated the relation between the PROP bitter-taste phenotype and acceptance and consumption of vegetables by young children. We hypothesized that nontasters of PROP would give higher hedonic ratings to bitter-tasting vegetables and would consume more bitter vegetables than would tasters of PROP. DESIGN: Sixty-five preschool children were identified as tasters (n = 24) or nontasters (n = 41) of PROP. Children were allowed to select from among 5 types of vegetables (black olives, cucumbers, carrots, red pepper, and raw broccoli) to consume in a free-choice intake test and to give hedonic ratings to the vegetables. RESULTS: The nontaster children consumed more vegetables than did the taster children during the free-choice test (0.91 servings compared with 0.48 servings; P < 0.05). This difference reflected the higher consumption of the more bitter-tasting vegetables (olives, cucumber, and broccoli) by the nontaster children (P < 0.05). Only 8% of the nontaster children consumed no vegetables in the free-choice test compared with 32% of taster children (P < 0.03). The nontaster children also liked raw broccoli more than did the taster children in the hedonic test (P < 0.05). CONCLUSIONS: The nontaster children consumed more vegetables, particularly the vegetables that were bitter tasting, than did the taster children during a free-choice intake test. These novel findings suggest that the PROP bitter-taste phenotype contributes to the development of vegetable acceptance and consumption patterns during early childhood.

Child, Preschool↗
PubMed2003

Bitter melon (Momordica charantia): a review of efficacy and safety.

The pharmacology, clinical efficacy, adverse effects, drug interactions, and place in therapy of bitter melon are described. Bitter melon (Momordica charantia) is an alternative therapy that has primarily been used for lowering blood glucose levels in patients with diabetes mellitus. Components of bitter melon extract appear to have structural similarities to animal insulin. Antiviral and antineoplastic activities have also been reported in vitro. Four clinical trials found bitter melon juice, fruit, and dried powder to have a moderate hypoglycemic effect. These studies were small and were not randomized or double-blind, however. Reported adverse effects of bitter melon include hypoglycemic coma and convulsions in children, reduced fertility in mice, a favism-like syndrome, increases in gamma-glutamyltransferase and alkaline phosphatase levels in animals, and headaches. Bitter melon may have additive effects when taken with other glucose-lowering agents. Adequately powered, randomized, placebo-controlled trials are needed to properly assess safety and efficacy before bitter melon can be routinely recommended. Bitter melon may have hypoglycemic effects, but data are not sufficient to recommend its use in the absence of careful supervision and monitoring.

Animals↗
PubMed2001

The science and complexity of bitter taste.

Food choices and eating habits are largely influenced by how foods taste. Without being the dominant taste sensation, bitter taste contributes to the complexity and enjoyment of beverages and foods. Compounds that are perceived as bitter do not share a similar chemical structure. In addition to peptides and salts, bitter compounds in foods may include plant-derived phenols and polyphenols, flavonoids, catechins, and caffeine. Recent studies have shown that humans possess a multitude of bitter taste receptors and that the transduction of bitter taste may differ between one compound and another. Studies of mixture interactions suggest further that bitter compounds suppress or enhance sweet and sour tastes and interact with volatile flavor molecules. Caffeine, a natural ingredient of tea, coffee, and chocolate, has a unique flavor profile. Used as a flavoring agent, it enhances the sensory appeal of beverages. Research developments on the genetics and perception of bitter taste add to our understanding of the role of bitterness in relation to food preference.

Aging↗
PubMed2001

Taste receptor cells that discriminate between bitter stimuli.

Recent studies showing that single taste bud cells express multiple bitter taste receptors have reignited a long-standing controversy over whether single gustatory receptor cells respond selectively or broadly to tastants. We examined calcium responses of rat taste receptor cells in situ to a panel of bitter compounds to determine whether individual cells distinguish between bitter stimuli. Most bitter-responsive taste cells were activated by only one out of five compounds tested. In taste cells that responded to multiple stimuli, there were no significant associations between any two stimuli. Bitter sensation does not appear to occur through the activation of a homogeneous population of broadly tuned bitter-sensitive taste cells. Instead, different bitter stimuli may activate different subpopulations of bitter-sensitive taste cells.

Animals↗
PubMed2002

Contribution of Lactococcus lactis cell envelope proteinase specificity to peptide accumulation and bitterness in reduced-fat Cheddar cheese.

Bitterness is a flavor defect in Cheddar cheese that limits consumer acceptance, and specificity of the Lactococcus lactis extracellular proteinase (lactocepin) is widely believed to be a key factor in the development of bitter cheese. To better define the contribution of this enzyme to bitterness, we investigated peptide accumulation and bitterness in 50% reduced-fat Cheddar cheese manufactured with single isogenic strains of Lactococcus lactis as the only starter. Four isogens were developed for the study; one was lactocepin negative, and the others produced a lactocepin with group a, e, or h specificity. Analysis of cheese aqueous extracts by reversed-phase high-pressure liquid chromatography confirmed that accumulation of alpha(S1)-casein (f 1-23)-derived peptides f 1-9, f 1-13, f 1-16, and f 1-17 in cheese was directly influenced by lactocepin specificity. Trained sensory panelists demonstrated that Cheddar cheese made with isogenic starters that produced group a, e, or h lactocepin was significantly more bitter than cheese made with a proteinase-negative isogen and that propensity for bitterness was highest in cells that produced group h lactocepin. These results confirm the role of starter proteinase in bitterness and suggest that the propensity of some industrial strains for production of the bitter flavor defect in cheese could be altered by proteinase gene exchange or gene replacement.

Cheese↗
PubMed1996

Rapid kinetics of second messenger production in bitter taste.

The tasting of bitter compounds may have evolved as a protective mechanism against ingestion of potentially harmful substances. We have identified second messengers involved in bitter taste and show here for the first time that they are rapid and transient. Using a quench-flow system, we have studied bitter taste signal transduction in a pair of mouse strains that differ in their ability to taste the bitter stimulus sucrose octaacetate (SOA); however, both strains taste the bitter agent denatonium. In both strains of mice, denatonium (10 mM) induced a transient and rapid increase in levels of the second messenger inositol 1,4,5-trisphosphate (IP3) with a maximal production near 75-100 ms after stimulation. In contrast, SOA (100 microM) brought about a similar increase in IP3 only in SOA-taster mice. The response to SOA was potentiated in the presence of GTP (1 microM). The GTP-enhanced SOA-response supports a G protein-mediated response for this bitter compound. The rapid kinetics, transient nature, and specificity of the bitter taste stimulus-induced IP3 formation are consistent with the role of IP3 as a second messenger in the chemoelectrical transduction of bitter taste.

Animals↗
PubMed2003

Effect of bitter melon (Momordica charantia Linn) on level and function of natural killer cells in cervical cancer patients with radiotherapy.

Cervical cancer patients have a defective immune system. There is a decrease of total white blood cell count including lymphocytes and natural killer (NK) cells. NK cells, one type of lymphocytes, play a role to eliminate cancer cells by antibody dependent cell mediated cytotoxicity (ADCC) mechanism. Previous studies have shown that P-glycoprotein (170 kDa, transmembrane protein) may be a transporter for cytokine releasing in ADCC mechanism. This study proposed to explore the role of bitter melon intake in cervical cancer patients undergoing normal treatment (radiotherapy). Subjects were divided into three groups: 1) normal control (women 35-55 years, n = 35), 2) patient control (n = 30) and 3) patient treatment (n = 30) groups. Patient control and patient treatment groups were cervical cancer patients (stage II or III) treated with radiotherapy (without or with bitter melon ingestion). Blood samples of patient control and patient treatment groups were analyzed for NK cells percentage and P-glycoprotein level. Bitter melon is a Thai herb. Previous studies have shown that bitter melon can stimulate lymphocyte activity in vitro and in vivo (mouse). The authors hope that bitter melon could stimulate the increase of NK cells percentage and P-glycoprotein level on the membrane in blood samples from cervical cancer patients who ingest bitter melon. The results showed an increased percentage of NK cells in patient control and patient treatment groups. The increase in each group is significant (p < 0.05) when compared with the percentage of NK cells from second and third blood sampling time (after radiation with of without bitter melon intake for 45 and 90 days) with first blood sampling time (before treatment). The results also show a significant decrease of P-glycoprotein level (p < 0.05) in second and third blood sampling times when compared with first blood sampling time of the patient treatment group. There was no significant difference of P-glycoprotein (P-gp) level from first, second and third blood sampling times in patient control group. Bitter melon ingestion did not affect NK cell level but it affected the decrease of P-gp level on NK cell membrane.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2003

Modification of bitter taste in children.

The palatability of oral medications, many of which are quite bitter, plays an important role in achieving compliance in pediatric patients. We tested the hypothesis that the addition of a sodium salt to some, but not all, bitter tasting liquids enhances acceptance and reduces the perceived bitterness in 7- to 10-year-old children and their mothers. For both children and adults, sodium gluconate significantly suppressed the perceived bitterness and enhanced the acceptance of urea and caffeine whereas the reverse was true for another bitter stimulus, Tetralone. Because children preferred salted solutions more than did adults, these data suggest that the use of sodium salts may be an especially effective strategy for reducing the bitterness of some medicines and facilitating compliance among pediatric populations. However, based on sodium's differential ability to inhibit bitterness, as has been shown here with children and adults, clearly each drug of interest must be evaluated separately.

Administration, Oral↗
PubMed2007

Quantitative structure-activity relationship study of bitter di- and tri-peptides including relationship with angiotensin I-converting enzyme inhibitory activity.

Bitterness represents a major challenge in industrial application of food protein hydrolysates or bioactive peptides and is a major factor that controls the flavor of formulated therapeutic products. The aim of this work was to apply quantitative structure-activity relationship modeling as a tool to determine the type and position of amino acids that contribute to bitterness of di- and tri-peptides. Datasets of bitter di- and tri-peptides were constructed using values from available literature, followed by modeling using partial least square (PLS) regression based on the three z-scores of 20 coded amino acids. Prediction models were validated using cross-validation and permutation tests. Results showed that a single-component model could explain 52 and 50% of the Y variance (bitterness threshold) of bitter di- and tri-peptides, respectively. Using PLS regression coefficients, it was determined that hydrophobic amino acids at the carboxyl-terminus and bulky amino acid residues adjacent to the carboxyl terminal are the major determinants of the intensity of bitterness of di- and tri-peptides. However, there was no significant (p > 0.05) correlation between bitterness of di- and tri-peptides and their angiotensin I-converting enzyme-inhibitory properties.

Amino Acid Sequence↗
PubMed1996

Lipoprotein that selectively inhibits taste nerve responses to bitter substances.

The development of a specific inhibitor for bitter taste has been widely required in the fields of taste physiology and pharmaceutical sciences, but no inhibitor has been available. We found that lipoproteins, PA-LG composed of phosphatidic acid (PA) and beta-lactoglobulin (LG) and PA-LA composed of PA and alpha-lactalbumin (LA) reversibly suppressed the responses of the frog glossopharyngeal nerve to the bitter substances. The frog tongue was treated with PA-LG solution for 10 min and then stimulated by a stimulus dissolved in water. The responses to the bitter substances such as quinine hydrochloride, papaverine hydrochloride, caffeine and L-leucine were completely suppressed by PA-LG, while those to the salt type bitter substances such as CsCl, MgCl2 and tetraethylammonium chloride were not suppressed. The responses to NaCl, galactose, acetic acid and L-alanine were unchanged or only slightly increased. The results suggested that binding of PA-LG to the hydrophobic region of the receptor membranes leads to suppression of the responses to the bitter substances. It was pointed out that PA-LG is useful not only for elucidating the receptor mechanisms of bitter substances, but also can be safely used to mask the bitter taste of foods and drugs, since PA, LG and LA are prepared from foods (soybean and milk).

Animals↗
PubMed2005

The molecular basis of individual differences in phenylthiocarbamide and propylthiouracil bitterness perception.

Individual differences in perception are ubiquitous within the chemical senses: taste, smell, and chemical somesthesis . A hypothesis of this fact states that polymorphisms in human sensory receptor genes could alter perception by coding for functionally distinct receptor types . We have previously reported evidence that sequence variants in a presumptive bitter receptor gene (hTAS2R38) correlate with differences in bitterness recognition of phenylthiocarbamide (PTC) . Here, we map individual psychogenomic pathways for bitter taste by testing people with a variety of psychophysical tasks and linking their individual perceptions of the compounds PTC and propylthiouracil (PROP) to the in vitro responses of their TAS2R38 receptor variants. Functional expression studies demonstrate that five different haplotypes from the hTAS2R38 gene code for operatively distinct receptors. The responses of the three haplotypes we also tested in vivo correlate strongly with individuals' psychophysical bitter sensitivities to a family of compounds. These data provide a direct molecular link between heritable variability in bitter taste perception to functional variations of a single G protein coupled receptor that responds to compounds such as PTC and PROP that contain the N-C=S moiety. The molecular mechanisms of perceived bitterness variability have therapeutic implications, such as helping patients to consume beneficial bitter-tasting compounds-for example, pharmaceuticals and selected phytochemicals.

Animals↗
PubMed2003

Sensory activity, chemical structure, and synthesis of Maillard generated bitter-tasting 1-oxo-2,3-dihydro-1H-indolizinium-6-olates.

Thermal treatment of aqueous solutions of xylose, rhamnose, and l-alanine led to a rapid development of a bitter taste of the reaction mixture. To characterize the key compounds causing this bitter taste, the recently developed taste dilution analysis (TDA), which is based on the determination of the taste threshold of reaction products in serial dilutions of HPLC fractions, was performed to locate the most intense taste compounds in the complex mixture of Maillard reaction products. By application of this TDA, 26 fractions were obtained, among which seven fractions were evaluated with a high taste impact. LC/MS and NMR spectroscopy as well as synthetic experiments revealed the 1-oxo-2,3-dihydro-1H-indolizinium-6-olates 1-5 as the key compounds contributing the most to the intense bitter taste of the Maillard mixture. Calculation of the taste impact of these compounds based on a dose/activity relationship indicated that these five compounds already accounted for 56.8% of the overall bitterness of the Maillard mixture, thus demonstrating this class of 1-oxo-2,3-dihydro-1H-indolizinium-6-olates as the key bitter compounds. First synthetic studies on the relationship between the chemical structure and the human psychobiological activity of 1-oxo-2,3-dihydro-1H-indolizinium-6-olates revealed that substitution of the furan rings of 1 by 5-methylfuryl moieties (compounds 3-5) or by 5-(hydroxymethyl)furyl groups (compound 6) led to a significant increase of the bitter threshold. In contrast, the substitution of the oxygen atoms in the furan rings of 1 by sulfur atoms induced a significant decrease of the detection threshold of the 1-oxo-2,3-dihydro-1H-indolizinium-6-olate; for example, the thiophene derivative 7 showed the extraordinarily low bitter detection threshold of 6.3 x 10(-5) mmol/kg (water).

Alanine↗
PubMed2006

New bitter-masking compounds: hydroxylated benzoic acid amides of aromatic amines as structural analogues of homoeriodictyol.

Starting from the known bitter-masking flavanones eriodictyol and homoeriodictyol from herba santa some structurally related hydroxybenzoic acid amides of benzylamines were synthesized and evaluated as masking agents toward bitterness of caffeine by sensory methods. The closest structural relatives of homoeriodictyol, the hydroxybenzoic acid vanillylamides 5-9, were the most active and were able to reduce the bitterness of a 500 mg L(-1) caffeine solution by about 30% at a concentration of 100 mg L(-1). 2,4-Dihydroxybenzoic acid vanillylamide 7 showed a clear dose-dependent activity as inhibitor of the bitter taste of caffein between 5 and 500 mg L(-1). Additionally, it was possible to reduce the bitterness of quinine and salicine but not of the bitter peptide N-l-leucyl-l-tryptophan. Combinations of homoeriodictyol and amide 7 showed no synergistic or antagonistic changes in activity. The results for model compound 7 suggested that the hitherto unknown masking mechanism is probably the same for flavanones and the new amides. In the future, the new amides may be alternatives for the expensive flavanones to create flavor solutions to mask bitterness of pharmaceuticals or foodstuffs.

Amides↗
PubMed1999

Blocking taste receptor activation of gustducin inhibits gustatory responses to bitter compounds.

Gustducin, a transducin-like guanine nucleotide-binding regulatory protein (G protein), and transducin are expressed in taste receptor cells where they are thought to mediate taste transduction. Gustducin and transducin are activated in the presence of bovine taste membranes by several compounds that humans perceive to be bitter. We have monitored this activation with an in vitro assay to identify compounds that inhibited taste receptor activation of transducin by bitter tastants: AMP and chemically related compounds inhibited in vitro responses to several bitter compounds (e.g., denatonium, quinine, strychnine, and atropine). AMP also inhibited behavioral and electrophysiological responses of mice to bitter tastants, but not to NaCl, HCl, or sucrose. GMP, although chemically similar to AMP, inhibited neither the bitter-responsive taste receptor activation of transducin nor the gustatory responses of mice to bitter compounds. AMP and certain related compounds may bind to bitter-responsive taste receptors or interfere with receptor-G protein coupling to serve as naturally occurring taste modifiers.

Adenosine Monophosphate↗