Sweet Response Research Articles

Modulations of sweet taste responses by salts, acids and bitter compounds in the mouse chorda tympani nerve

Modulations of sweet taste responses by salts, acids and bitter compounds in the mouse chorda tympani nerve

Temperature modulation of gurmarin sensitive sweet responses in the mouse chorda tympani nerve

Knockout (KO) mice missing the taste signaling protein Trpm5 have greatly attenuated sweetener preferences but develop strong preferences for glucose in 24-h tests, which is attributed to post-oral sugar conditioning. Trpm5 KO mice express mild preferences for galactose but no preferences for fructose in 24-h tests, which suggests that these sugars differ in their post-oral reinforcing effects. Here we investigated sugar-conditioned flavor preferences in Trpm5 KO and C57BL/6J wildtype (B6) mice. The mice were trained to consume a flavored (CS+, e.g. grape) 8% sugar solution and flavored (CS−, e.g., cherry) water on alternating days followed by two-bottle choice tests with CS+ vs. CS− flavors in water and with unflavored sugar vs. water. The KO mice displayed strong preferences (> 80%) for the CS+ glucose and CS+ galactose but not for the CS + fructose flavor. They also preferred glucose and galactose, but not fructose to water. In contrast, the B6 mice preferred all three CS + flavors to the CS− flavor, and all three sugars to water. In tests with the non-metabolizable sugar α-methyl-d-glucopyranoside (MDG), the KO and B6 mice preferred 8% MDG to water but did not prefer the CS+ 8% MDG to CS−. However, they preferred a CS + flavor mixed with 4% MDG over the CS− flavor. Trpm5 KO mice also preferred galactose and MDG to fructose in direct choice tests. The Trpm5 KO data indicate that glucose and, to a lesser extent, galactose and MDG have post-oral reinforcing actions that stimulate intake and preference while fructose has a much weaker effect. The CS+ flavor and sugar preferences of B6 mice may be mediated by the sweet taste and/or post-oral actions of the various sugars. Glucose, galactose, and MDG, but not fructose, are ligands for the sodium–glucose transporter 1 (SGLT1) which is implicated in post-oral sugar conditioning in B6 mice.

A Taste Receptor Required for the Caffeine Response In Vivo

Caffeine is a methylxanthine present in the coffee tree, tea plant, and other naturally occurring sources and is among the most commonly consumed drugs worldwide. Whereas the pharmacological action of caffeine has been studied extensively, relatively little is known concerning the molecular mechanism through which this substance is detected as a bitter compound. Unlike most tastants, which are detected through cell-surface G protein-coupled receptors, it has been proposed that caffeine and related methylxanthines activate taste-receptor cells through inhibition of a cyclic nucleotide phosphodiesterase (PDE) . Here, we show that the gustatory receptor Gr66a is expressed in the dendrites of Drosophila gustatory receptor neurons and is essential for the caffeine response. In a behavioral assay, the aversion to caffeine was specifically disrupted in flies missing Gr66a. Caffeine-induced action potentials were also eliminated, as was the response to theophylline, the methylxanthine in tea. The Gr66a mutant exhibited normal tastant-induced action potentials upon presentation of theobromine, a methylxanthine in cocoa. Given that theobromine and caffeine inhibit PDEs with equal potencies , these data further support the role of Gr66a rather than a PDE in mediating the caffeine response. Gr66a is the first gustatory receptor shown to be essential for caffeine-induced behavior and activity of gustatory receptor cells in vivo.

Persistent sucrose stimulation of ovine fetal ingestion: Lack of adaptation responses

Objective. Sweet taste responsiveness is reduced in adult rats and humans following continued oral sucrose. We have previously demonstrated that sublingual sucrose stimulates near term ovine fetal swallowing, suggesting intact taste responsiveness. We sought to determine if prolonged oral sucrose infusion to the near term ovine fetus will evoke adaptation, as manifested by reduced swallowing stimulation.Methods. Time-dated pregnant ewes and fetuses (n = 4) were chronically prepared with fetal vascular and sublingual catheters, and electrocorticogram and esophageal electromyogram electrodes and studied at 129 ± 1d gestation. Following an initial 2 h basal period, sucrose (2.5%) was infused sublingually (0.25 ml/min) to the fetus for 8 h. Fetal swallowing activity, blood pressure and heart rate were continuously recorded while maternal and fetal arterial blood samples were taken at timed intervals.Results. During the basal period, fetal swallowing averaged 0.9 ± 0.1 swallows/min. Fetal swallowing increased significantly following sublingual 2.5% sucrose infusion and remained significantly elevated at 2, 4, 6 and 8 h after initiation of sucrose infusion (1.3 ± 0.1, 1.2 ± 0.1, 1.3 ± 0.1, 1.3 ± 0.1 swallows/min; p < 0.001). There were no significant changes in fetal cardiovascular or arterial blood parameters.Conclusions. Although oral sucrose significantly stimulates near term ovine fetal ingestive behavior, sweet taste adaptation or habituation does not occur, in contrast to that observed in adult animals and human. The lack of taste adaptation in the fetus/newborn may facilitate increased neonatal food intake and accelerated growth.

Mouse Strain Differences in Gurmarin-sensitivity of Sweet Taste Responses Are Not Associated with Polymorphisms of the Sweet Receptor Gene, Tas1r3

Gurmarin (Gur) is a peptide that selectively inhibits responses of the chorda tympani (CT) nerve to sweet compounds in rodents. In mice, the sweet-suppressing effect of Gur differs among strains. The inhibitory effect of Gur is clearly observed in C57BL/6 mice, but only slightly, if at all, in BALB/c mice. These two mouse strains possess different alleles of the sweet receptor gene, Sac (Tas1r3) (taster genotype for C57BL/6 and non-taster genotype for BALB/c mice), suggesting that polymorphisms in the gene may account for differential sensitivity to Gur. To investigate this possibility, we examined the effect of Gur in another Tas1r3 non-taster strain, 129 X 1/Sv mice. The results indicated that unlike non-taster BALB/c mice but similar to taster C57BL/6 mice, 129 X 1/Sv mice exhibited significant inhibition of CT responses to various sweet compounds by Gur. This suggests that the mouse strain difference in the Gur inhibition of sweet responses of the CT nerve may not be associated with polymorphisms of Tas1r3.

Sweet Corn Hybrid Sensitivity to Clopyralid

Limited information exists on sweet corn tolerance to postemergence (POST) applications of clopyralid under Ontario growing conditions. Eight sweet corn hybrids were evaluated for tolerance to clopyralid in three field experiments conducted in 2001 and 2002 in Ontario. Clopyralid was applied POST at 200 and 400 g ai/ha, the proposed and twice the proposed registered rate for use in sweet corn in Ontario. Sweet corn response to clopyralid did not vary among the hybrids tested. In 2001, visual injury among hybrids 7 d after treatment (DAT) with clopyralid at 400 g/ha was less than 3%. Subsequent visual injury evaluations at 14 and 28 DAT showed no differences among sweet corn hybrids at either rate of clopyralid evaluated. The application of clopyralid at 200 and 400 g/ ha had no detrimental effect on plant height or marketable yield of any of the eight sweet corn hybrids. On the basis of visual injury, height, and marketable yield response ‘Calico Belle’, ‘CNS 710’, ‘DelMonte 2038’, ‘GG 222’, ‘GG 246’, ‘GH 2684’, ‘Reveille’, and ‘Rival’ are all tolerant to the POST application of clopyralid.

EXTINCTION TRAINING OF SWEET CHERRIES IN FRANCE - APPRAISAL AFTER SIX YEARS

For a number of years in France, the Solaxe training system has been proposed for sweet cherries as a way of increasing tree density/ha and reducing time before the first commercial crop. Planting distances usually are 4.5 to 5 m between the rows and 1.5 to 2 m within each row, giving tree densities ranging from 1000 to 1500 trees/ha. Bending, rather than heading cuts, is used to control the vegetative growth of the trunk (at a height of 2.5 to 3.5 m) and side branches. For certain cultivars, bending also is used to increase fruiting. More recently, the removal of fruiting spurs from side branches has been suggested as a training tool for improving the balance between vegetative growth and fruit load. This method, known as extinction, has now been integrated in training programs in several commercial orchards with the collaboration of the applied research network Mafcot (Maitrise de la Fructification - Concepts et Techniques; Fruiting Control - Concepts and Applications). This paper presents two experiments carried out (i) on 10- and 6year-old trees to compare standard winter heading cuts and extinction, and (ii) on 6year-old trees to evaluate how cultivar ('Burlat', 'Duroni 3', 'Sumele', 'Summit') affects sweet cherry growth and fruiting responses to various heading cuts and extinction treatments, all involving the removal of ~30% of the fruiting spurs. Synthesis of these experiments confirms the benefits of the extinction method, as compared to standard heading cuts, for improving fruit size while maintaining a good balance between vegetative growth and fruiting. Although not quantified in this study, these extinction experiments resulted in two unexpected side effects that are now being studied carefully: enhanced fruit maturity (by 2 to 4 days) in the early-ripening 'Burlat' and reduced sensitivity to European brown rot. The better light and air penetration within the canopy brought about by extinction training may explain these observations.

Brazzein, a Small, Sweet Protein: Effects of Mutations on its Structure, Dynamics and Functional Properties

The demand for non-calorigenic protein-based sweeteners with favorable taste properties is high. The optimal design of such sweeteners requires knowledge about structure–function relationships and the identification of chemical entities that trigger the sweetness response. Among the known, naturally occurring, sweet-tasting proteins, brazzein has properties that make it particularly attractive as a potential economic sweetener. It is highly stable over wide temperature and pH ranges and has taste properties that resemble those of carbohydrate sweeteners. Brazzein is a single polypeptide of 54 standard amino acids and contains no carbohydrate. The brazzein protein originally was purified from the fruit of Pentadiplandra brazzeana, a climbing vine that grows in Gabon, Zaire and Cameroon (Ming and Hellekant, 1994). The fruit is consumed by the local population and is prized for its sweetness. Pure brazzein has been shown to elicit sweetness responses in humans by taste trials and in a non-human primate (rhesus monkey) as determined from electrophysiological recordings of signals from the chorda tympani (van der Wel et al., 1989). Recently receptor proteins have been discovered that are responsive to sweet ligands. The human receptor appears to be a heterodimer of two conventional seven-transmembrane-helix Gcoupled type receptors (T1R2/T1R3) but with unusually large ectodomains ((Nelson et al., 2001; Li et al., 2002); P. Jiang and M. Max, personal communication). Different sweet proteins interact with and activate the same heterodimeric receptor in somewhat different ways and tentative models for such interactions have been elaborated ((Temussi, 2002); M. Max, personal communication). The discovery of the sweet taste heteroreceptor opens up exciting new avenues for research on the mechanism of action of sweet substances. Brazzein is an excellent candidate for experimental investigations of the chemical and structural requirements for extracellular triggering of a sweet response in humans and for understanding the mechanism of the signal transduction.

Taste response functions of adults and children using different rating scales

The ability of children to estimate the strength of suprathreshold taste stimuli has received minimal investigation, and there have been few attempts to compare their responses directly with those of adults. Accordingly, the present study investigated three rating procedures for establishing the sweetness response functions of 87 adults and 8–9-year old children for sucrose following training with the visual stimulus, length. Similar sweetness response functions were obtained for both subject groups using a category scale or magnitude estimation procedure, whilst the functions for adults and children were different using a hand-separation procedure. The similar sweetness response functions for adults and children obtained with two of the procedures suggest that the sense of taste has reached maturity for the perception of suprathreshold sucrose stimuli by mid-childhood.

Gurmarin suppression of licking responses to sweetener-quinine mixtures in C57BL mice.

Gurmarin (Gur) is a peptide that selectively suppresses responses of the chorda tympani nerve to sweet substances in rats and mice. In the present study, we examined the effect of Gur on behavioral responses to sweet substances in C57BL mice. To accomplish this, we developed a new short-term lick test and measured numbers of licks for 10 s for sweet substances mixed with quinine hydrochloride (QHCl) in water-deprived mice. Numbers of licks for sucrose mixed with 1 or 3 mM QHCl increased with increasing concentration of sucrose from 0.01 to 1.0 M. Oral infusion with 30 micro g/ml Gur produced significant decreases in responses to concentration series for sucrose mixed with 3 mM QHCl, whereas no such effect by Gur was observed in responses to QHCl alone or QHCl-mixed HCl, NaCl or monosodium glutamate. The Gur suppression of QHCl-mixed sucrose responses, which otherwise lasted for 2-3 h, rapidly returned to approximately 80% of control levels after oral infusion with beta-cyclodextrin. These results are comparable to neural data previously found in chorda tympani responses, and thereby provide further evidence for Gur as a sweet response inhibitor in C57BL mice. In the other aspect, our newly developed short-term test can also provide a tool for measurements of taste-guided behavioral responses to sweeteners.

Ion channels and second messengers involved in transduction and modulation of sweet taste in mouse taste cells

Abstract Leptin, a hormone released from the adipose tissue, inhibits food intake and increases energy expenditure. We have found a novel function of leptin as a modulator of sweet taste sensitivity in mice. In lean normal mice, the gustatory nerve responses to sweet stimuli were selectively suppressed depending on plasma leptin level after an intraperitoneal injection of recombinant leptin. Patch-clamp studies using isolated taste cells of lean mice showed that extracellular leptin enhanced K+ currents of sweet-responsive taste cells, which led to membrane hyperpolarization and a reduction of sweetener-induced depolarization. Reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization analyses demonstrated specific expression of mRNA of the long-form functional leptin receptor (Ob-Rb) in taste tissue and cells of lean mice. The genetically diabetic db/db mice, which have defects in Ob-Rb, demonstrated neither a suppression of gustatory neural responses to sweeteners nor an increment of whole-cell K+ conductance of taste cells even with high doses of leptin. These results suggest that Ob-Rb is specifically expressed in sweet-responsive taste cells of lean mice and that leptin suppresses sweetener-induced depolarization via activation of K+ channels, leading to a decrease in impulses of sweet-best fibers. The enhanced sweet responses of db/db mice may result from the lack of inhibitory modulation by leptin.

Glutamate transduction mechanism in mouse taste cells

In order to clarify the role of group III metabotropic glutamate receptor (including mGluR4) in transduction for umami taste, we investigated the effects of monosodium glutamate (MSG) and 2-amino-4-phosphonobutyrate (L-AP4), a mGluR4 agonist, on taste cells by use of electrophysiological and biochemical methods, and Ca2+ imaging in C57BL mice. The responses of the chorda tympani (CT) nerve to MSG were suppressed by gurmarin, a sweet response inhibitor, indicating that the MSG response may be partly mediated by sweet receptors, while the CT responses to L-AP4 and the glossopharyngeal (GL) nerve responses to MSG were little suppressed by gurmarin suggesting that these responses may be mediated by only umami receptors. Biochemical study demonstrated that MSG stimulation significantly elevated both adenosine 3′, 5′-cyclic monophosphate (cAMP) and inositol 1,4,5-triphosphate (IP3) levels in the fungiform papillae. The increase in cAMP might occur through sweet receptors, which is consistent with CT nerve responses. The increase in IP3 levels may relate to intracellular events mediated by group III mGluRs, because MSG and L-AP4 induced increment of intracellular Ca2+ concentration in some taste cells. Whole-cell patchclamp recording from isolated taste cells showed that L-AP4 induced not only outward currents with a conductance decreases but also inward currents with conductance increases at about resting potentials. These inward currents reversed at +10-+30 mV suggesting that cation conductance was activated by L-AP4. These results strongly support the idea that phospholipase C activation mediated by group III mGluRs is involved in transduction mechanism for umami taste, and also suggest the possibility that stimulation of the mGluRs may cause activation of cation conductance as well as [Ca2+]i elevation.

Tas1r3, encoding a new candidate taste receptor, is allelic to the sweet responsiveness locus Sac.

The ability to taste the sweetness of carbohydrate-rich foodstuffs has a critical role in the nutritional status of humans. Although several components of bitter transduction pathways have been identified, the receptors and other sweet transduction elements remain unknown. The Sac locus in mouse, mapped to the distal end of chromosome 4 (refs. 7-9), is the major determinant of differences between sweet-sensitive and -insensitive strains of mice in their responsiveness to saccharin, sucrose and other sweeteners. To identify the human Sac locus, we searched for candidate genes within a region of approximately one million base pairs of the sequenced human genome syntenous to the region of Sac in mouse. From this search, we identified a likely candidate: T1R3, a previously unknown G protein-coupled receptor (GPCR) and the only GPCR in this region. Mouse Tas1r3 (encoding T1r3) maps to within 20,000 bp of the marker closest to Sac (ref. 9) and, like human TAS1R3, is expressed selectively in taste receptor cells. By comparing the sequence of Tas1r3 from several independently derived strains of mice, we identified a specific polymorphism that assorts between taster and non-taster strains. According to models of its structure, T1r3 from non-tasters is predicted to have an extra amino-terminal glycosylation site that, if used, would interfere with dimerization.

Sweet taste transduction in hamster: role of protein kinases.

Two different second-messenger pathways have been implicated in sweet taste transduction: sugars produce cyclic AMP (cAMP), whereas synthetic sweeteners stimulate production of inositol 1,4, 5-tris-phosphate (IP(3)) and diacylglycerol (DAG). Both sugars and sweeteners depolarize taste cells by blocking the same resting K(+) conductance, but the intermediate steps in the transduction pathways have not been examined. In this study, the loose-patch recording technique was used to examine the role of protein kinases and other downstream regulatory proteins in the two sweet transduction pathways. Bursts of action currents were elicited from approximately 35% of fungiform taste buds in response to sucrose (200 mM) or NC-00274-01 (NC-01, 200 microM), a synthetic sweetener. To determine whether protein kinase C (PKC) plays a role in sweet transduction, taste buds were stimulated with the PKC activator PDBu (10 microM). In all sweet-responsive taste buds tested (n = 11), PDBu elicited burst of action currents. In contrast, PDBu elicited responses in only 4 of 19 sweet-unresponsive taste buds. Inhibition of PKC by bisindolylmaleimide I (0.15 microM) resulted in inhibition of the NC-01 response by approximately 75%, whereas the response to sucrose either increased or remained unchanged. These data suggest that activation of PKC is required for the transduction of synthetic sweeteners. To determine whether protein kinase A (PKA) is required for the transduction of sugars, sweet responses were examined in the presence of the membrane-permeant PKA inhibitor H-89 (10 and 19 microM). Surprisingly, H-89 did not decrease responses to either sucrose or NC-01. Instead, responses to both compounds were increased in the presence of the inhibitor. These data suggest that PKA is not required for the transduction of sugars, but may play a modulatory role in both pathways, such as adaptation of the response. We also examined whether Ca(2+)-calmodulin dependent cAMP phosphodiesterase (CaM-PDE) plays a role in sweet taste transduction, by examining responses to sucrose and synthetic sweeteners in the presence of the CaM-PDE inhibitor W-7 (100 microM). Inhibition resulted in an increase in the response to sucrose, whereas the response to NC-01 remained unchanged. These data suggest that the pathways for sugars and sweeteners are negatively coupled; the Ca(2+) that is released from intracellular stores during stimulation with synthetic sweeteners may inhibit the response to sucrose by activation of CaM-PDE.

Responses to Umami Substances in Taste Bud Cells Innervated by the Chorda Tympani and Glossopharyngeal Nerves

The chorda tympani (CT) and glossopharyngeal (GL) nerves of several mammalian species respond differently to umami substances (US) such as monosodium glutamate (MSG), disodium 5'-inosinate (IMP) and disodium 5'-guanylate (GMP). In mice and rhesus monkeys, responses to US are greater in the GL than the CT nerve, with the GL nerve containing larger numbers of MSG-sensitive fibers. Gurmarin, a sweet response inhibitor, suppresses the mouse CT responses to the mixture of MSG and IMP to approximately 65% of control levels but not to the metabotropic and ionotropic glutamate agonists 2-amino-4-phophonobutyrate and N-methyl-D-aspartate. Gurmarin does not inhibit any taste responses in the GL. In mice, CT responses to MSG may be masked by their greater sensitivity to sodium ions. Calcium imaging studies demonstrate that some mouse taste cells isolated from the fungiform papilla innervated by the CT respond selectively (as indicated by a rise in intracellular Ca(2+) concentrations) to MSG and/or IMP or GMP. These MSG responses are not suppressed notably by reducing the Ca(2+) concentration of the stimulus solution, suggesting that the observed Ca(2+) release is from intracellular stores. Measurements of second messengers in the mouse fungiform papilla have revealed consistently that MSG elicits increases in both inositol 1,4,5-trisphosphate and adenosine 3', 5'-cyclic monophosphate levels. Together, these results suggest that US may stimulate two different transduction mechanisms in the fungiform papilla. They also suggest that gurmarin-insensitive components of receptors for US, including metabotropic and ionotropic glutamate receptors, may be commonly involved in transduction for umami taste in taste cells on both anterior and posterior parts of the tongue.

POTENCY OF SWEETNESS OF ASPARTAME, D‐TRYPTOPHAN AND THAUMATIN EVALUATED BY SINGLE VALUE AND TIME‐INTENSITY MEASUREMENTS

ABSTRACTPerceived sweetness of sucrose, aspartame, D‐tryptophan and thaumatin in a sour, citric acid background was analyzed in terms of the potency of these compounds relative to sucrose‐water combinations. Potencies of the sweeteners were determined from (1) maximum intensity using single value and time‐intensity (T‐I) measurements and (2) average intensity calculated as the ratio of area under the T‐I curve and total perceived time. Stevens’ law was applied to sweet responses, either in static or dynamic conditions. It was found that the exponent of the concentration‐response function reflected the relative capacity of a compound to sweeten a given food and stressed differences of potency among sweeteners. Aspartame, D‐tryptophan and thaumatin exhibited a decrease in sweetness potency relative to sucrose as sweetness increased from 10 to 100% of the full scale of response. Across the entire sweetness range, thaumatin showed the greatest potency but its long persistence time led to differentiate this intense sweetener from the other sweeteners evaluated.

Relationships of sweet, bitter, and roasted peanut sensory attributes with carbohydrate components in peanuts.

Certain roasted peanut quality sensory attributes have been shown to be heritable. Currently the only means of measuring these traits is the use of a trained sensory panel. This is a costly and time-consuming process. It is desirable, from a cost, time, and sample size perspective, to find other methodologies for estimating these traits. Because sweetness is the most heritable trait and it has a significant positive relationship to the roasted peanut trait, the possible relationships between heritable sensory traits and 18 carbohydrate components (inositol, glucose, fructose, sucrose, raffinose, stachyose, and 12 unknown peaks) in raw peanuts from 52 genotypes have been investigated. Previously reported correlations among sweet, bitter, and roasted peanut attributes were evident in this study as well. Where there was positive correlation of total sugars with sweetness, there also was positive correlation of total sugars with roasted peanut attribute and negative correlation of total sugars with bitterness and astringency. The expected generalized relationship of total sugars or sucrose to sweetness could not be established because the relationship was not the same across all market-types. Further work is needed to determine the nature of the chemical components related to the bitter principle, which appear to modify the sweet response and interfere with the sensory perception of sweetness, particularly in the Virginia market-type. Also, certain carbohydrate components showed significant relationships with sensory attributes in one market-type and not another. These differential associations demonstrate the complexity of the interrelationships among sweet, bitter, and roasted peanut sensory attributes. Within two market-types it is possible to improve the efficiency of selection for sweetness and roasted peanut quality by assaying for total carbohydrates. On the basis of the regression values the greatest efficiency would occur in the fastigiate market-type and then the runner.

Induction of Membrane Chloride Currents in Xenopus Laevis Oocytes By of Sulfonyl Amide Sweeteners Acesulfame K and Saccharin

Sweet receptors have remained elusive. In Xenopus oocytes sulfonyl amide sweeteners but not sweet compounds belonging to other chemical classes dose dependently induced membrane chloride currents via the inositol trisphosphate/calcium pathway. Induction of membrane currents was exclusively observed following extracellular application of sulfonyl amides but not by intracellular pressure injection, suggesting the involvement of a plasma membrane receptor. The presence of this receptor in oocytes and the observed seasonal variation of the sweet response offers an opportunity for a molecular cloning approach.

Modeling the sweetness response using time–intensity data

A general mathematical model for the temporal intensity response to a transient sweet stimulus was developed. The model is a set of nonlinear ordinary differential equations, expressing the rates of diffusion across a saliva boundary layer and adsorption and desorption to receptor site proteins on the taste bud cells. In this model, the perceived intensity is considered to be the product of a scaling factor and the amount of stimulus bound to receptor sites at any given time. A parameter estimation routine was used to fit the differential equations to the time–intensity (TI) curves for five equisweet stimuli (sucrose, aspartame, thaumatin, monellin, and brazzein). Model parameters were computed for each of 19 trained judges. The predicted TI curves were close to the observed time-intensity responses for all judges and sweeteners. TI parameters varied significantly across both judges and compounds, while model predicted parameters, such as adsorption and desorption coefficients, varied significantly only across compounds. Except for one model parameter (predicted plateau time), there were no significant differences across judges for the model-predicted parameters, indicating that all judges responded similarly to each compound.

A study of the solution properties of selected binary mixtures of bulk and intense sweeteners in relation to their psychophysical characteristics

The solution properties of binary mixtures of two bulk sweeteners (sucrose and maltitol) and three intense sweeteners (acesulfame K, aspartame and sodium cyclamate) were studied. The parameters measured were apparent specific volumes, isentropic compressibilities and compressibility hydration numbers. An attempt has been made to correlate the solution properties of some of the mixtures with their sweetness responses. Both specific volume and isentropic compressibility data have been used to interpret the possibility of synergism or suppression in the mixtures in terms of the affinity of the solutes for the surrounding solvent structure, and hence the effectiveness of transport of the molecules to their appropriate receptor sites. However, an understanding of the nature and stereochemistry of the individual components in the mixtures is necessary for predicting the packing characteristics of molecules in water and their accession to receptor sites. The intense sweeteners seem to play an important role in modifying the structure of water in solution. Although there is no clear proof of how this affects perception, fine differences in solution behaviour can be observed with isentropic apparent specific compressibility measurements. The study supports the idea that receptors lie at different depths in the lingual epithelium, and also that in two-component systems, one species may alter the packing efficiency of the other in solution sufficiently to effect a change in taste quality or intensity.