Sweet Thermal Taste: Perceptual Characteristics in Water and Dependence on TAS1R2/TAS1R3.

The initial objective of this study was to determine if activation of the sweet taste receptor TAS1R2/TAS1R3 is necessary for perception of sweet thermal taste (swTT). Our approach was to inhibit the receptor with the inverse agonist lactisole using a temperature-controlled flow gustometer. Because all prior studies of thermal taste (TT) used metal thermodes to heat the tongue tip, we first investigated whether it could be generated in heated water. Experiment 1 showed that sweetness could be evoked when deionized water was heated from 20 to 35 °C, and testing with static temperatures between 20 and 35 °C demonstrated the importance of heating from a cool temperature. As in previous studies, thermal sweetness was reported by only a subset of participants, and replicate measurements found variability in reports of sweetness across trials and between sessions. Experiment 2 then showed that exposure to 8 mM lactisole blocked perception of swTT. Confirmation of the involvement of TAS1R2/TAS1R3 led to an investigation of possible sensory and cognitive interactions between thermal and chemical sweetness. Using sucrose as a sweet stimulus and quinine as a nonsweet control, we found that dynamic heating capable of producing thermal sweetness did not increase the sweetness of sucrose compared with static heating at 35 °C. However, swTT was disrupted if trials containing sucrose (but not quinine) were interspersed among heating-only trials. These findings provide new information relevant to understanding the perceptual processes and receptor mechanisms of swTT, as well as the heat sensitivity of sweet taste in general.

Selective Effects of Temperature on the Sensory Irritation but not Taste of NaCl and Citric Acid.

This study investigated the effect of temperature on taste and chemesthetic sensations produced by the prototypical salty and sour stimuli NaCl and citric acid. Experiment 1 measured the perceived intensity of irritation (burning, stinging) and taste (saltiness, sourness) produced on the tongue tip by brief (3 s) exposures to suprathreshold concentrations of NaCl and citric acid at 3 different temperatures (12, 34, and 42 °C). No significant effects of temperature were found on the taste or sensory irritation of either stimulus. Experiment 2 investigated the potential effects of temperature on sensory irritation at peri-threshold concentrations and its sensitization over time. Measurements were again made on the tongue tip at the same 3 temperatures. Heating was found to enhance the perception of irritation at peri-threshold concentrations for both stimuli, whereas cooling suppressed sensitization of irritation for NaCl but not for citric acid. These results (i) confirm prior evidence that perception of suprathreshold salty and sour tastes are independent of temperature; (ii) demonstrate that heat has only weak effects on sensory irritation produced by brief exposures to NaCl and citric acid; and (iii) suggest that sensitization of the irritation produced by NaCl and citric acid occur via different peripheral mechanisms that have different thermal sensitivities. Overall, the results are consistent with involvement of the heat-sensitive channel TRPV1 in the sensory irritation of both stimuli together with one or more additional channels (e.g., acid-sensing channel, epithelial sodium channel, TRPA1) that are insensitive to heat and may possibly be sensitive to cooling.

Differential modulation of the lactisole 'Sweet Water Taste' by sweeteners.

Pre-exposure to taste stimuli and certain chemicals can cause water to have a taste. Here we studied further the 'sweet water taste' (SWT) perceived after exposure to the sweet taste inhibitor lactisole. Experiment 1 investigated an incidental observation that presenting lactisole in mixture with sucrose reduced the intensity of the SWT. The results confirmed this observation and also showed that rinsing with sucrose after lactisole could completely eliminate the SWT. The generalizability of these findings was investigated in experiment 2 by presenting 5 additional sweeteners before, during, or after exposure to lactisole. The results found with sucrose were replicated with fructose and cyclamate, but the 3 other sweeteners were less effective suppressors of the SWT, and the 2 sweeteners having the highest potency initially enhanced it. A third experiment investigated these interactions on the tongue tip and found that the lactisole SWT was perceived only when water was actively flowed across the tongue. The same experiment yielded evidence against the possibility that suppression of the SWT following exposure to sweeteners is an aftereffect of receptor activation while providing additional support for a role of sweetener potency. Collectively these results provide new evidence that complex inhibitory and excitatory interactions occur between lactisole and agonists of the sweet taste receptor TAS1R2-TAS1R3. Receptor mechanisms that may be responsible for these interactions are discussed in the context of the current model of the SWT and the possible contribution of allosteric modulation.

The Effect of Temperature on Umami Taste.

The effect of temperature on umami taste has not been previously studied in humans. Reported here are 3 experiments in which umami taste was measured for monopotassium glutamate (MPG) and monosodium glutamate (MSG) at solution temperatures between 10 and 37 °C. Experiment 1 showed that for subjects sensitive to MPG on the tongue tip, 1) cooling reduced umami intensity whether sampled with the tongue tip or in the whole mouth, but 2) had no effect on the rate of umami adaptation on the tongue tip. Experiment 2 showed that temperature had similar effects on the umami taste of MSG and MPG on the tongue tip but not in the whole mouth, and that contrary to umami taste, cooling to 10 °C increased rather than decreased the salty taste of both stimuli. Experiment 3 was designed to investigate the contribution of the hT1R1-hT1R3 glutamate receptor to the cooling effect on umami taste by using the T1R3 inhibitor lactisole. However, lactisole failed to block the umami taste of MPG at any temperature, which supports prior evidence that lactisole does not block umami taste for all ligands of the hT1R1-hT1R3 receptor. We conclude that temperature can affect sensitivity to the umami and salty tastes of glutamates, but in opposite directions, and that the magnitude of these effects can vary across stimuli and modes of tasting (i.e., whole mouth vs. tongue tip exposures).

Temperature Affects Human Sweet Taste via At Least Two Mechanisms.

The reported effects of temperature on sweet taste in humans have generally been small and inconsistent. Here, we describe 3 experiments that follow up a recent finding that cooling from 37 to 21 °C does not reduce the initial sweetness of sucrose but increases sweet taste adaptation. In experiment 1, subjects rated the sweetness of sucrose, glucose, and fructose solutions at 5-41 °C by dipping the tongue tip into the solutions after 0-, 3-, or 10-s pre-exposures to the same solutions or to H2O; experiment 2 compared the effects of temperature on the sweetness of 3 artificial sweeteners (sucralose, aspartame, and saccharin); and experiment 3 employed a flow-controlled gustometer to rule out the possibility the effects of temperature in the preceding experiments were unique to dipping the tongue into a still taste solution. The results (i) confirmed that mild cooling does not attenuate sweetness but can increase sweet taste adaptation; (ii) demonstrated that cooling to 5-12 °C can directly reduce sweetness intensity; and (iii) showed that both effects vary across stimuli. These findings have implications for the TRPM5 hypothesis of thermal effects on sweet taste and raise the possibility that temperature also affects an earlier step in the T1R2-T1R3 transduction cascade.

Verbal descriptors influence hypothalamic response to low-calorie drinks.

Messages describing foods constitute a pervasive form of reward cueing. Different descriptions may produce particular appeal depending upon the individual. To examine the extent to which verbal descriptors and individual differences interact to influence food preferences, we used functional magnetic resonance imaging to measure brain responses to the same low-calorie drinks preceded by the spoken verbal descriptor "treat" or "healthy" in 27 subjects varying in BMI, eating style and reward sensitivity. Subjects also sampled a prototypical milkshake treat. Despite the fact that the verbal descriptor had no influence on pleasantness ratings, preferential responses to the low-calorie drinks labeled "treat" vs. "healthy" were observed in the midbrain and hypothalamus. These same regions were also preferentially responsive to the prototypical treat. These results reveal a previously undocumented influence of verbal descriptors on brain circuits regulating energy homeostasis.

Somatosensory factors in taste perception: effects of active tasting and solution temperature.

Touch and temperature are recognized as important factors in food perception, but much remains to be learned about how they contribute to the perception of flavor. The present paper describes human psychophysical studies that investigated two recently discovered effects of temperature and mechanical stimulation on taste: (1) enhancement of the savory taste of MSG by active tongue and mouth movements, and (2) modulation of the rate of adaptation to sucrose sweetness by temperature. The first study provides evidence that for MSG but not other taste stimuli, movement of the tongue against the palate enhances taste intensity both by increasing spatial summation between opposing gustatory surfaces and by a hypothesized interaction with touch/kinesthesis. The second study shows that the rate of adaptation to sucrose sweetness (but not quinine bitterness) on the tongue tip is strongly influenced by temperature. It is hypothesized that warming slows adaptation to sucrose by increasing the sensitivity of an early stage of taste transduction. Together these results demonstrate that models of flavor perception must include somatosensory stimuli both as components of flavor perception and as modulators of taste.

Enhancement of retronasal odors by taste.

Psychophysical studies of interactions between retronasal olfaction and taste have focused most often on the enhancement of tastes by odors, which has been attributed primarily to a response bias (i.e., halo dumping). Based upon preliminary evidence that retronasal odors could also be enhanced by taste, the present study measured both forms of enhancement using appropriate response categories. In the first experiment, subjects rated taste ("sweet," "sour," "salty," and "bitter") and odor ("other") intensity for aqueous samples of 3 tastants (sucrose, NaCl, and citric acid) and 3 odorants (vanillin, citral, and furaneol), both alone and in taste-odor mixtures. The results showed that sucrose, but not the other taste stimuli, significantly increased the perceived intensity of all 3 odors. Enhancement of tastes by odors was inconsistent and generally weaker than enhancement of odors by sucrose. A second experiment used a flavored beverage and a custard dessert to test whether the findings from the first experiment would hold for the perception of actual foods. Adding sucrose significantly enhanced the intensity of "cherry" and "vanilla" flavors, whereas adding vanillin did not significantly enhance the intensity of sweetness. It is proposed that enhancement of retronasal odors by a sweet stimulus results from an adaptive sensory mechanism that serves to increase the salience of the flavor of nutritive foods.

The insular taste cortex contributes to odor quality coding.

Despite distinct peripheral and central pathways, stimulation of both the olfactory and the gustatory systems may give rise to the sensation of sweetness. Whether there is a common central mechanism producing sweet quality sensations or two discrete mechanisms associated independently with gustatory and olfactory stimuli is currently unknown. Here we used fMRI to determine whether odor sweetness is represented in the piriform olfactory cortex, which is thought to code odor quality, or in the insular taste cortex, which is thought to code taste quality. Fifteen participants sampled two concentrations of a pure sweet taste (sucrose), two sweet food odors (chocolate and strawberry), and two sweet floral odors (lilac and rose). Replicating prior work we found that olfactory stimulation activated the piriform, orbitofrontal and insular cortices. Of these regions, only the insula also responded to sweet taste. More importantly, the magnitude of the response to the food odors, but not to the non-food odors, in this region of insula was positively correlated with odor sweetness rating. These findings demonstrate that insular taste cortex contributes to odor quality coding by representing the taste-like aspects of food odors. Since the effect was specific to the food odors, and only food odors are experienced with taste, we suggest this common central mechanism develops as a function of experiencing flavors.

Taste mixture interactions: suppression, additivity, and the predominance of sweetness.

Most of what is known about taste interactions has come from studies of binary mixtures. The primary goal of this study was to determine whether asymmetries in suppression between stimuli in binary mixtures predict the perception of tastes in more complex mixtures (e.g., ternary and quaternary mixtures). Also of interest was the longstanding question of whether overall taste intensity derives from the sum of the tastes perceived within a mixture (perceptual additivity) or from the sum of the perceived intensities of the individual stimuli (stimulus additivity). Using the general labeled magnitude scale together with a sip-and-spit procedure, we asked subjects to rate overall taste intensity and the sweetness, sourness, saltiness and bitterness of approximately equi-intense sucrose, NaCl, citric acid and QSO(4) stimuli presented alone and in all possible binary, ternary and quaternary mixtures. The results showed a consistent pattern of mixture suppression in which sucrose sweetness tended to be both the least suppressed quality and the strongest suppressor of other tastes. The overall intensity of mixtures was found to be predicted best by perceptual additivity. A second experiment that was designed to rule out potentially confounding effects of the order of taste ratings and the temperature of taste solutions replicated the main findings of the first experiment. Overall, the results imply that mixture suppression favors perception of sweet carbohydrates in foods at the expense of other potentially harmful ingredients, such as high levels of sodium (saltiness) and potential poisons or spoilage (bitterness and sourness).

The role of the human orbitofrontal cortex in taste and flavor processing.

The human orbitofrontal cortex (OFC) plays an important role in representing taste, flavor, and food reward. The primary role of the OFC in taste is thought to be the encoding of affective value and the computation of perceived pleasantness. The OFC also encodes retronasal olfaction and oral somatosensation. During eating, distinct sensory inputs fuse into a unitary flavor percept, and there is evidence that this percept is encoded in the orbital cortex. Studies examining the effect of internal state on neural representation of food and drink further suggest that processing in the OFC is critical for representing the reward value of foods. Thus, it is likely that, in addition to serving as higher-order gustatory cortex, the OFC integrates multiple sensory inputs and computes reward value to guide feeding behavior.