Explore the vast range of titles available.

Despite the apparent simplicity of the go/no-go (GNG) task, in which individuals selectively respond or withhold responses, there is strong evidence supporting its efficacy in terms of modulating food preferences. Herein, we manipulated sweet taste perception and investigated the no-go devaluation effect that is typically observed due to GNG training with respect to sweet and savory food items. Prior to engaging in a GNG task, one group of participants rinsed their mouths with a liquid solution containing gymnemic acid, thereby transiently and selectively inhibiting sweet taste perception, while another group used a placebo solution. The participants who rinsed their mouths with gymnemic acid exhibited a stronger overall decrease in food evaluations from pre to post training. Furthermore, a pronounced no-go devaluation effect was observed for sweet foods, irrespective of the rinsing solution. Overall, our results support the notion that training in the GNG task can induce changes in the valuation of food stimuli, particularly for sweet foods.

Natural genetic variation can have a pronounced influence on human taste perception, which in turn may influence food preference and dietary choice. Genome-wide association studies represent a powerful tool to understand this influence. To help optimize the design of future genome-wide-association studies on human taste perception we have used the well-known TAS2R38-PROP association as a tool to determine the relative power and efficiency of different phenotyping and data-analysis strategies. The results show that the choice of both data collection and data processing schemes can have a very substantial impact on the power to detect genotypic variation that affects chemosensory perception. Based on these results we provide practical guidelines for the design of future GWAS studies on chemosensory phenotypes. Moreover, in addition to the TAS2R38 gene past studies have implicated a number of other genetic loci to affect taste sensitivity to PROP and the related bitter compound PTC. None of these other locations showed genome-wide significant associations in our study. To facilitate further, target-gene driven, studies on PROP taste perception we provide the genome-wide list of p-values for all SNPs genotyped in the current study.

Rationale The effect of caffeine mouth rinsing (CAF-MR) on cognitive performance has not been thoroughly investigated. Objectives To evaluate the effects of different concentrations of CAF-MR on selective attention in relation to perceived taste intensity. Methods A total of 30 healthy and recreationally active male subjects were included in this randomized, double-blind, placebo-controlled crossover trial. Interventions included MR for 20 s at rest with three different caffeine solutions (0.24% [60 mg/ 25 mL ], 0.6% [150 mg/ 25 mL ], and 1.2% [300 mg/25 mL]), MR with 25 mL water (placebo), and no MR (control). Data on Victoria Stroop Test (VST) and the perceived taste intensity were recorded at five sessions. Results CAF-MR-300 mg intervention significantly decreased completion time (from 62.93 ± 19.07 to 57.01 ± 16.74 s, p  = 0.002 in Part D), while CAF-MR-150 mg intervention significantly decreased number of errors in Part D (7.00 ± 6.21 vs. 5.63 ± 5.76, p  = 0.04) and Part C ( 8.77  ± 8.80 vs. 7.10 ± 7.11, p  = 0.02). Perceived difficulty was significantly decreased both after CAF-MR with 150 mg (5.57 ± 1.65 vs. 4.77 ± 1.98, p  = 0.006) and 300 mg (5.95 ± 1.77vs. 4.67 ± 1.96, p  < 0.001). Perceived taste intensity for 300 mg of caffeine was negatively correlated with completion time (r: ranged, 0.37 to 0.46, p ranged, 0.045 to 0.009) after 300 mg, 150 mg (p ranged, 0.04 to 0.005) and placebo (p ranged 0.044 to 0.03) interventions. Conclusions This study is the first to demonstrate that CAF-MR shows dose-dependent effects on selective attention in healthy recreational males, such as improved speed (for 300 mg caffeine), reduced error rate (for 150 mg caffeine) and decrease in perceived difficulty (for 150 and 300 mg caffeine).

Animal models suggest that sucrose activates taste afferents differently than non-caloric sweeteners. Little information exists how artificial sweeteners engage central taste pathways in the human brain. We assessed sucrose and sucralose taste pleasantness across a concentration gradient in 12 healthy control women and applied 10% sucrose and matched sucralose during functional magnet resonance imaging. The results indicate that (1) both sucrose and sucralose activate functionally connected primary taste pathways; (2) taste pleasantness predicts left insula response; (3) sucrose elicits a stronger brain response in the anterior insula, frontal operculum, striatum and anterior cingulate, compared to sucralose; (4) only sucrose, but not sucralose, stimulation engages dopaminergic midbrain areas in relation to the behavioral pleasantness response. Thus, brain response distinguishes the caloric from the non-caloric sweetener, although the conscious mind could not. This could have important implications on how effective artificial sweeteners are in their ability to substitute sugar intake.

Salt taste sensitivity can change after heart failure (HF) hospitalization, however the relation between changes in salt taste sensitivity with HF symptoms, biomarkers, and outcomes is unknown. We assessed salt taste sensitivity over 12 weeks following HF hospitalization using a validated, point-of-care salt taste test. Subjects were divided into 2 groups: increase or no increase in salt taste sensitivity. HF biomarkers and outcomes were compared using 2-sample t tests and log-transformed t tests for non-normally distributed parameters. Baseline characteristics generally did not differ for subjects with an increase in salt taste sensitivity over 12 weeks compared with those without an increase in salt taste sensitivity. The total number of 12-week hospital days was 60 versus 121 days, with an average number of hospital days of 5.45 [3.88] versus 11.00 [6.74] (p = 0.03) among those hospitalized in the groups with an increase versus no increase in salt taste sensitivity, respectively. In conclusion, changes in salt taste sensitivity occurred in some but not all subjects in a 12-week period following HF hospitalization. Subjects with increased salt taste sensitivity over this time period were rehospitalized for fewer days. Improved salt taste sensitivity may represent a novel prognostic factor in postdischarge patients with HF.

Suppression of oral sweet sensation (OSS) acutely reduces intake of sweet-tasting food due to lower liking. However, little is known about other physiological responses during both the prandial and postprandial phase. Here, we explored the effects of Gymnema sylvestre (GS)-based suppression of OSS of several types of sweet-tasting food (muffin, sweet yogurt, banana) on gastric emptying, blood glucose (BG), plasma insulin (PI), appetite indices (hunger, fullness and prospective consumption), satisfaction and desire for tastes. Fifteen healthy subjects (22 ± 3 years, 9 women) took part in the study. Subjects rinsed their mouth with either GS solution or distilled water before eating the sweet-tasting food. Subjects felt decreased sweet taste intensity and reduced taste liking associated with GS rinsing after consuming each food, compared with rinsing with distilled water (p < 0.05). Gastric emptying, BG, PI and appetite indices during and after the prandial phase did not significantly change with GS rinsing compared to rinsing with distilled water (p > 0.05). Higher desire for sweet taste as well as lower satisfaction (p < 0.05) in the postprandial phase were observed with GS rinsing. These results suggest that the suppression of OSS does not affect gastric emptying, glycemic response and appetite during and after consumption of sweet-tasting food.

To identify molecules that could enhance sweetness perception, we undertook the screening of a compound library using a cell-based assay for the human sweet taste receptor and a panel of selected sweeteners. In one of these screens we found a hit, SE-1, which significantly enhanced the activity of sucralose in the assay. At 50 μM, SE-1 increased the sucralose potency by >20-fold. On the other hand, SE-1 exhibited little or no agonist activity on its own. SE-1 effects were strikingly selective for sucralose. Other popular sweeteners such as aspartame, cyclamate, and saccharin were not enhanced by SE-1 whereas sucrose and neotame potency were increased only by 1.3- to 2.5-fold at 50 μM. Further assay-guided chemical optimization of the initial hit SE-1 led to the discovery of SE-2 and SE-3, selective enhancers of sucralose and sucrose, respectively. SE-2 (50 μM) and SE-3 (200 μM) increased sucralose and sucrose potencies in the assay by 24- and 4.7-fold, respectively. In human taste tests, 100 μM of SE-1 and SE-2 allowed for a reduction of 50% to >80% in the concentration of sucralose, respectively, while maintaining the sweetness intensity, and 100 μM SE-3 allowed for a reduction of 33% in the concentration of sucrose while maintaining the sweetness intensity. These enhancers did not exhibit any sweetness when tasted on their own. Positive allosteric modulators of the human sweet taste receptor could help reduce the caloric content in food and beverages while maintaining the desired taste.

Abstract Purpose Obesity is associated with alterations in appetite, gastrointestinal hormone levels and excessive fat mass. We previously published a double-blind, placebo-controlled, randomized, 16-week trial on effects of once-daily glucagon-like peptide-1 (GLP-1) analog, liraglutide on weight, satiation, and gastric functions in obese volunteers. The aim of this substudy is to compare to placebo the effects of liraglutide on appetite, taste preference, regional body fat stores, and anthropometric measurements. Methods Forty obese adults received standard instruction for weight management, monthly behavioral intervention utilizing motivational interviews, and 16-week treatment of once-daily liraglutide (escalated to 3 mg SQ daily). At baseline and 16 weeks, the following were measured: appetite and taste preferences rated every 30 min for 5 h after ingesting 300 mL Ensure®; maximal tolerated volume (MTV) with a nutrient drink test; fasting and postprandial bioactive GLP-1 (7–36) and peptide YY (PYY) levels; total and regional body fat with dual-energy X-ray absorptiometry, and waist and hip circumference. Results Thirty-five participants (17 liraglutide; 18 placebo) completed the trial. Compared to placebo group, liraglutide group had significant reductions in MTV; prospective food consumption score; desire to eat something sweet, salty, savory or fatty; and an increase in perceived fullness. Postprandial plasma levels of GLP-1 decreased and PYY levels increased with liraglutide relative to baseline. Significant reductions in total body, trunk, and upper and lower body fat without reduction in lean body mass were observed. Conclusion Liraglutide 3 mg SQ modulates appetite, taste preference, gut hormones, and regional body fat stores in adults with obesity without reduction in lean body mass.

In our diet, we ingest a variety of compounds that are TRPV1 modulators. It is important to understand if these compounds alter neural and behavioral responses to taste stimuli representing all taste qualities. Here, we will summarize the effects of capsaicin, resiniferatoxin, cetylpyridinium chloride, ethanol, nicotine, N-geranyl cyclopropylcarboxamide, Kokumi taste peptides, pH, and temperature on neural and behavioral responses to taste stimuli in rodent models and on human taste perception. The above TRPV1 agonists produced characteristic biphasic effects on chorda tympani taste nerve responses to NaCl in the presence of amiloride, an epithelial Na+ channel blocker, at low concentrations enhancing and at high concentrations inhibiting the response. Biphasic responses were also observed with KCl, NH4Cl, and CaCl2. In the presence of multiple stimuli, the effect is additive. These responses are blocked by TRPV1 antagonists and are not observed in TRPV1 knockout mice. Some TRPV1 modulators also increase neural responses to glutamate but at concentrations much above the concentrations that enhance salt responses. These modulators also alter human salt and glutamate taste perceptions at different concentration ranges. Glutamate responses are TRPV1-independent. Sweet and bitter responses are TRPV1-independent but the off-taste of sweeteners is TRPV1-dependent. Aversive responses to acids and ethanol are absent in animals in which both the taste system and the TRPV1-trigeminal system are eliminated. Thus, TRPV1 modulators differentially alter responses to taste stimuli.

Taste sensitivity to PROP varies greatly among individuals and is associated with polymorphisms in the bitter receptor gene TAS2R38, and with differences in fungiform papilla density on the anterior tongue surface. Recently we showed that the PROP non-taster phenotype is strongly associated with the G variant of polymorphism rs2274333 (A/G) of the gene that controls the salivary trophic factor, gustin. The aims of this study were 1) to investigate the role of gustin gene polymorphism rs2274333 (A/G), in PROP sensitivity and fungiform papilla density and morphology, and 2) to investigate the effect of this gustin gene polymorphism on cell proliferation and metabolic activity. Sixty-four subjects were genotyped for both genes by PCR techniques, their PROP sensitivity was assessed by scaling and threshold methods, and their fungiform papilla density, diameter and morphology were determined. In vitro experiments examined cell proliferation and metabolic activity, following treatment with saliva of individuals with and without the gustin gene mutation, and with isolated protein, in the two iso-forms. Gustin and TAS2R38 genotypes were associated with PROP threshold (p=0.0001 and p=0.0042), but bitterness intensity was mostly determined by TAS2R38 genotypes (p<0.000001). Fungiform papillae densities were associated with both genotypes (p<0.014) (with a stronger effect for gustin; p=0.0006), but papilla morphology was a function of gustin alone (p<0.0012). Treatment of isolated cells with saliva from individuals with the AA form of gustin or direct application of the active iso-form of gustin protein increased cell proliferation and metabolic activity (p<0.0135). These novel findings suggest that the rs2274333 polymorphism of the gustin gene affects PROP sensitivity by acting on fungiform papilla development and maintenance, and could provide the first mechanistic explanation for why PROP super-tasters are more responsive to a broad range of oral stimuli.