Effect of oral or intragastric delivery of the bitter tastant quinine on food intake and appetite sensations: a randomised crossover trial.

Stimulation of gastrointestinal taste receptors affects eating behaviour. Intraduodenal infusion of tastants leads to increased satiation and reduced food intake, whereas intraileal infusion of tastants does not affect eating behaviour. Currently, it is unknown whether oral- or intragastric administration of tastants induces a larger effect on eating behaviour. This study investigated the effects of oral- and/or intragastric administration of quinine on food intake, appetite sensations and heart rate variability (HRV). In a blinded randomised crossover trial, thirty-two healthy volunteers participated in four interventions with a 1-week washout: oral placebo and intragastric placebo (OPGP), oral quinine and intragastric placebo (OQGP), oral placebo and intragastric quinine (OPGQ) and oral quinine and intragastric quinine (OQGQ). On test days, 150 min after a standardised breakfast, subjects ingested a capsule containing quinine or placebo and were sham-fed a mixture of quinine or placebo orally. At 50 min after intervention, subjects received an ad libitum meal to measure food intake. Visual analogue scales for appetite sensations were collected, and HRV measurements were performed at regular intervals. Oral and/or intragastric delivery of the bitter tastant quinine did not affect food intake (OPGP: 3273·6 (sem 131·8) kJ, OQGP: 3072·7 (sem 132·2) kJ, OPGQ: 3289·0 (sem 132·6) kJ and OQGQ: 3204·1 (sem 133·1) kJ, P = 0·069). Desire to eat and hunger decreased after OQGP and OPGQ compared with OPGP (P < 0·001 and P < 0·05, respectively), whereas satiation, fullness and HRV did not differ between interventions. In conclusion, sole oral sham feeding with and sole intragastric delivery of quinine decreased desire to eat and hunger, without affecting food intake, satiation, fullness or HRV.

Quinine Ingestion During the Latter Stages of a 3,000-m Time Trial Fails to Improve Cycling Performance.

The ingestion of quinine, a bitter tastant, improves short-term (30 s) cycling performance, but it is unclear whether this effect can be integrated into the last effort of a longer race. The purpose of this study was to determine whether midtrial quinine ingestion improves 3,000-m cycling time-trial (TT) performance. Following three familiarization TTs, 12 well-trained male cyclists (mean ± SD: mass = 76.6 ± 9.2 kg, maximal aerobic power = 390 ± 50 W, maximal oxygen uptake = 4.7 ± 0.6 L/min) performed four experimental 3,000-m TTs on consecutive days. This double-blind, crossover design study had four randomized and counterbalanced conditions: (a) Quinine 1 (25-ml solution, 2 mM of quinine); (b) Quinine 2, replicate of Quinine 1; (c) a 25-ml sweet-tasting no-carbohydrate solution (Placebo); and (d) 25 ml of water (Control) consumed at the 1,850-m point of the TT. The participants completed a series of perceptual scales at the start and completion of all TTs, and the power output was monitored continuously throughout all trials. The power output for the last 1,000 m for all four conditions was similar: mean ± SD: Quinine 1 = 360 ± 63 W, Quinine 2 = 367 ± 63 W, Placebo = 364 ± 64 W, and Control = 367 ± 58 W. There were also no differences in the 3,000-m TT power output between conditions. The small perceptual differences between trials at specific 150-m splits were not explained by quinine intake. Ingesting 2 mM of quinine during the last stage of a 3,000-m TT did not improve cycling performance.

Sensing Senses: Optical Biosensors to Study Gustation.

The five basic taste modalities, sweet, bitter, umami, salty and sour induce changes of Ca2+ levels, pH and/or membrane potential in taste cells of the tongue and/or in neurons that convey and decode gustatory signals to the brain. Optical biosensors, which can be either synthetic dyes or genetically encoded proteins whose fluorescence spectra depend on levels of Ca2+, pH or membrane potential, have been used in primary cells/tissues or in recombinant systems to study taste-related intra- and intercellular signaling mechanisms or to discover new ligands. Taste-evoked responses were measured by microscopy achieving high spatial and temporal resolution, while plate readers were employed for higher throughput screening. Here, these approaches making use of fluorescent optical biosensors to investigate specific taste-related questions or to screen new agonists/antagonists for the different taste modalities were reviewed systematically. Furthermore, in the context of recent developments in genetically encoded sensors, 3D cultures and imaging technologies, we propose new feasible approaches for studying taste physiology and for compound screening.

Intragastric quinine administration decreases hedonic eating in healthy women through peptide-mediated gut-brain signaling mechanisms.

Objectives: Intragastric bitter tastants may decrease appetite and food intake. We aimed to investigate the gut-brain signaling and brain mechanisms underlying these effects.Methods: Brain responses to intragastric quinine-hydrochloride (QHCl, 10 µmol/kg) or placebo infusion were recorded using functional magnetic resonance imaging in 15 healthy women. Appetite-related sensations, plasma levels of gastrointestinal hormones and hedonic food intake (ad libitum drink test) were assessed.Results: Lower octanoylated ghrelin (P<0.04), total ghrelin (P<0.01), and motilin (P<0.01) plasma levels were found after QHCl administration, along with lower prospective food consumption ratings (P<0.02) and hedonic food intake (P<0.05). QHCl increased neural activity in the hypothalamus and hedonic (anterior insula, putamen, caudate, pallidum, amygdala, anterior cingulate cortex, orbitofrontal cortex, midbrain) regions, but decreased activity in the homeostatic medulla (all pFWE-corrected<0.05). Differential brain responses to QHCl versus placebo covaried with subjective and hormonal responses and predicted differences in hedonic food intake.Discussion: Intragastric QHCl decreases prospective and actual food intake in healthy women by interfering with homeostatic and hedonic brain circuits in a ghrelin- and motilin-mediated fashion. These findings suggest a potential of bitter tastants to reduce appetite and food intake, through the gut-brain axis.

Challenges in relating concentrations of aromas and tastes with flavor features of foods.

Flavor sensations in food are highly influenced by the aroma and taste compounds. Reviewing the extensive literature of recent years in this field has shown that the reconstitution of flavor based on aroma and taste compounds poses numerous problems. These are of different nature and include among others (a) chemical transformations among these compounds, (b) changes in the concentrations of the compounds responsible for the perceived flavor, (c) interactions among the chemical compounds that enhance or reduce a specific flavor sensation, and finally, (d) the complexity of the different food matrices and its influence in the flavor perception. Another difficulty that flavor scientists must face is how to properly model and visualize the complex relationships existing between the chemical composition of foods and the flavor perception. These problems have repercussions on the reconstitution of the flavor signature of food based on the natural concentrations of its key aroma and taste compounds. Therefore, the main aim of this review is to deal with all these issues to propose potential solutions for a robust transformation in a science-based quality approach.

Membrane-permeable tastants amplify ß2-adrenergic receptor signaling and delay receptor desensitization via intracellular inhibition of GRK2's kinase activity.

BACKGROUND: Amphipathic sweet and bitter tastants inhibit purified forms of the protein kinases GRK2, GRK5 and PKA activities. Here we tested whether membrane-permeable tastants may intracellularly interfere with GPCR desensitization at the whole cell context. METHODS: ß2AR-transfected cells and cells containing endogenous ß2AR were preincubated with membrane-permeable or impermeable tastants and then stimulated with isoproterenol (ISO). cAMP formation, ß2AR phosphorylation and ß2AR internalization were monitored in response to ISO stimulation. IBMX and H89 inhibitors and GRK2 silencing were used to explore possible roles of PDE, PKA, and GRK2 in the tastants-mediated amplification of cAMP formation and the tastant delay of ß2AR phosphorylation and internalization. RESULTS: Membrane-permeable but not impermeable tastants amplified the ISO-stimulated cAMP formation in a concentration- and time-dependent manner. Without ISO stimulation, amphipathic tastants, except caffeine, had no effect on cAMP formation. The amplification of ISO-stimulated cAMP formation by the amphipathic tastants was not affected by PDE and PKA activities, but was completely abolished by GRK2 silencing. Amphipathic tastants delayed the ISO-induced GRK-mediated phosphorylation of ß2ARs and GRK2 silencing abolished it. Further, tastants also delayed the ISO-stimulated ß2AR internalization. CONCLUSION: Amphipathic tastants significantly amplify ß2AR signaling and delay its desensitization via their intracellular inhibition of GRK2. GENERAL SIGNIFICANCE: Commonly used amphipathic tastants may potentially affect similar GPCR pathways whose desensitization depends on GRK2's kinase activity. Because GRK2 also modulates phosphorylation of non-receptor components in multiple cellular pathways, these gut-absorbable tastants may permeate into various cells, and potentially affect GRK2-dependent phosphorylation processes in these cells as well.

Bitter tastants induce relaxation of rat thoracic aorta precontracted with high K(+).

It has been reported that bitter tastants decrease blood pressure and relax precontracted vascular smooth muscle. However, the underlying mechanisms remain unclear. The aim of the present study was to determine the mechanism underlying the vasorelaxant effect of the bitter tastants. Thoracic aortic rings were isolated from Wistar rats and contractions were measured using an isometric myograph. Intracellular Ca(2+) ([Ca(2+)]i) in single rat thoracic aortic smooth muscle cells was recorded by calcium imaging. Calcium currents in single cells were recorded using patch-clamp techniques. High K(+) (140 mmol/L) induced contractions in rat thoracic aortic rings that were inhibited by 3 mmol/L chloroquine, 3 mmol/L denatonium and 10 µmol/L nifedipine. In single rat thoracic aortic smooth muscle cells, high K(+) increased [Ca(2+)]i and this effect was also blocked by 3 mmol/L chloroquine and 10 µmol/L nifedipine. Under Ca(2+) -free conditions, high K(+) failed to induce contractions in rat thoracic aortic rings. On its own, chloroquine had no effect on the muscle tension of rat aortic rings and [Ca(2+) ]i. The vasorelaxant effects of chloroquine on precontracted rat thoracic aortic rings were not altered by either 1 µg/mL pertussis toxin (PTX), an inhibitor of Gαo/i-protein, or 1 mmol/L gallein, an inhibitor of Gßγ-protein. The results of patch-clamp analysis in single cells indicate that 1 mmol/L chloroquine blocks voltage-dependent L-type Ca(2+) channel (VDLCC) currents from both extracellular and intracellular sides. Together, the results indicate that chloroquine can block VDLCC, independent of PTX- and gallein-sensitive G-proteins, resulting in relaxation of high K(+)-precontracted thoracic aortic smooth muscle.

Self-Healing E-tongue.

Self-healing materials inspire the next generation of multifunctional wearables and Internet of Things appliances. They expand the realm of thin film fabrication, enabling seamless conformational coverage irrespective of the shape complexity and surface geometry for electronic skins, smart textiles, soft robotics, and energy storage devices. Within this context, the layer-by-layer (LbL) technique is versatile for homogeneously dispersing materials onto various matrices. Moreover, it provides molecular level thickness control and coverage on practically any surface, with poly(ethylenimine) (PEI) and poly(acrylic acid) (PAA) being the most used materials primarily employed in self-healing LbL structures operating at room temperature. However, achieving thin film composites displaying controlled conductivity and healing ability is still challenging under ambient conditions. Here, PEI and PAA are mixed with conductive fillers (gold nanorods, poly(3,4-ethylene dioxythiophene): polystyrenesulfonate (PEDOT:PSS), reduced graphene oxides, and multiwalled carbon nanotubes) in distinct LbL film architectures. Electrical (AC and DC), optical (Raman spectroscopy), and mechanical (nanoindentation) measurements are used for characterizing composite structures and properties. A delicate balance among electrical, mechanical, and structural characteristics must be accomplished for a controlled design of conductive self-healing composites. As a proof-of-concept, four LbL composites were chosen as sensing units in the first reported self-healing e-tongue. The sensor can easily distinguish basic tastes at low molar concentrations and differentiate trace levels of glucose in artificial sweat. The formed nanostructures enable smart coverages that have unique features for solving current technological challenges.

A survey on computational taste predictors.

Taste is a sensory modality crucial for nutrition and survival, since it allows the discrimination between healthy foods and toxic substances thanks to five tastes, i.e., sweet, bitter, umami, salty, and sour, associated with distinct nutritional or physiological needs. Today, taste prediction plays a key role in several fields, e.g., medical, industrial, or pharmaceutical, but the complexity of the taste perception process, its multidisciplinary nature, and the high number of potentially relevant players and features at the basis of the taste sensation make taste prediction a very complex task. In this context, the emerging capabilities of machine learning have provided fruitful insights in this field of research, allowing to consider and integrate a very large number of variables and identifying hidden correlations underlying the perception of a particular taste. This review aims at summarizing the latest advances in taste prediction, analyzing available food-related databases and taste prediction tools developed in recent years. Supplementary Information: The online version contains supplementary material available at 10.1007/s00217-022-04044-5.

Different tastants and low-caloric sweeteners induce differential effects on the release of satiety hormones.

Recent studies have found different types of taste receptors located along the intestine. However, the effect of tastants, and in particular sweet tastants, on satiety hormone release is still unknown. STC-1 cells were incubated with different concentrations of bitter, sour, sweet, salty, and umami tastants. After incubation with different time-periods, cholecystokinin (CCK) and glucagons-like peptide 1 (GLP-1) concentrations were measured in the supernatant. All tastants increased the CCK levels both dose- and time-dependently. GLP-1 release dose-dependently increased after the addition of all tastants, with the exception of acetic acid. GLP-1 was released in a time-dependent manner after the addition of all tastants, but bitter tastants stimulated GLP-1 release only during the first 15min of exposure. All commercial sweeteners elevated CCK and GLP-1 levels, with Tagatesse exerting the strongest effects. Tastants, and in particular sweet, play a role in the regulation of satiety hormone release, both in a concentration- and time-dependent manner.

Comparative Evaluation of Altered Taste Perception among Oral Submucous Fibrosis Patients.

BACKGROUND: Taste perception is an important factor in sustaining human life. Impairment of taste is one of the important features of oral submucous fibrosis (OSMF), and it has not received much attention, owing to limited research work in the field. Therefore, the present study was conducted to determine taste alteration in OSMF patients. MATERIALS AND METHODS: A total of 200 participants, both males and females with the age range of 20 years to 55 years, were included in the study. Four basic tastants (i.e., sweet, salt, sour, and bitter) were prepared as follows: sucrose for sweet (0.1-1.0 mol/l), sodium chloride for salty (0.01-1.0 mol/l), citric acid for sour (0.320-0.032 mol/l), and quinine sulfate for bitter (0.01-1.0 mol/l) and full mouth rinse test was performed for a complete taste response examination, after which punch biopsy was taken from buccal mucosa to determine histopathological staging. The data obtained were tabulated and analyzed by the Pearson Chi-square test; P < 0.05 was considered statistically significant. RESULTS: The overall results suggested that there was a significant alteration of taste. The sweet taste was altered followed by salty and bitter was least affected. CONCLUSION: The study points out at the significance of alteration in taste perception is OSMF patients related to sweet, salt, sour, and bitter taste by using physiological stimuli tastants.

Review on the Regional Effects of Gastrointestinal Luminal Stimulation on Appetite and Energy Intake: (Pre)clinical Observations.

Macronutrients in the gastrointestinal (GI) lumen are able to activate "intestinal brakes", feedback mechanisms on proximal GI motility and secretion including appetite and energy intake. In this review, we provide a detailed overview of the current evidence with respect to four questions: (1) are regional differences (duodenum, jejunum, ileum) present in the intestinal luminal nutrient modulation of appetite and energy intake? (2) is this "intestinal brake" effect macronutrient specific? (3) is this "intestinal brake" effect maintained during repetitive activation? (4) can the "intestinal brake" effect be activated via non-caloric tastants? Recent evidence indicates that: (1) regional differences exist in the intestinal modulation of appetite and energy intake with a proximal to distal gradient for inhibition of energy intake: ileum and jejunum > duodenum at low but not at high caloric infusion rates. (2) the "intestinal brake" effect on appetite and energy appears not to be macronutrient specific. At equi-caloric amounts, the inhibition on energy intake and appetite is in the same range for fat, protein and carbohydrate. (3) data on repetitive ileal brake activation are scarce because of the need for prolonged intestinal intubation. During repetitive activation of the ileal brake for up to 4 days, no adaptation was observed but overall the inhibitory effect on energy intake was small. (4) the concept of influencing energy intake by intra-intestinal delivery of non-caloric tastants is intriguing. Among tastants, the bitter compounds appear to be more effective in influencing energy intake. Energy intake decreases modestly after post-oral delivery of bitter tastants or a combination of tastants (bitter, sweet and umami). Intestinal brake activation provides an interesting concept for preventive and therapeutic approaches in weight management strategies.

Structure-dependent effects of sweet and sweet taste affecting compounds on their sensorial properties.

A reduction in sugar consumption is desirable from a health point of view. However, the sensory profiles of alternative sweet tasting compounds differ from sucrose regarding their temporal profile and undesired side tastes, reducing consumers' acceptance. The present study describes a sensory characterization of a variety of sweet and sweet taste affecting compounds followed by a comparison of similarity to sucrose and a multivariate regression analysis to investigate structural determinants and possible interactions for the temporal profile of the sweetness and side-tastes. The results of the present study suggest a pivotal role for the number of ketones, aromatic rings, double bonds and the M LogP in the temporal profile of sweet and sweet taste affecting compounds. Furthermore, interactions between aggregated physicochemical descriptors demonstrate the complexity of the sensory response, which should be considered in future models to predict a comprehensive sensory profile of sweet and sweet taste affecting compounds.

Ingesting a Bitter Solution: The Sweet Touch to Increasing Short-Term Cycling Performance.

Purpose: The authors investigated the potential benefit of ingesting 2 mM of quinine (bitter tastant) on a 3000-m cycling time-trial (TT) performance. Methods: Nine well-trained male cyclists (maximal aerobic power: 386 [38] W) performed a maximal incremental cycling ergometer test, three 3000-m familiarization TTs, and four 3000-m intervention TTs (∼4 min) on consecutive days. The 4 interventions were (1) 25 mL of placebo, (2) a 25-mL sweet solution, and (3) and (4) repeat 25 mL of 2-mM quinine solutions (Bitter1 and Bitter2), 30 s before each trial. Participants self-selected their gears and were only aware of distance covered. Results: Overall mean power output for the full 3000 m was similar for all 4 conditions: placebo, 348 (45) W; sweet, 355 (47) W; Bitter1, 354 (47) W; and Bitter2, 355 (48) W. However, quinine administration in Bitter1 and Bitter2 increased power output during the first kilometer by 15 ± 11 W and 21 ± 10 W (mean ± 90% confidence limits), respectively, over placebo, followed by a decay of 34 ± 32 W during Bitter1 and Bitter2 during the second kilometer. Bitter2 also induced a 11 ± 13-W increase during the first kilometer compared with the sweet condition. Conclusions: Ingesting 2 mM of quinine can improve cycling performance during the first one-third of a 3000-m TT and could be used for sporting events lasting ∼80 s to potentially improve overall performance.

Intraintestinal Delivery of Tastants Using a Naso-Duodenal-Ileal Catheter Does Not Influence Food Intake or Satiety.

Intraduodenal activity of taste receptors reduces food intake. Taste receptors are expressed throughout the entire gastrointestinal tract. Currently, there are no data available on the effects of distal taste receptor activation. In this study, we investigate the effect of intraduodenal and/or intraileal activation of taste receptors on food intake and satiety. In a single-blind randomized crossover trial, fourteen participants were intubated with a naso-duodenal-ileal catheter and received four infusion regimens: duodenal placebo and ileal placebo (DPIP), duodenal tastants and ileal placebo (DTIP), duodenal placebo and ileal tastants (DPIT), duodenal tastants and ileal tastants (DTIT). Fifteen minutes after cessation of infusion, subjects received an ad libitum meal to measure food intake. Visual analog scale scores for satiety feelings were collected at regular intervals. No differences in food intake were observed between the various interventions (DPIP: 786.6 ± 79.2 Kcal, DTIP: 803.3 ± 69.0 Kcal, DPIT: 814.7 ± 77.3 Kcal, DTIT: 834.8 ± 59.2 Kcal, p = 0.59). No differences in satiety feelings were observed. Intestinal infusion of tastants using a naso-duodenal-ileal catheter did not influence food intake or satiety feelings. Possibly, the burden of the four-day naso-duodenal-ileal intubation masked a small effect that tastants might have on food intake and satiety.

Characterization of Bitter Compounds via Modulation of Proton Secretion in Human Gastric Parietal Cells in Culture.

Humans perceive bitterness via around 25 different bitter receptors. Therefore, the identification of antagonists remains a complex challenge. We previously demonstrated several bitter-tasting compounds such as caffeine to induce acid secretion in the stomach and in a human gastric tumor cell line (HGT-1). Here, the results of a fluorescent-based in vitro assay using HGT-1 cells and a human sensory panel testing nine selected potential bitter modulators, with or without the bitter compounds caffeine or theobromine, were compared. Of the bitter-modulating compounds tested, eriodictyol, matairesinol, enterolacton, lariciresinol, and homoeriodictyol reduced the effect of caffeine on proton secretion by -163 ± 14.0, -152 ± 12.4, -74 ± 16.4, -58 ± 7.2, and -44.6 ± 16.5%, respectively, and reduced the bitter intensity of caffeine in the human sensory panel. In contrast, naringenin and 5,7-dihydroxy-4(4-hydroxyphenyl)chroman-2-one neither reduced the caffeine-induced proton secretion in HGT-1 cells nor showed an effect on bitter intensity perceived by the sensory panel. Results for theobromine were not as pronounced as those for caffeine, but followed a similar trend. The results demonstrate that the HGT-1 in vitro assay is a useful tool to identify potential bitter-masking compounds. Nevertheless, a sensory human panel is necessary to quantify the bitter-masking potency.

Bitter tastant responses in the amoeba Dictyostelium correlate with rat and human taste assays.

Treatment compliance is reduced when pharmaceutical compounds have a bitter taste and this is particularly marked for paediatric medications. Identification of bitter taste liability during drug discovery utilises the rat in vivo brief access taste aversion (BATA) test which apart from animal use is time consuming with limited throughput. We investigated the suitability of using a simple, non-animal model, the amoeba Dictyostelium discoideum to investigate taste-related responses and particularly identification of compounds with a bitter taste liability. The effect of taste-related compounds on Dictyostelium behaviour following acute exposure (15 minutes) was monitored. Dictyostelium did not respond to salty, sour, umami or sweet tasting compounds, however, cells rapidly responded to bitter tastants. Using time-lapse photography and computer-generated quantification to monitor changes in cell membrane movement, we developed an assay to assess the response of Dictyostelium to a wide range of structurally diverse known bitter compounds and blinded compounds. Dictyostelium showed varying responses to the bitter tastants, with IC50 values providing a rank order of potency. Comparison of Dictyostelium IC50 values to those observed in response to a similar range of compounds in the rat in vivo brief access taste aversion test showed a significant (p = 0.0172) positive correlation between the two models, and additionally a similar response to that provided by a human sensory panel assessment test. These experiments demonstrate that Dictyostelium may provide a suitable model for early prediction of bitterness for novel tastants and drugs. Interestingly, a response to bitter tastants appears conserved from single-celled amoebae to humans.

Intraduodenal infusion of a combination of tastants decreases food intake in humans.

BACKGROUND: Taste receptors are expressed not only in taste buds but also in the gastrointestinal tract. It has been hypothesized that these receptors may play a role in satiety and food intake. OBJECTIVE: This study investigated the effect of intraduodenal tastant infusions (bitter, sweet, and umami) on food intake, hunger and fullness, gastrointestinal symptoms, and gastrointestinal peptide release. DESIGN: Fifteen healthy volunteers [6 male; mean ± SEM age: 23.9 ± 2.0 y; mean ± SEM body mass index (in kg/m(2)): 22.4 ± 0.3] received 5 treatments in a double-blind, randomized, placebo-controlled crossover design. Test days started with the insertion of a nasoduodenal catheter followed by a standardized liquid breakfast. Participants received an intraduodenal infusion 150 min after breakfast, containing quinine (bitter), rebaudioside A (sweet), monosodium glutamate (umami), a combination of the 3 tastants, or placebo (tap water) over a period of 60 min. Food intake was measured during an ad libitum meal, and visual analog scales were used to monitor gastrointestinal complaints and hunger and fullness scores. Blood samples were drawn at regular intervals for cholecystokinin, glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) analysis. RESULTS: Infusion of the combination of tastants substantially decreased food intake (422 ± 97 compared with 486 ± 104 kcal for placebo, P < 0.05), whereas both a combination of tastants and umami decreased hunger scores compared with placebo. No change in cholecystokinin, GLP-1, or PYY concentrations was observed during the infusions. Intraduodenal infusions of the tastants did not result in gastrointestinal symptoms. CONCLUSIONS: Intraduodenal infusion of umami and a combination of tastants inhibits feelings of hunger, but only the latter also reduces food intake. However, these alterations were not accompanied by changes in the plasma concentrations of the gut-derived peptides cholecystokinin, GLP-1, or PYY. This trial was registered at clinicaltrials.gov as NCT01956838.

Bitter tastants alter gastric-phase postprandial haemodynamics.

ETHNOPHARMACOLOGICAL RELEVANCE: Since Greco-Roman times bitter tastants have been used in Europe to treat digestive disorders, yet no pharmacological mechanism has been identified which can account for this practice. This study investigates whether the bitter tastants, gentian root (Gentian lutea L.) and wormwood herb (Artemisia absinthium L.), stimulate cephalic and/or gut receptors to alter postprandial haemodynamics during the gastric-phase of digestion. MATERIALS AND METHODS: Normal participants ingested (1) 100 mL water plus capsules containing either cellulose (placebo-control) or 1000 mg of each tastant (n=14); or (2) 100mL of water flavoured with 500 or 1500 mg of each tastant (a) gentian (n=12) and (b) wormwood (n=12). A single beat-to-beat cardiovascular recording was obtained for the entire session. Pre/post-ingestion contrasts with the control were analysed for (1) the encapsulated tastants, in the "10 to 15" minute post-ingestion period, and (2) the flavoured water in the "5 to 10" minute post-ingestion period. RESULTS: Water, the placebo-control, increased cardiac contraction force and blood pressure notwithstanding heart rate decreases. Encapsulated tastants did not further alter postprandial haemodynamics. In contrast gentian (500 and 1500 mg) and wormwood (1500 mg) flavoured water elicited increased peripheral vascular resistance and decreased cardiac output, primarily by reducing stroke volume rather than heart rate. CONCLUSIONS: Drinking 100mL water elicits a pressor effect during the gastric-phase of digestion due to increased cardiac contraction force. The addition of bitter tastants to water elicits an additional and parallel pressor effect due to increased peripheral vascular resistance; yet the extent of the post-prandial blood pressure increases are unchanged, presumably due to baroreflex buffering. The vascular response elicited by bitter tastants can be categorised as a sympathetically-mediated cephalic-phase response. A possible mechanism by which bitter tastants could positively influence digestion is altering gastric-phase postprandial haemodynamics and supporting postprandial hyperaemia.