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The molecular basis of sweet taste toward various amino acids has not been fully elucidated. In this study, by correlation of their sweetness intensities with molecular properties, it is revealed that hydrophobic or dispersion force between side chains and sweet taste receptor (Tas1R2/Tas1R3) plays a prominent role for eliciting sweetness. Furthermore, the interaction modes of 13 amino acids with receptor indicate that amino (AH) and carboxyl (B) glucophores of different amino acids interact with identical residues of receptor, while the hydrophobic side chains (X glucophores) conduct distinct topological orientations with receptor, determining their chirality selection and sweetness intensities. Molecular dynamics analysis shows that sweet d‐amino acids move toward the hydrophobic transmembrane domain during activation with more contact numbers with receptor than nonsweet l‐amino acids, providing a mechanistic elucidation of previous inconsistent sensory evaluation results of specific amino acids. Moreover, by comparison with the interactions of a dipeptide sweetener, aspartame with Tas1R2/Tas1R3 and nonsweet l‐glutamate with class C G protein‐coupled receptors, we conclude that a complementary interaction mode with both hydrophilic and hydrophobic contacts accounts for the molecular origin of their sweet taste, presenting in‐depth insights and valuable guidelines for further molecular designs or modifications of amino acids‐derived sweeteners. [ABSTRACT FROM AUTHOR]

Sodium and two popular artificial sweeteners, sucralose and acesulfame, are poorly removed by conventional water and wastewater treatment. The drinking water industry must prepare for the presence of these tastants in tap water and develop strategies to minimize effects on the public. [ABSTRACT FROM AUTHOR]

The oral detection of sugars relies on two types of receptor systems. The first is the G-protein-coupled receptor TAS1R2/TAS1R3. When activated, this receptor triggers a downstream signaling cascade involving gustducin, phospholipase Cβ2 (PLCβ2), and transient receptor potential channel M5 (TRPM5). The second type of receptor is the glucose transporter. When glucose enters the cell via this transporter, it is metabolized to produce ATP. This ATP inhibits the opening of KATP channels, leading to cell depolarization. Beside these receptor systems, sweet-sensitive taste cells have mechanisms to regulate their sensitivity to sweet substances based on internal and external states of the body. Sweet taste receptors are not limited to the oral cavity; they are also present in extraoral organs such as the gastrointestinal tract, pancreas, and brain. These extraoral sweet receptors are involved in various functions, including glucose absorption, insulin release, sugar preference, and food intake, contributing to the maintenance of energy homeostasis. Additionally, sweet receptors may have unique roles in certain organs like the trachea and bone. This review summarizes past and recent studies on sweet receptor systems, exploring the molecular mechanisms and physiological functions of sweet (sugar) detection in both oral and extraoral organs. [ABSTRACT FROM AUTHOR]

This article discusses the history of the perception of sugar from antiquity to the Middle Ages. The author shows how changes in society can be demonstrated by changes in the reflection of dietary attitudes towards sweet taste. Medieval society was influenced by ambiguous attitudes towards sugar and sweets in general. On one hand, sweet taste was associated with the risk of mental malaise, which contradicted religious devotion to the Christian faith; on the other hand, the description of sweet taste was often used symbolically in the Bible as an allegory of reward for strong faith. Sugar, however, found its way into pharmacy as a medicine and, above all, as a sweetener. Medieval trade between Europe and its Arab neighbours and the development of urban and international trade eventually opened the way for sugar cane to enter Europe. European merchants learned to produce sugar and, from the 16th century onwards, took their technological knowledge or knowledge of the organisation of cane sugar production to the newly discovered territories in America. The transfer of knowledge was the precursor to the Industrial Revolution and medieval concepts of sugar were forgotten. This article therefore provides a brief overview of medieval mindset regarding sugar and sweet taste. [ABSTRACT FROM AUTHOR]

Background: Recent research has shown obesity to be associated with e-cigarette use and appeal, but models have yet to examine how weight status may be related to e-cigarette dependence among e-cigarette users. Objectives: To increase our understanding of pathways from body mass index (BMI) to e-cigarette dependence, the present cross-sectional observational study investigated a model in which BMI, sweet taste responsiveness, and the interaction of BMI and sweet taste responsiveness are associated with e-cigarette dependence indirectly via seven conceptually-distinct motives for e-cigarette use. Data from several e-cigarette clinical laboratory research studies were pooled and analyzed; only current e-cigarette users were included in the analyses (N=330). Structural equation modeling was used to analyze the hypothesized model. Results: BMI was positively associated with lower social/environmental goad motives and higher weight control motives, and BMI x sweet taste interaction terms found that sweet taste responsiveness strengthened the association of BMI and weight control motives. BMI was not directly or indirectly associated with e-cigarette dependence nor was there a bivariate association between BMI and e-cigarette dependence. Sweet taste responsiveness was positively associated with greater affiliative attachment motives, cognitive enhancement motives, cue exposure-associative process motives, weight control motives, and affect enhancement motives. Sweet taste responsiveness was bivariately associated with e-cigarette dependence and mediation paths show indirect relations to e-cigarette dependence via three of the seven motives. Conclusions: The findings suggest that sweet taste responsiveness, opposed to BMI, is associated with a wider range of e-cigarette use motives and indirectly relates to e-cigarette dependence via several e-cigarette use motives. [ABSTRACT FROM AUTHOR]

Introduction and purpose: Sugar is the primary energy substrate for the brain. Consuming sweet products releases dopamine, which activates the reward system. In this aspect, excessive consumption of sugar is similar to drug use and leads to many health risks. The aim of the study is to systematize information on sugar addiction, highlight the need for preventive measures and create treatment algorithms covering areas such as psychotherapy, pharmacotherapy and the positive impact of physical activity. Materials and metods: A literature search was conducted using the medical databases PubMed and Google Scholar. Articles were retrieved in English, employing the key words: “sugar addiction”, “sweet taste”, „sugar diabetes” and „sugar sport” in appropriate configurations. The analysis encompassed data from 34 scientific references published between 2007 and 2024. Conclusions: Many factors contribute to sugar addiction. It is a self-perpetuating cycle, as obese and sugar addicts need more sugar to feel satisfied. At the same time, sugar negatively affects body weight, behavior, mood, cardiovascular, nervous, digestive systems. Which is why steps should be taken to increase public understanding and awareness of the mechanism of sugar addiction and its risks.

BackgroundTo understand age-related changes in sweet taste perception in daily life, it is important to understand taste intensity at the suprathreshold level. Previous studies have attempted to characterize the temporal aspects of human taste perception in terms of time–intensity evaluations. The perception of dynamic taste intensity in older adults increases slowly for salty taste; however, there have been no previous studies on time–intensity sensory evaluation of sweet taste in older adults. We hypothesized that older adults perceive sweet taste intensity more slowly than young adults.MethodsFifty young and 40 older adults participated in the study and glucose solutions of 0.6 M and 1.5 M were used as stimuli. The study comprised two experiments: (1) a cup tasting test (static taste perception in the mouth), and (2) a time–intensity sensory evaluation, in which the solutions were presented using a custom-made delivery system. The intra-oral device was made to fit each participant’s dentition. Further, the level of gag reflex was taken into consideration for each participant in the design of the intra-oral device. A suction tube was placed across the posterior tongue near the throat to remove solution and saliva. The solution delivery system was controlled by an original computer program.ResultsOlder adults presented significantly different maximum intensity timing and slope for both concentrations compared with young adults (slope for 1.5 M, p < 0.01; others, p < 0.05). No significant differences were found between the older and young adults for reaction timing and maximum intensity.ConclusionWe conclude that older adults perceived sweetness more slowly than young adults, and ultimately perceived almost the same intensity as young adults. This is the first reported characterization of the time–intensity profile of sweet taste intensity of glucose in older adults. Using a standardized system enabled us to assess and compare feedback on taste intensities among different age groups in real-time. Based on this, we recommend older adults “savor” to perceive sweet tastes at the same level experienced by young adults.

Sweet and umami taste receptors recognize chemicals such as sugars and amino acids on their extracellular side and transmit signals into the cytosol of the taste cell. In contrast to ligands that act on the extracellular side of these receptors, little is known regarding the molecules that regulate receptor functions within the cytosol. In this study, we analysed the interaction between sweet and umami taste receptors and calmodulin, a representative Ca2+-dependent cytosolic regulatory protein. High prediction scores for calmodulin binding were observed on the C-terminal cytosolic side of mouse taste receptor type 1 subunit 3 (T1r3), a subunit that is common to both sweet and umami taste receptors. Pull-down assay and surface plasmon resonance analyses showed different affinities of calmodulin to the C-terminal tails of distinct T1r subtypes. Furthermore, we found that T1r3 and T1r2 showed the highest and considerable binding to calmodulin, whereas T1r1 showed weaker binding affinity. Finally, the binding of calmodulin to T1rs was consistently higher in the presence of Ca2+ than in its absence. The results suggested a possibility of the Ca2+-dependent feedback regulation process of sweet and umami taste receptor signaling by calmodulin. [ABSTRACT FROM AUTHOR]

BACKGROUND: Increased consumption of sweet and high-calorie foods leads to weight gain in humans and the development of metabolic syndrome. Great attention is given to a personalized approach to nutrition correction based on genetic testing. The genetic basis for human taste sensitivity to sweet stimuli remains is understudied. The role of the g.18853330 A>G (rs4920566) polymorphism of the TAS1R2 gene in preference for sweets has not been fully studied.AIM: To investigate the possible relationship between rs4920566 polymorphism in TAS1R2 gene and sensitivity to natural sugars and food preference of high-calorie sweet foods in humans.MATERIALS AND METHODS: A single-sample experimental study was carried out. The study participants were conditionally healthy students who voluntarily agreed to conduct it. Sugar sensitivity was assessed in two tasting tests. Sucrose sensitivity thresholds (STS) were determined by staircase procedure (solutions: 8.0 to 500 mM/l). To assess food preferences for sweet foods, specially designed questionnaires with a checklist of products were used. Genomic DNA samples from all study participants were obtained from buccal epithelial cells. Genomic DNA was extracted from buccal epithelial cells using the adsorption of DNA with an inorganic sorbent in the presence of a chaotropic agent. Typing of the rs4920566 polymorphism in TAS1R2 gene was performed using asymmetric real-time PCR.RESULTS: The study included 26 young men and 110 young women which the average age was 20.8±4.8 (SD) years. Gender was a significant factor affecting the taste perception of the sweetness sugars (maltose, glucose, sucrose and fructose) in students. Young men more often than young women could not distinguish the taste of four sugars (β=-2.93(0.99), p=0.003). The rs4920566 polymorphism in TAS1R2 gene did not affect the ability of students to distinguish the taste of four natural sugars. It was found that the variation series of STS values for sucrose in young women with the A allele (16.0[16.0–31.0] versus 16.0[8.0–16.0] mmol/l, pcor=0.002) and A/G genotype (16.0[16.0–31.0] vs. 16.0[8.0–16.0] mmol/l, pcor=0.010) were significantly lower compared to young men. Separately, in young women with the G/G genotype the range of STS is shifted towards higher concentrations of sucrose compared with women with the A/G genotype (16.0[16.0–31.0] vs. 16.0[8.0 -16.0] mmol/l, pcor=0.039). Testing the hypothesis about the randomness of the relationship between the rs4920566 genotypes of the TAS1R2 gene and the liking rating of foods with a sweet taste using Kruskal-Wallis test did not allow us to conclude that the A/A, A/G and G/G genotypes of the TAS1R2 gene influence the choice of sugary high-calorie foods in students.CONCLUSION: Our results are consistent with the literature data and confirm that rs4920566 polymorphism of TAS1R2 gene cannot be an informative marker for the diagnosis of metabolic conditions associated with the consumption of high-calorie sweet foods. Likely, its functions are related to the mechanisms of neurotransduction of the sweet taste signal.

A commercial strain of Hafnia alvei (H. alvei) 4597 bacteria was shown to reduce food intake and promote weight loss, effects possibly induced by the bacterial protein ClpB, an antigen-mimetic of the anorexigenic α-melanocyte-stimulating hormone. A decrease in the basal plasma glucose levels was also observed in overweight fasted humans and mice receiving H. alvei. However, it is not known whether H. alvei influences sweet taste preference and whether its protein extract or ClpB are sufficient to increase glucose tolerance; these are the objectives tested in the present study. C57BL/6J male mice were kept under standard diet and were gavaged daily for 17 days with a suspension of H. alvei (4.5 × 107 CFU/animal) or with H. alvei total protein extract (5 μg/animal) or saline as a control. Sweet taste preference was analyzed via a brief-access licking test with sucrose solution. Glucose tolerance tests (GTT) were performed after the intraperitoneal (IP) or intragastric (IG) glucose administration at the 9th and 15th days of gavage, respectively. The expression of regulatory peptides' mRNA levels was assayed in the hypothalamus. In another experiment performed in non-treated C57BL/6J male mice, effects of acute IP administration of recombinant ClpB protein on glucose tolerance were studied by both IP- and IG-GTT. Mice treated with the H. alvei protein extract showed an improved glucose tolerance in IP-GTT but not in IG-GTT. Both groups treated with H. alvei bacteria or protein extract showed a reduction of pancreatic tissue weight but without significant changes to basal plasma insulin. No significant effects of H. alvei bacteria or its total protein extract administration were observed on the sweet taste preference, insulin tolerance and expression of regulatory peptides' mRNA in the hypothalamus. Acute administration of ClpB in non-treated mice increased glucose tolerance during the IP-GTT but not the IG-GTT, and reduced basal plasma glucose levels. We conclude that both the H. alvei protein extract introduced orally and the ClpB protein administered via IP improve glucose tolerance probably by acting at the glucose postabsorptive level. Moreover, H. alvei probiotic does not seem to influence the sweet taste preference. These results justify future testing of both the H. alvei protein extract and ClpB protein in animal models of diabetes. [ABSTRACT FROM AUTHOR]

On the tongue, the T1R-independent pathway (comprising glucose transporters, including sodium–glucose cotransporter (SGLT1) and the KATP channel) detects only sugars, whereas the T1R-dependent (T1R2/T1R3) pathway can broadly sense various sweeteners. Cephalic-phase insulin release, a rapid release of insulin induced by sensory signals in the head after food-related stimuli, reportedly depends on the T1R-independent pathway, and the competitive sweet taste modulators leptin and endocannabinoids may function on these two different sweet taste pathways independently, suggesting independent roles of two oral sugar-detecting pathways in food intake. Here, we examined the effect of adrenomedullin (ADM), a multifunctional regulatory peptide, on sugar sensing in mice since it affects the expression of SGLT1 in rat enterocytes. We found that ADM receptor components were expressed in T1R3-positive taste cells. Analyses of chorda tympani (CT) nerve responses revealed that ADM enhanced responses to sugars but not to artificial sweeteners and other tastants. Moreover, ADM increased the apical uptake of a fluorescent D-glucose derivative into taste cells and SGLT1 mRNA expression in taste buds. These results suggest that the T1R-independent sweet taste pathway in mouse taste cells is a peripheral target of ADM, and the specific enhancement of gustatory nerve responses to sugars by ADM may contribute to caloric sensing and food intake. [ABSTRACT FROM AUTHOR]

The search for novel, natural, high-sweetness, low-calorie sweeteners remains open and challenging. In the present study, the structure-based machine learning modeling and sweetness recognition mechanism were investigated to assist this process. It was found that whether or not a compound was sweet was closely related to molecular connectivity and composition (the number of hydrogen bond acceptors and donors), tpsaEfficiency, structural complexity, and shape (nAtomP and Fsp3). While the relative sweetness of sweet compounds was more determined by the molecular properties (tpsaEfficiency and Log P), structural complexity and composition (nAtomP and ATSm 1). The built machine learning models exhibited very good performance for classifying the sweet/non-sweet compounds and predicting the relative sweetness of the compounds. Moreover, a specific binding pocket was found for sweet compounds, and the sweet compounds mainly interacted with the VFT domain of the T1R2-T1R3 through hydrogen bonds. In addition, the results indicated that among the sweet compounds, those that were sweeter bound to the VFT domain stronger than those that had low sweetness. This study provides very useful information for developing new sweeteners. [ABSTRACT FROM AUTHOR]

Abstract Background Several health organizations recommend lowering the consumption of sweet-tasting foods. The rationale behind this recommendation is that a lower exposure to sweet foods may reduce preferences for sweet tasting foods, thus lowering sugar and energy intake, and in turn aiding in obesity prevention. However, empirical data supporting this narrative are lacking. In fact, relatively little is known about the contribution of long-term sweet taste exposure on one’s sweetness preferences. Methods The primary objective of this randomized controlled trial is to assess the effect of low, regular and high dietary sweetness exposure on preference for sweet foods and beverages, and to compare these effects between intervention groups. One hundred and eighty adults aged 18–65 years with a BMI of 18.5–30.0 kg/m2 will be recruited and randomly allocated to either: low dietary sweetness exposure (LSE) (10–15% daily energy from sweet tasting foods), regular dietary sweetness exposure (RSE) (25–30% daily energy from sweet tasting foods), or high dietary sweetness exposure (HSE) (40–45% daily energy from sweet tasting foods), for 6 months, followed by a 4-month follow up. Intervention foods are provided ad libitum, covering approximately 50% of the daily number of food items, to include sugar-sweetened, low-calorie-sweetener-sweetened and non-sweet foods. The primary outcome measure is the difference in change in sweetness preference from baseline to 6 months between intervention groups. Secondary outcomes include: change in sweet taste preferences at different time-points; taste intensity perception; behavioral outcomes: food choice and intake, sweet-liker type, food cravings, dietary taste preferences and dietary taste patterns; anthropometric outcomes: body composition, waist-hip circumference, body weight; and biochemical outcomes: glucose variability and biomarkers related to CVD and diabetes. Discussion This study will generate important data on the effect of dietary sweetness exposure on sweetness preferences in terms of effect size and change, duration of change and its impact on food intake, body weight status and associated health outcomes. Trial Registration The study protocol has been registered on ClinicalTrials.gov (ID no. NCT04497974, Registered 4 August 2020, https://clinicaltrials.gov/ct2/show/NCT04497974 ) and approved by Wageningen’s Medical Ethical Committee (ABR no. NL72134).

Diet therapy for diabetes involves controlling carbohydrate intake in order to manage blood glucose concentrations. Simple carbohydrates, like sucrose, quickly and potently raise blood glucose when ingested, and are typically perceived as sweet. Sweetness is innately pleasurable and contributes to the positive hedonic evaluation of foods and beverages. There is some evidence to suggest that individuals with diabetes mellitus may be less able to detect sweetness, which could result in increased intake and, thus, more difficulty managing blood glucose. A systematic review that included PubMed, PsycInfo, and Embase databases was conducted. Inclusion criteria included observational studies that investigated the sweet taste function of adults with and without diabetes mellitus (Prospero CRD42021225058). The quality of the final included studies was assessed using the Academy of Nutrition and Dietetics' Evidence Analysis Library Quality Criteria Checklist: Primary Research tool. Eighteen studies that compared sweet taste thresholds, intensity ratings, or hedonic responses in adults both with and without diabetes were included. Differences in sweet taste thresholds, both detection and recognition, indicated that individuals with diabetes were less sensitive than healthy controls. The same findings were observed for intensity ratings. Only two studies examined hedonic responses; results were inconclusive. [ABSTRACT FROM AUTHOR]

Background: Several health organizations recommend lowering the consumption of sweet-tasting foods. The rationale behind this recommendation is that a lower exposure to sweet foods may reduce preferences for sweet tasting foods, thus lowering sugar and energy intake, and in turn aiding in obesity prevention. However, empirical data supporting this narrative are lacking. In fact, relatively little is known about the contribution of long-term sweet taste exposure on one's sweetness preferences. Methods: The primary objective of this randomized controlled trial is to assess the effect of low, regular and high dietary sweetness exposure on preference for sweet foods and beverages, and to compare these effects between intervention groups. One hundred and eighty adults aged 18–65 years with a BMI of 18.5–30.0 kg/m2 will be recruited and randomly allocated to either: low dietary sweetness exposure (LSE) (10–15% daily energy from sweet tasting foods), regular dietary sweetness exposure (RSE) (25–30% daily energy from sweet tasting foods), or high dietary sweetness exposure (HSE) (40–45% daily energy from sweet tasting foods), for 6 months, followed by a 4-month follow up. Intervention foods are provided ad libitum, covering approximately 50% of the daily number of food items, to include sugar-sweetened, low-calorie-sweetener-sweetened and non-sweet foods. The primary outcome measure is the difference in change in sweetness preference from baseline to 6 months between intervention groups. Secondary outcomes include: change in sweet taste preferences at different time-points; taste intensity perception; behavioral outcomes: food choice and intake, sweet-liker type, food cravings, dietary taste preferences and dietary taste patterns; anthropometric outcomes: body composition, waist-hip circumference, body weight; and biochemical outcomes: glucose variability and biomarkers related to CVD and diabetes. Discussion: This study will generate important data on the effect of dietary sweetness exposure on sweetness preferences in terms of effect size and change, duration of change and its impact on food intake, body weight status and associated health outcomes. Trial Registration: The study protocol has been registered on ClinicalTrials.gov (ID no. NCT04497974, Registered 4 August 2020, https://clinicaltrials.gov/ct2/show/NCT04497974) and approved by Wageningen's Medical Ethical Committee (ABR no. NL72134). [ABSTRACT FROM AUTHOR]

Taste function impairment is observed in people with type 1 diabetes (T1D). It is most often related to sweet taste. It is associated with such factors as diabetic neuropathy, smoking, age, duration of the disease and a rigorous diet that eliminates easily digestible carbohydrates. The aim of the study was to compare sensitivity to sweet and salty tastes between healthy children and adolescents and children and adolescents with T1D. The study group consisted of children with T1D (n = 35), with at least 5 years of disease history, while the group of healthy children included 46 individuals selected in terms of age, gender and BMI. A study concerning the perception of sweet and salty taste was carried out with the use of the specific gustometry method (examining the recognition and assessment of the intensity of taste sensations, performing a hedonic assessment). Children and adolescents from both groups had trouble recognising tastes. Children and adolescents with T1D were more likely to recognise sweet taste correctly even at its lower concentrations compared to healthy individuals (p = 0.04). Salty taste was significantly more often correctly identified by healthy children compared to T1D patients (p = 0.01). Children and adolescents with T1D reported a stronger intensity of perceived tastes than healthy ones. No significant differences in perceived pleasure were noted at lower sucrose concentrations in any group. The intensity score was higher in individuals with T1D at higher sucrose concentrations. No significant differences occurred in the assessment of salty taste intensity. The hedonic scoring of solutions with higher concentrations of sweet taste was higher in people with T1D than in healthy ones, while salty taste was assessed neutrally. Children and adolescents with T1D were demonstrated to have some taste recognition disorders. Therefore, monitoring taste function in pediatric diabetic clinical practice seems relevant, as it may be associated with important implications for the intake of a particular type of food and for the development of eating habits and preferences. [ABSTRACT FROM AUTHOR]

Abstract Background Strong evidence suggests that maternal-infant skin-to-skin contact (SSC) is effective in reducing behavioural responses to pain. Given the multi-sensory benefits of SSC, it is highly likely that SSC provided during pain in early life may reduce pain-induced brain activity. The aim of this study is to examine the effect of SSC compared to 24% sucrose on pain-induced activity in the preterm infant brain during a medically required heel lance. Secondary objectives include determining (a) differences between behavioural pain response and noxious-related brain activity during heel lance and (b) rate of adverse events across groups. Methods We will randomly assign 126 babies (32 to 36 completed weeks gestational age) admitted to the neonatal intensive care unit, and their mothers within the first seven days of age to receive (i) SSC plus sterile water and (ii) 24% oral sucrose. Each baby will receive a medically indicated heel lance, following a no treatment baseline period. The primary outcome is noxious-related brain activity measured using an electroencephalogram (EEG) pain-specific event-related potential. Secondary outcomes include pain intensity measured using a bio-behavioural infant pain assessment tool (Premature Infant Pain Profile-Revised) and rate of adverse events. Discussion This will be the first clinical trial to compare the effect of SSC and 24% sucrose on pain-induced brain activity in the preterm infant brain during a clinical noxious stimulus, measured using EEG. Given the negative neurodevelopmental outcomes associated with unmanaged pain, it is imperative that preterm babies receive the most effective pain-reducing treatments to improve their health outcomes. Our findings will have important implications in informing optimal pain assessment and management in preterm infants. Trial registration ClinicalTrials.gov NCT03745963 . Registered on November 19, 2018.

From the root barks of a Central African tree Millettia dubia De Wild. (Fabaceae), ten previously undescribed oleanane-type glycosides were isolated by various chromatographic protocols. Their structures were elucidated by spectroscopic methods, mainly 2D NMR experiments and mass spectrometry, as mono- and bidesmosidic glycosides of mesembryanthemoidigenic acid, hederagenin and oleanolic acid. The stimulation of the sweet taste receptor TAS1R2/TAS1R3 by these glycosides was evaluated, and structure/activity relationships were proposed. Two of them showed an agonist effect on TAS1R2/TAS1R3. [Display omitted] • Ten different oleanolic acid glycosides were isolated. • Their structures were elucidated by extensive 2D NMR analyses. • The stimulation of the sweet taste receptors TAS1R2/TAS1R3 was evaluated. • Some structure/activity relationships were discussed. [ABSTRACT FROM AUTHOR]

Summary: Taste sensation enables humans to make nutritionally important decisions such as food preference and consumption. It functions as deterministic factors for unpropitious eating behavior, leading to overweight and obesity. The hedonistic feeling on consumption of fat and sugar‐rich meals, in particular, has a negative influence on health. In addition, impairment in the taste receptors alters the downstream signaling of taste transduction pathway. Hence, genetic polymorphism in typical taste receptors is a predictor of taste sensitivity variance across individuals. The present review summarizes the effect of a single nucleotide polymorphism (SNP) in sweet taste receptors (T1R2/T1R3) on taste perception among individuals of various body mass index (BMI). Furthermore, in the context of obesity, we discussed the possibility of crosstalk between fat and sweet receptors as well as taste dysfunction in diseased individuals. In overall, a greater understanding of the physiological relationship between taste receptors, altered taste sensitivity, and genetic polymorphisms should lead to more effective obesity prevention approaches. [ABSTRACT FROM AUTHOR]

Human research has shown interactions between rewards and cognitive control. In animal models of affective neuroscience, reward administration typically involves administering orosensory sugar signals (OSS) during caloric-deprived states. We adopted this procedure to investigate neurophysiological mechanisms of reward-cognitive control interactions in humans. We predicted that OSS would affect neurophysiological and behavioral indices of error processing oppositely, depending on the relative weight of the OSS-induced 'wanting' and 'liking' components of reward. We, therefore, conducted a double-blind, non-nutritive sweetener-controlled study with a within-subject design. Fasted (16 hr) participants (N = 61) performed a modified Flanker task to assess neurophysiological (error-related negativity [Ne/ERN]) and behavioral (post-error adaptations) measures of error processing. Non-contingent to task performance, we repeatedly administered either a sugar (glucose) or non-nutritive sweetener (aspartame) solution, which had to be expulsed after short oral stimulation to prevent post-oral effects. Consistent with our hypothesis on how 'liking' would affect Ne/ERN amplitude, we found the latter to be decreased for sugar compared to aspartame. Unexpectedly, we found post-error accuracy, instead of post-error slowing, to be reduced by sugar relative to aspartame. Our findings suggest that OSS may interact with error processing through the 'liking' component of rewards. Adopting our reward-induction procedure (i.e. administering OSS in a state of high reward sensitivity [i.e. fasting], non-contingent to task performance) might help future research investigating the neural underpinnings of reward-cognitive control interactions in humans. [ABSTRACT FROM AUTHOR]

The phytochemical study of Wisteria sinensis (Sims) DC. (Fabaceae), commonly known as the Chinese Wisteria, led to the isolation of seven oleanane-type glycosides from an aqueous-ethanolic extract of the roots. Among the seven isolated saponins, two have never been reported before: 3-O-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranosyl-(1→2)-β-D-glucuronopyranosyl-22-O-acetylolean-12-ene-3β,16β,22β,30-tetrol, and 3-O-β-D-xylopyranosyl-(1→2)-β-D-glucuronopyranosylwistariasapogenol A. Based on the close structures between the saponins from W. sinensis, and the glycyrrhizin from licorice, the stimulation of the sweet taste receptor TAS1R2/TAS1R3 by these glycosides was evaluated. [ABSTRACT FROM AUTHOR]

Non-sugar sweeteners (NSS), low- or no-calorie alternatives to sugar, are marketed for weight loss and improved blood glucose control in people with diabetes. However, their health effects remain controversial. This review provides a brief overview of sweet taste perception and summarizes experimental findings of the impact of NSS on cardiometabolic health in animal models and humans. We also review evidence suggesting that many NSS are not metabolically inert, highlighting the challenges in related human studies. Given the conflicting and unclear data on health outcomes, additional mechanistic studies, particularly in animal models, are necessary to clarify how NSS influence feeding behaviors and energy homoeostasis., Competing Interests: Declaration of interests No interests are declared., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

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, NH 4 Cl, and CaCl 2 . 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.

The aim of the study is to analyze the association of different bitter and sweet gene receptor polymorphisms and bitter and sweet food consumption on formation of dental caries in Turkish adult population.

IntroductionWhile sweet taste perception is a potential determinant of feeding behavior in obesity, the supporting evidence is inconsistent and is typically associated with methodological limitations. Notably, possible associations between sweet taste perception and measures of food reward remain undetermined.Materials and methodsWe conducted a cross-sectional analysis comparing 246 individuals with severe obesity and 174 healthy volunteers using a validated method for taste perception assessment. We included gustatory variables, namely intensity and pleasantness ratings of sour, salt, sweet, and bitter tastants, and taste thresholds assessed by electrogustometry. Reward-related feeding behavior, including hedonic hunger, food addiction, feeding behavior traits, and acceptance of foods and alcohol, was evaluated using self-rated scales for comparison with gustatory measures.ResultIn logistic regressions adjusted for age, gender, educational level, and research center, we found that a greater likelihood of belonging to the obesity group was associated with higher sweet intensity ratings (OR = 1.4, P = 0.01), hedonic hunger, food addiction symptoms, restrained and emotional eating (1.7 < OR ≤ 4.6, all P ≤ 0.001), and lower alcohol acceptance (OR = 0.6, P = 0.0002). Using principal component analysis, we found that while hedonic hunger, food addiction, and emotional eating were strongly interrelated, they were not associated with sweet intensity perception that, in turn, had a closer relationship with alcohol acceptance and restrained eating.ConclusionWe found that individuals with obesity report higher sweet taste intensity ratings than healthy controls. Furthermore, while psychological measures of reward-related feeding behavior assess a common construct, sweet intensity perception may represent a different obesity-related dimension.

The human sweet taste receptor is a heterodimeric receptor composed of two distinct G-protein-coupled receptors (GPCRs), TAS1R2 and TAS1R3. The TAS1R2 and TAS1R3 subunits are members of a small family of class C GPCRs whose members share the same architecture, comprising a Venus Flytrap (VFT) module linked to the seven transmembrane domains (TMDs) by a short cysteine-rich region (CRR). The VFT module of TAS1R2 contains the primary binding site for most of the sweet-tasting compounds, including natural sugars and artificial and natural sweeteners. However, cellular assays, molecular docking and site-directed mutagenesis studies have revealed that the VFT, CRR and TMD of TAS1R3 interact with some sweeteners, including the sweet-tasting protein brazzein. The aim of this study was to better understand the contribution of TAS1R2-VFT in the binding of sweet stimuli. To achieve this, we heterologously expressed human TAS1R2-VFT (hTAS1R2-VFT) in Escherichia coli. Circular dichroism spectroscopic studies revealed that hTAS1R2-VFT was properly folded with evidence of secondary structures. Using size-exclusion chromatography coupled with light scattering, we found that hTAS1R2-VFT behaves as a monomer. Ligand binding quantified by intrinsic tryptophan fluorescence showed that hTAS1R2-VFT is capable of binding sweet stimuli with Kd values, in agreement with physiological detection. Furthermore, we investigated whether the impact of point mutations, already shown to have deleterious effects on cellular assays, could impact the ability of hTAS1R2-VFT to bind sweet ligands. As expected, the ligand affinities of hTAS1R2-VFT were drastically reduced through the introduction of single amino acid substitutions (D278A and E382A) known to abolish the response of the full-length TAS1R2/TAS1R3 receptor. This study demonstrates the feasibility of producing milligram quantities of hTAS1R2-VFT to further characterize the mechanism of binding interaction and perform structural studies. [ABSTRACT FROM AUTHOR]

ABSTRACT: Elucidating the taste sensing systems in chickens will enhance our understanding of poultry nutrition and improve the feeding strategies used in poultry farming. It is known that chickens lack the sweet taste receptor subunit, taste receptor type 1 member 2 (T1R2), in their genome. Thus, the present study investigated T1R2-independent sweet-sensing pathways in chickens. RT-PCR analysis revealed that glucose transporters known to play an important role in T1R2-independent sweet sensing in mammals—namely sodium-glucose cotransporter 1 (SGLT1) and ATP-gated K+ channel subunits—are expressed in the palate, the main taste organ in chickens. In behavioral tests, chickens slightly preferred glucose, galactose, sucrose, maltose, lactose, and stevioside, while high doses of sucrose and fructose were rejected. Chickens did not show any preference for noncaloric sweeteners or sugar alcohol, such as acesulfame K, aspartame, saccharin, sucralose, or sorbitol. The preference for galactose was inhibited by an inhibitor of SGLT1 in a dose-dependent manner. In addition, we found that glucagon-like peptide 1 (GLP-1) and mRNA of the GLP-1 receptor, which are involved specifically in sweet transmission in mice, are also present in the oral tissues of chickens. The present results imply that chickens can sense various sweet compounds via T1R2-independent pathways in oral tissues.

Using mouth rinse (MR) with carbohydrate during exercise has been shown to act as an ergogenic aid. Purpose: To investigate if nutritive or nonnutritive sweetened MR affects exercise performance and to assess the influence of sweetness intensity on endurance performance during a time trial (TT). Methods: This randomized, single-blinded study had 4 treatment conditions. Sixteen subjects (9 men, 7 women) completed a 12.8-km TT 4 different times. During each TT, subjects mouth-rinsed and expectorated a different solution at time 0 and every 12.5% of the TT. The 4 MR solutions were sucrose (S) (sweet taste and provides energy of 4 kcal/g), a lower-intensity sucralose (S1:1) (artificial sweetener that provides no energy but tastes sweet), a higher-intensity sucralose (S100:1), and water as control (C). Completion times for each TT, heart rate (HR), and ratings of perceived exertion (RPE) were also recorded. Results: Completion time for S was faster than for C (1:03:47 ± 00:02:17 vs 1:06:56 ± 00:02:18, respectively; P < .001) and showed a trend to be faster vs S100:1 (1:03:47 ± 00:02:17 vs 1:05:38 ± 00:02:12, respectively; P = .07). No other TT differences were found. Average HR showed a trend to be higher for S vs C (P = .08). The only difference in average or maximum RPE was for higher maximum RPE in C vs S1:1 (P = .02). Conclusion: A sweet-tasting MR did improve endurance performance compared with water in a significant manner (mean 4.5% improvement; 3+ min.); however, the presence of energy in the sweet MR appeared necessary since the artificial sweeteners did not improve performance more than water alone. [ABSTRACT FROM AUTHOR]

The search for novel, natural, high-sweetness, low-calorie sweeteners remains open and challenging. In the present study, the structure-based machine learning modeling and sweetness recognition mechanism were investigated to assist this process. It was found that whether or not a compound was sweet was closely related to molecular connectivity and composition (the number of hydrogen bond acceptors and donors), tpsaEfficiency, structural complexity, and shape (nAtomP and Fsp3). While the relative sweetness of sweet compounds was more determined by the molecular properties (tpsaEfficiency and Log P), structural complexity and composition (nAtomP and ATSm 1). The built machine learning models exhibited very good performance for classifying the sweet/non-sweet compounds and predicting the relative sweetness of the compounds. Moreover, a specific binding pocket was found for sweet compounds, and the sweet compounds mainly interacted with the VFT domain of the T1R2-T1R3 through hydrogen bonds. In addition, the results indicated that among the sweet compounds, those that were sweeter bound to the VFT domain stronger than those that had low sweetness. This study provides very useful information for developing new sweeteners.

Schisandra sphenanthera (Schisandra sphenanthera Rehd. et Wils.) is the dried mature fruit of Schisandra sphenanthera, a plant in the Magnoliaceae family. It was used in the treatment of diabetes mellitus in the Jade Fluid Decoction and the Xiaoke pills, which were recorded in ancient books. However, its mechanism of action in the treatment of type 2 diabetes mellitus (T2DM) was unclear and needs further study. This research aimed to investigate the chemical composition and lignan content of Schisandra sphenanthera petroleum ether parts (SPEP) and to evaluate the effects of SPEP on sweet taste receptors (STRs) and intestinal flora in rats on a high-fat diet (HFD). Additionally, the relationships between SPEP and hyperglycemia and insulin resistance were examined. GC-MS was used to determine the chemical composition of SPEP, and HPLC was used to determine the lignin content. A combination of the HFD and the administration of streptozotocin (STZ) was employed to generate a rat model of T2DM. Petroleum ether extracts from Schisandra sphenanthera were used as the focus of the research to evaluate the effects of these extracts on the glucolipid metabolism of T2DM rats, as well as the underlying mechanisms. Analysis of the GC-MS spectrum of SESP revealed a total of 58 compounds. HPLC analysis revealed that SPEP had the highest concentration of Schisandrin A and the lowest concentration of Schisandrol A. The drug administration intervention resulted in a significant decrease in body weight and pancreatic weight of diabetic rats compared to the Normal group. When compared to the Model group, the body weight of rats in the drug administration group and the Metformin group had a more moderate decrease, while the pancreatic weight and pancreatic-to-body ratio increased. The Model group shown significant increases in FBG, OGTT, GHb, TC, TG, LDL-C, ALT, AST, MDA, FINS, and NEFA, as well as significant decreases in HDL-C and SOD, when compared to the Normal group (P < 0.05). The administration of each group was found to be significantly effective in decreasing FBG, OGTT, GHb, TC, TG, LDL-C, ALT, AST, MDA, FINS, NEFA, while increasing HDL-C and SOD when compared to the Model group. The application of SPEP had a positive impact on hepatocyte swelling, hepatocyte degeneration, and necrosis, as well as the morphological structure of pancreatic islet cells. Furthermore, the protein expression levels of T1R2, TRPM5 and GLP-1 in the small intestine of the Model group were reduced. After a period of six weeks, the protein expression levels began to align more closely with those of the Normal group of rats. Analysis of 16S rRNA sequencing revealed that the intestinal microbiota of diabetic rats was significantly disrupted, with a decrease in the abundance of the Firmicutes phylum and an increase in the abundance of the Bacteroidetes phylum. Furthermore, the composition of the dominant genus was distinct from that of the control group. After the drug intervention, the microbiota of diabetic rats was significantly altered, exhibiting a higher abundance and diversity, as well as a significant enrichment of the community. The SPEP treatment resulted in a significant increase in acetic acid, propionic acid, and butyric acid. The findings of this research indicated that SPEP could be effective in treating T2DM through the regulation of STRs, the adjustment of disturbed metabolite levels, and the alteration of intestinal flora. [Display omitted] • SPEP can improve the regulation of glucose and lipid metabolism in diabetic rats. • SPEP may improve the pathological status of T2DM rats by regulating the expression of intestinal T1R2, TRPM5 and GLP-1 proteins. • SPEP regulates T2DM by regulating intestinal flora balance. [ABSTRACT FROM AUTHOR]

• Volumetric and Taste Behavior of D(+)-Glucose and D(-)-Fructose in Aqueous Solutions of Ethanolammoium Acetate. • Taste analysed by measuring apparent specific volume and isentropic compressibility. • Ethanolammonium acetate interacted strongly with aldohexose compared to aldoketose. • Hydrophilic interactions exist between monosaccharide and ethanolammonium acetate. • Monosaccharides were sweet even in aqueous ethanolammonium acetate solutions. The hydration and taste behaviour of glucose and fructose in aqueous ethanolammonium acetate solutions were investigated by measuring volumetric properties. Density and speed of sound were measured at four different temperatures. Apparent and partial molar volumes, apparent specific compressibility, apparent specific volume, transfer volumes, and hydration numbers were determined from the measured density and speed of sound data. Positive transfer properties of saccharides from water to aqueous ethanolammonium acetate solutions suggested the dominance of hydrophilic-ionic interactions. However, such interactions weakened with incremental concentrations of ethanolammonium acetate. The transfer properties increased in the order: glucose > fructose, indicating stronger interactions between glucose and ethanolammonium acetate. The apparent specific volume and apparent specific isentropic compressibility values for monosaccharides in water and in aqueous ethanolammonium acetate were found to fall within the sweet taste modality. [ABSTRACT FROM AUTHOR]

Background: Strong evidence suggests that maternal-infant skin-to-skin contact (SSC) is effective in reducing behavioural responses to pain. Given the multi-sensory benefits of SSC, it is highly likely that SSC provided during pain in early life may reduce pain-induced brain activity. The aim of this study is to examine the effect of SSC compared to 24% sucrose on pain-induced activity in the preterm infant brain during a medically required heel lance. Secondary objectives include determining (a) differences between behavioural pain response and noxious-related brain activity during heel lance and (b) rate of adverse events across groups.Methods: We will randomly assign 126 babies (32 to 36 completed weeks gestational age) admitted to the neonatal intensive care unit, and their mothers within the first seven days of age to receive (i) SSC plus sterile water and (ii) 24% oral sucrose. Each baby will receive a medically indicated heel lance, following a no treatment baseline period. The primary outcome is noxious-related brain activity measured using an electroencephalogram (EEG) pain-specific event-related potential. Secondary outcomes include pain intensity measured using a bio-behavioural infant pain assessment tool (Premature Infant Pain Profile-Revised) and rate of adverse events.Discussion: This will be the first clinical trial to compare the effect of SSC and 24% sucrose on pain-induced brain activity in the preterm infant brain during a clinical noxious stimulus, measured using EEG. Given the negative neurodevelopmental outcomes associated with unmanaged pain, it is imperative that preterm babies receive the most effective pain-reducing treatments to improve their health outcomes. Our findings will have important implications in informing optimal pain assessment and management in preterm infants.Trial Registration: ClinicalTrials.gov NCT03745963 . Registered on November 19, 2018. [ABSTRACT FROM AUTHOR]

In Drosophila melanogaster , gustatory receptor neurons (GRNs) for sugar taste coexpress various combinations of gustatory receptor (Gr) genes and are found in multiple sites in the body. To determine whether diverse sugar GRNs expressing different combinations of Gr s have distinct behavioral roles, we examined the effects on feeding behavior of genetic manipulations which promote or suppress functions of GRNs that express either or both of the sugar receptor genes Gr5a (Gr5a + GRNs) and Gr61a (Gr61a + GRNs). Cell-population-specific overexpression of the wild-type form of Gr5a (Gr5a+) in the Gr5a mutant background revealed that Gr61a + GRNs localized on the legs and internal mouthpart critically contribute to food choice but not to meal size decisions, while Gr5a + GRNs, which are broadly expressed in many sugar-responsive cells across the body with an enrichment in the labella, are involved in both food choice and meal size decisions. The legs harbor two classes of Gr61a expressing GRNs, one with Gr5a expression (Gr5a+/Gr61a+ GRNs) and the other without Gr5a expression (Gr5a−/Gr61a+ GRNs). We found that blocking the Gr5a+ class in the entire body reduced the preference for trehalose and blocking the Gr5a - class reduced the preference for fructose. These two subsets of GRNsare also different in their central projections: axons of tarsal Gr5a +/ Gr61a + GRNs terminate exclusively in the ventral nerve cord, while some axons of tarsal Gr5a −/ Gr61a + GRNs ascend through the cervical connectives to terminate in the subesophageal ganglion. We propose that tarsal Gr5a+ / Gr61a+ GRNs and Gr5a −/ Gr61a+ GRNs represent functionally distinct sensory pathways that function differently in food preference and meal-size decisions. [ABSTRACT FROM AUTHOR]

Sleep is a universally conserved physiological state which contributes toward basic organismal functions, including cognitive operations such as learning and memory. Intriguingly, organisms can sometimes form memory even without sleep, such that Drosophila display sleep-dependent and sleep-independent memory in an olfactory appetitive training paradigm. Sleep-dependent memory can be elicited by the perception of sweet taste, and we now show that a mixed-sex population of flies maintained on sorbitol, a tasteless but nutritive substance, do not require sleep for memory consolidation. Consistent with this, silencing sugar-sensing gustatory receptor neurons in fed flies triggers a switch to sleep-independent memory consolidation, whereas activating sugar-sensing gustatory receptor neurons results in the formation of sleep-dependent memory in starved flies. Sleep-dependent and sleep-independent memory relies on distinct subsets of reward signaling protocerebral anterior medial dopaminergic neurons (PAM DANs) such that PAM-β92mp DANs mediate memory in fed flies whereas PAM-α1 DANs are required in starved flies. Correspondingly, we observed a feeding-dependent calcium increase in PAM-β92mp DANs, but not in PAM-α1 DANs. Following training, the presence of sweet sugars recruits PAM-β92mp DANs, whereas tasteless medium increases calcium in PAM-α1 DANs. Together, this work identifies mechanistic underpinnings of sleep-dependent memory consolidation, in particular demonstrating a role for the processing of sweet taste reward signals. [ABSTRACT FROM AUTHOR]

Background: Taste perception is an integral part of a person’s life. This perception gets altered due to many factors, one of which is diabetes mellitus. There is limited data on the taste alteration for sweet in Type 1 diabetics. Objective: To evaluate the sweet taste perception in subjects with type 1 diabetes by the mouth threshold index test. Methods: A cross-sectional study with 200 subjects inclusive of both sexes. The subjects were grouped into 2:100 control, composed of non-diabetics, and 100 tests, with Type 1 diabetic patients were recruited from Endocrinology Out patient department at Osmania General Hospital, Hyderabad to take part in this study. Sensitivity test in determining threshold index for sensory perception was analyzed. The tests were conducted on 5 sections containing different concentrations of glucose. Statistical analysis: The two groups were statistically analyzed using Chi square test with P value < 0.05 was considered statistically significant. Results: Among the study population, majority of participants had 0.25M (51 (51%) in non-diabetic and 28 (28%) in diabetic), 0.50M (26 (26%) in non-diabetic and 37 (37%) in diabetic) and 1M (11 (11%) in non-diabetic and 23 (23%) in diabetic) as concentration at which sweet taste was perceived. Type diabetics showed less sensitive to sweet stimuli compared to controls. Conclusion: Type 1 diabetes patients showed greater threshold index for sweet taste perception, this finding could further result in increased sweet intake leading increased blood sugar levels in these patients.

The first studies were published on the possible pathogenetic role of so-called ectopically localized taste receptors in bronchial asthma. The receptors for bitter and sweet taste, may, apparently, have opposite functions, but in available literature there is no data on the balance of sensitivity for bitter and sweet tastes in the same patients with bronchial asthma. The aim of the present work is to simultaneously assess the sensitivity of canonical lingual receptors to bitter and sweet taste in the same patients with different clinical variants of bronchial asthma by methods applicable in wide clinical practice. 16 healthy persons and 35 patients with bronchial asthma were examined at the M.V. Chernorutsky Clinics of Hospital Therapy at First St. Petersburg State I. Pavlov Medical University. The sensitivity for bitter taste was assessed using The Frey Scientific 569885 PTC Taste Paper test strip kit containing phenylthiourea solution. Sucrose solutions at concentrations of 0.3; 0,4; 0,5; 0,6; 0,7; 0,8; 0,9 % for determination of individual value of taste thresholds to sweet taste were used. The bitter-to-sweet taste sensitivity balance was assessed on the basis of an original “bitter/sweet taste sensitivity” index. The highest values of index of bitter/sweet taste was found in the allergic variant of bronchial asthma: its values are significantly different from those in healthy persons only at low sucrose concentrations (0.3-0.4%). The factor analysis revealed an association between taste imbalance (a shift towards high sensitivity to sweet taste) and key characteristics of bronchial asthma, including severity of bronchial asthma course, duration of inhaled glucocorticosteroid use and inefficiency of β2-agonists use at pre-clinical stage. It has been revealed by gustometry that in the allergic variant of bronchial asthma there is a decreased sensitivity for bitter test substance (phenylthiourea), along with higher sensitivity for sweet taste (sucrose).

In Drosophila melanogaster, gustatory receptor neurons (GRNs) for sugar taste coexpress various combinations of gustatory receptor (Gr) genes and are found in multiple sites in the body. To determine whether diverse sugar GRNs expressing different combinations of Grs have distinct behavioral roles, we examined the effects on feeding behavior of genetic manipulations which promote or suppress functions of GRNs that express either or both of the sugar receptor genesGr5a (Gr5a+ GRNs) and Gr61a (Gr61a+ GRNs). Cell-population-specific overexpression of the wild-type form of Gr5a (Gr5a+) in the Gr5a mutant background revealed that Gr61a+ GRNs localized on the legs and internal mouthpart critically contribute to food choice but not to meal size decisions, while Gr5a+ GRNs, which are broadly expressed in many sugar-responsive cells across the body with an enrichment in the labella, are involved in both food choice and meal size decisions. The legs harbor two classes of Gr61a expressing GRNs, one with Gr5a expression (Gr5a+/Gr61a+ GRNs) and the other without Gr5aexpression (Gr5a−/Gr61a+ GRNs). We found that blocking the Gr5a+ class in the entire body reduced the preference for trehalose and blocking the Gr5a- class reduced the preference for fructose. These two subsets of GRNsare also different in their central projections: axons of tarsal Gr5a+/Gr61a+ GRNs terminate exclusively in the ventral nerve cord, while some axons of tarsal Gr5a−/Gr61a+ GRNs ascend through the cervical connectives to terminate in the subesophageal ganglion. We propose that tarsal Gr5a+/Gr61a+ GRNs and Gr5a−/Gr61a+ GRNs represent functionally distinct sensory pathways that function differently in food preference and meal-size decisions.

Emerging evidence points to a major role of salivary flow and viscoelastic properties in taste perception and mouthfeel. It has been proposed that sweet-tasting compounds influence salivary characteristics. However, whether perceived differences in the sensory properties of structurally diverse sweet-tasting compounds contribute to salivary flow and saliva viscoelasticity as part of mouthfeel and overall sweet taste perception remains to be clarified. In this study, we hypothesized that the sensory diversity of sweeteners would differentially change salivary characteristics in response to oral sweet taste stimulation. Therefore, we investigated salivary flow and saliva viscoelasticity from 21 healthy test subjects after orosensory stimulation with sucrose, rebaudioside M (RebM), sucralose, and neohesperidin dihydrochalcone (NHDC) in a crossover design and considered the basal level of selected influencing factors, including the basal oral microbiome. All test compounds enhanced the salivary flow rate by up to 1.51 ± 0.12 g/min for RebM compared to 1.10 ± 0.09 g/min for water within the 1st min after stimulation. The increase in flow rate was moderately correlated with the individually perceived sweet taste (r = 0.3, p < 0.01) but did not differ between the test compounds. The complex viscosity of saliva was not affected by the test compounds, but the analysis of covariance showed that it was associated (p < 0.05) with mucin 5B (Muc5B) concentration. The oral microbiome was of typical composition and diversity but was strongly individual-dependent (permutational analysis of variance (PERMANOVA): R2 = 0.76, p < 0.001) and was not associated with changes in salivary characteristics. In conclusion, this study indicates an impact of individual sweet taste impressions on the flow rate without measurable changes in the complex viscosity of saliva, which may contribute to the overall taste perception and mouthfeel of sweet-tasting compounds.

Excessive consumption of sugar-rich foods is currently one of the most important factors that has led to the development of the global pandemic of obesity. On the other hand, there is evidence that obesity contributes to reduced sensitivity to sweet taste and hormonal changes affecting appetite, leading to an increased craving for sweets. A high intake of sugars increases the caloric value of the diet and, consequently, leads to weight gain. Moreover, attention is drawn to the concept of the addictive properties of sugar and sugary foods. A potential method to reduce the energy value of diet while maintaining the sweet taste is using non-nutritive sweeteners (NNS). NNS are commonly used as table sugar substitutes. This wide group of chemical compounds features high sweetness almost without calories due to its high sweetening strength. NNS include aspartame, acesulfame-K, sucralose, saccharin, cyclamate, neohesperidin dihydrochalcone (neohesperidin DC), neotame, taumatin, and advantame. The available evidence suggests that replacing sugar with NNS may support weight control. However, the effect of NNS on the regulation of appetite and sweet taste perception is not clear. Therefore, the review aimed to summarize the current knowledge about the use of NNS as a potential strategy for weight loss and their impact on sweet taste perception. Most studies have demonstrated that consumption of NNS-sweetened foods does not increase sweetness preference orenergy intake. Nonetheless, further research is required to determine the long-term effects of NNS on weight management. [ABSTRACT FROM AUTHOR]

Dopamine plays a key role in food rewards and sweet-taste stimulation. We examined the basis for behavioral responses to sweet taste in dopamine D3 receptor-deficient (D3−/−) mice by determining whether the absence of D3 receptors affects the sensitivity to dilute sucrose solutions. In experiment 1, we measured the intensity generalization threshold of conditioned taste aversion (CTA) to a 0.2 M sucrose solution. Results showed that the generalization thresholds were 0.025–0.05 M in D3−/− mice and 0.0025–0.005 M in wild-type (WT) mice. In experiment 2, we found that D3−/− and WT mice had similar capabilities to form and extinguish CTAs. Since the intensity generalization threshold is mainly due to a combination of sweet-taste sensitivity and the robust nature of CTA formation, the results showed that taste sensitivity to sucrose in D3−/− mice was lower than that in WT mice. In experiment 3, to test whether the peripheral sensory signaling may also be affected by the disruption of the dopamine D3 receptors, the mRNA expression levels of sweet-taste-related proteins in taste buds of D3−/− mice were determined. The T1R1 and BDNF mRNA expression levels in D3−/− mice were higher than the controls, whereas T1R2, T1R3, α-gustducin, and TRPM5 mRNA were similar. These findings suggest that disruption of dopamine D3 receptor-mediated signaling decreases the sweet-taste sensitivity and alters the mRNA expression levels of some taste-related molecules. [ABSTRACT FROM AUTHOR]

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Due to the lack of comprehensive evaluation of all metabolites in wampee, the metabolic reasons for taste differences are unclear. Here, two local varieties YF1 (sweet taste) and YF2 (sweet–sour taste), were selected for quality analysis, followed by ultra-performance liquid chromatography–tandem mass spectrometry (UPLC–MS/MS) based widely targeted metabolomic analysis. YF1 and YF2 were clearly separated by principal component analysis (PCA) and cluster analysis, and 449 metabolites were different between the cultivars, including 29 carbohydrates and 29 organic acids. Among them, d-galactose, d-mannose, and d-fructose 6-phosphate contributed mainly to the sweet taste of the YF1 wampee. l-citramalic acid, 2-hydroxyglutaric acid, and 3-methylmalic acid were the dominant organic acids in YF2 wampee, and therefore, contributed primarily to the sweet–sour taste. The differential metabolites were significantly enriched in the “ascorbate and aldarate metabolism” and “C5-branched dibasic acid metabolism” pathways. Ascorbate played a crucial role in the regulation of sugars and organic acids through those pathways. In addition, high-performance liquid chromatography (HPLC) based quantitative verification exhibited the same specific cultivar variations.

This review summarizes current studies on the psychological effects of sweet taste and its role in overweight and obesity. Recent psychological studies demonstrate intriguing relationships between the experience of sweet taste and social perceptions and behavior. For example, studies show that experiencing sweet taste affects "helping behavior" or interest in initiating a romantic relationship. Furthermore, given that the role of sweet taste in obesity has been suggested, we reviewed studies on the relationship between sweet taste preference and eating behavior, thereby examining the role of sweet taste (and the preference for it) in the global rise of overweight and obesity in adults and children. Finally, we provide an outlook on future research perspectives on the psychological effects of sweet taste, and suggest some fundamental issues that future research should address to help provide a comprehensive understanding of how sweet taste and sweet taste preference affect our thinking and eating behaviors. [ABSTRACT FROM AUTHOR]

Here, we investigated whether or not the characteristics of the oxaliplatin-induced sweet taste sensitivity were altered by PEGylated liposomalization of oxaliplatin (liposomal oxaliplatin), which enhances its anticancer efficacy. Liposomal oxaliplatin and oxaliplatin were intravenously and intraperitoneally , respectively, administered to male Sprague-Dawley rats at the total dose of 8 mg/kg. A brief-access test for evaluation of sweet taste sensitivity on day 7 revealed that both liposomal oxaliplatin and oxaliplatin decreased the sensitivity of rats, the degree with the former being greater than in the case of the latter. Liposomalization of oxaliplatin increased the accumulation of platinum in lingual non-epithelial tissues, through which taste nerves passed. The lingual platinum accumulation induced by not only liposomal oxaliplatin but also oxaliplatin was decreased on cooling of the tongue during the administration. In the current study, we revealed that liposomalization of oxaliplatin exacerbated the oxaliplatin-induced decrease of sweet taste sensitivity by increasing the accumulation of platinum/oxaliplatin in lingual non-epithelial tissues. These findings may suggest that reduction of liposomal oxaliplatin distribution to the tongue on cooling during the administration prevents exacerbation of the decrease of sweet taste sensitivity, maintaining the quality of life and chemotherapeutic outcome in patients. [ABSTRACT FROM AUTHOR]