scholarly journals Gut T1R3 sweet taste receptors do not mediate sucrose-conditioned flavor preferences in mice

2010 ◽  
Vol 299 (6) ◽  
pp. R1643-R1650 ◽  
Author(s):  
Anthony Sclafani ◽  
Damien S. Glass ◽  
Robert F. Margolskee ◽  
John I. Glendinning
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Strong Preference ◽  
Choice Test ◽  
Wild Type ◽  
Conditioning Paradigm ◽  
Flavored Solution ◽  
Sweet Taste Receptors ◽  
Conditioned Flavor ◽  
Measured Preference

Most mammals prefer the sweet taste of sugars, which is mediated by the heterodimeric T1R2+T1R3 taste receptor. Sugar appetite is also enhanced by the post-oral reinforcing actions of the nutrient in the gut. Here, we examined the contribution of gut T1R3 (either alone or as part of the T1R3+T1R3 receptor) to post-oral sugar reinforcement using a flavor-conditioning paradigm. We trained mice to associate consumption of a flavored solution (CS+) with intragastric (IG) infusions of a sweetener, and a different flavored solution (CS-) with IG infusions of water (23 h/day); then, we measured preference in a CS+ vs. CS- choice test. In experiment 1, we predicted that if activation of gut T1R3 mediates sugar reinforcement, then IG infusions of a nutritive (sucrose) or nonnutritive (sucralose) ligand for this receptor should condition a preference for the CS+ in B6 wild-type (WT) mice. While the mice that received IG sucrose infusions developed a strong preference for the CS+, those that received IG sucralose infusions developed a weak avoidance of the CS+. In experiment 2, we used T1R3 knockout (KO) mice to examine the necessity of gut T1R2+T1R3 receptors for conditioned flavor preferences. If intact gut T1R3 (or T1R2+T1R3) receptors are necessary for flavor-sugar conditioning, then T1R3 KO mice should not develop a sugar-conditioned flavor preference. We found that T1R3 KO mice, like WT mice, acquired a strong preference for the CS+ paired with IG sucrose infusions. The KO mice were also like WT mice in avoiding a CS+ flavor paired with IG sucralose infusions These findings provide clear evidence that gut T1R3 receptors are not necessary for sugar-conditioned flavor preferences or sucralose-induced flavor avoidance in mice.

scholarly journals Contribution of the T1r3 Taste Receptor to the Response Properties of Central Gustatory Neurons

2009 ◽  
Vol 101 (5) ◽  
pp. 2459-2471 ◽  
Author(s):  
Christian H. Lemon ◽  
Robert F. Margolskee
Keyword(s):  
Normal Development ◽  
Nucleus Tractus Solitarius ◽  
Monosodium Glutamate ◽  
Taste Receptor ◽  
Residual Activity ◽  
Sweet Taste ◽  
Taste Receptors ◽  
Wild Type ◽  
Sweet Taste Receptors ◽  
Gustatory Neurons

T1r3 is a critical subunit of T1r sweet taste receptors. Here we studied how the absence of T1r3 impacts responses to sweet stimuli by taste neurons in the nucleus tractus solitarius (NTS) of the mouse. The consequences bear on the multiplicity of sweet taste receptors and how T1r3 influences the distribution of central gustatory neurons. Taste responses to glycine, sucrose, NaCl, HCl, and quinine were electrophysiologically recorded from single NTS neurons in anesthetized T1r3 knockout (KO) and wild-type (WT) C57BL/6 mice. Other stimuli included l-proline, d-fructose, d-glucose, d-sorbitol, Na-saccharin, acesulfame-K, monosodium glutamate, NaNO3, Na-acetate, citric acid, KCl, denatonium, and papaverine. Forty-one WT and 41 KO neurons were recorded. Relative to WT, KO responses to all sweet stimuli were significantly lower, although the degree of attenuation differed among stimuli, with near zero responses to sugars but salient residual activity to artificial sweeteners and glycine. Residual KO across-neuron responses to sweet stimuli were variably similar to nonsweet responses, as indexed by multivariate and correlation analyses. In some cases, this suggested that residual KO activity to “sweet” stimuli could be mediated by nonsweet taste receptors, implicating T1r3 receptors as primary contributors to NTS sweet processing. The influence of T1r3 on the distribution of NTS neurons was evaluated by comparing neuron types that emerged between WT and KO cells. Neurons tuned toward sweet stimuli composed 34% of the WT sample but did not appear among KO cells. Input from T1r3-containing receptors critically guides the normal development of NTS neurons oriented toward sweet tastants.

scholarly journals The effects of sweeteners and sweetness enhancers on obesity and diabetes: a review

2018 ◽  
Vol 4 ◽  
Author(s):  
Yanli Jiao ◽  
Yu Wang
Keyword(s):  
Metabolic Regulation ◽  
Hormone Secretion ◽  
Taste Receptor ◽  
Caloric Intake ◽  
Sweet Taste ◽  
The Body ◽  
Incretin Hormone ◽  
Obesity And Diabetes ◽  
Sweet Taste Receptors

Sweet taste, one of the five basic taste qualities, is not only important for evaluation of food quality, but also guides the dietary food choices of animals. Sweet taste involves a variety of chemical compounds and structures, including natural sugars, sugar alcohols, natural and artificial sweeteners, and sweet-tasting proteins. The preference for sweetness has induced the over-consumption of sugar, contributing to certain prevailing health problems, such as obesity, diabetes and cardiovascular disease. Non-nutritive sweeteners, including natural and synthetic sweeteners, and sweet-tasting proteins have been added to foods to reduce the caloric intake from sugar, but many of these sugar substitutes induce an off-taste or after taste that negatively impacts any pleasure derived from the sweet taste. Sweet taste is detected by sweet taste receptor, that also play an important role in the metabolic regulation of the body, such as glucose homeostasis and incretin hormone secretion. In this review, the role of sweet tastants and the sweet taste receptors involved in sweetness perception, and their effect on obesity and diabetes are summarized. Sweet taste enhancement, as a new way to solve the over-consumption of sugar, is discussed in this contribution. Sweet taste enhancers can bind with sweet tastans to potentiate the sweetness of food without producing any taste by itself. Various type of sweet taste enhancers, including synthetic compounds, food-processed substances and aroma compounds, are summarized. Notably, few natural, non-volatile compounds have been identified as sweetness enhancers.

scholarly journals Sweet Taste Receptor Signaling Network: Possible Implication for Cognitive Functioning

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Menizibeya O. Welcome ◽  
Nikos E. Mastorakis ◽  
Vladimir A. Pereverzev
Keyword(s):  
Cognitive Functioning ◽  
Transmembrane Protein ◽  
Taste Receptor ◽  
Sweet Taste ◽  
The Body ◽  
Taste Receptors ◽  
Receptor Signaling ◽  
Sweet Taste Receptor ◽  
Sweet Taste Receptors

Sweet taste receptors are transmembrane protein network specialized in the transmission of information from special “sweet” molecules into the intracellular domain. These receptors can sense the taste of a range of molecules and transmit the information downstream to several acceptors, modulate cell specific functions and metabolism, and mediate cell-to-cell coupling through paracrine mechanism. Recent reports indicate that sweet taste receptors are widely distributed in the body and serves specific function relative to their localization. Due to their pleiotropic signaling properties and multisubstrate ligand affinity, sweet taste receptors are able to cooperatively bind multiple substances and mediate signaling by other receptors. Based on increasing evidence about the role of these receptors in the initiation and control of absorption and metabolism, and the pivotal role of metabolic (glucose) regulation in the central nervous system functioning, we propose a possible implication of sweet taste receptor signaling in modulating cognitive functioning.

scholarly journals SGLT1 sugar transporter/sensor is required for post-oral glucose appetition

2016 ◽  
Vol 310 (7) ◽  
pp. R631-R639 ◽  
Author(s):  
Anthony Sclafani ◽  
Hermann Koepsell ◽  
Karen Ackroff
Keyword(s):  
Saccharin Solution ◽  
Glucose Transporter ◽  
Sweet Taste ◽  
Choice Test ◽  
Oral Glucose ◽  
Glucose Transporter 1 ◽  
Low Carbohydrate Diet ◽  
Flavored Solution ◽  
Low Carbohydrate

Recent findings suggest that the intestinal sodium-glucose transporter 1 (SGLT1) glucose transporter and sensor mediates, in part, the appetite-stimulation actions of intragastric (IG) glucose and nonmetabolizable α-methyl-d-glucopyranoside (MDG) infusions in mice. Here, we investigated the role of SGLT1 in sugar conditioning using SGLT1 knockout (KO) and C57BL/6J wild-type (WT) mice. An initial experiment revealed that both KO and WT mice maintained on a very low-carbohydrate diet display normal preferences for saccharin, which was used in the flavored conditioned stimulus (CS) solutions. In experiment 2, mice were trained to drink one flavored solution (CS+) paired with an IG MDG infusion and a different flavored solution (CS−) paired with IG water infusion. In contrast to WT mice, KO mice decreased rather than increased the intake of the CS+ during training and failed to prefer the CS+ over the CS− in a choice test. In experiment 3, the KO mice also decreased their intake of a CS+ paired with IG glucose and avoided the CS+ in a choice test, unlike WT mice, which preferred the CS+ to CS−. In experiment 4, KO mice, like WT mice preferred a glucose + saccharin solution to a saccharin solution. These findings support the involvement of SGLT1 in post-oral glucose and MDG conditioning. The results also indicate that sugar malabsorption in KO mice has inhibitory effects on sugar intake but does not block their natural preference for sweet taste.

scholarly journals T1r3 taste receptor involvement in gustatory neural responses to ethanol and oral ethanol preference

2010 ◽  
Vol 41 (3) ◽  
pp. 232-243 ◽  
Author(s):  
Susan M. Brasser ◽  
Meghan B. Norman ◽  
Christian H. Lemon
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Receptor Protein ◽  
Wild Type ◽  
Ethanol Preference ◽  
Background Strain ◽  
Neurobiological Substrates ◽  
High Concentrations ◽  
Gustatory Neurons ◽  
Deficient Mice

Elevated alcohol consumption is associated with enhanced preference for sweet substances across species and may be mediated by oral alcohol-induced activation of neurobiological substrates for sweet taste. Here, we directly examined the contribution of the T1r3 receptor protein, important for sweet taste detection in mammals, to ethanol intake and preference and the neural processing of ethanol taste by measuring behavioral and central neurophysiological responses to oral alcohol in T1r3 receptor-deficient mice and their C57BL/6J background strain. T1r3 knockout and wild-type mice were tested in behavioral preference assays for long-term voluntary intake of a broad concentration range of ethanol, sucrose, and quinine. For neurophysiological experiments, separate groups of mice of each genotype were anesthetized, and taste responses to ethanol and stimuli of different taste qualities were electrophysiologically recorded from gustatory neurons in the nucleus of the solitary tract. Mice lacking the T1r3 receptor were behaviorally indifferent to alcohol (i.e., ∼50% preference values) at concentrations typically preferred by wild-type mice (5–15%). Central neural taste responses to ethanol in T1r3-deficient mice were significantly lower compared with C57BL/6J controls, a strain for which oral ethanol stimulation produced a concentration-dependent activation of sweet-responsive NTS gustatory neurons. An attenuated difference in ethanol preference between knockouts and controls at concentrations >15% indicated that other sensory and/or postingestive effects of ethanol compete with sweet taste input at high concentrations. As expected, T1r3 knockouts exhibited strongly suppressed behavioral and neural taste responses to sweeteners but did not differ from wild-type mice in responses to prototypic salt, acid, or bitter stimuli. These data implicate the T1r3 receptor in the sensory detection and transduction of ethanol taste.

scholarly journals Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release

2010 ◽  
Vol 104 (10) ◽  
pp. 1415-1420 ◽  
Author(s):  
Andrew G. Renwick ◽  
Samuel V. Molinary
Keyword(s):  
Insulin Release ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Glucose Absorption ◽  
Enteroendocrine Cells ◽  
Low Energy ◽  
Taste Receptors ◽  
Sweet Taste Receptors

The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro,in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro,in situ or knockout studies in animals.

scholarly journals Drosophila sweet taste receptor

2002 ◽  
Vol 74 (7) ◽  
pp. 1159-1165 ◽  
Author(s):  
Kunio Isono ◽  
Kohei Ueno ◽  
Masayuki Ohta ◽  
Hiromi Morita
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
P Element ◽  
Taste Receptors ◽  
Wild Populations ◽  
Intracellular Loop ◽  
Sweet Taste Receptor ◽  
Loop Domain ◽  
Sweet Taste Receptors ◽  
Receptor Family

Like the Sac locus controlling sugar sensitivity in mice, the taste gene Tre of the fruitfly Drosophila was discovered in wild populations as a genetic dimorphism controlling gustatory sensitivity to a sugar trehalose. By activating a P-element transposon near the gene locus we obtained induced Tre mutations and analyzed the associated changes in gene organizations and the mRNA expressions. The analysis showed that Tre is identical to Gr5a, a gene that belongs to a novel seven-transmembrane receptor family expressed in chemosensory neurons and predicted to encode chemosensory receptors. Thus, Gr5a is a candidate sweet taste receptor in the fly. An amino acid substitution in the second intracellular loop domain was identified to be functionally correlated with the genetic dimorphism of Tre. Since Tre controls sweet taste sensitivity to a limited subset of sugars, other Gr genes phylogenetically related to Tre may also encode sweet taste receptors. Those candidate sweet taste receptors, however, are phylogenetically distinct from vertebrate sweet taste receptors, suggesting that the sweet taste receptors in animals do not share a common origin.

scholarly journals Expansion of sweet taste receptor genes in grass carp (Ctenopharyngodon idellus) coincided with vegetarian adaptation

2019 ◽  
Author(s):  
Xiao-Chen Yuan ◽  
Xu-Fang Liang ◽  
Wen-Jing Cai ◽  
Shan He ◽  
Wen-Jie Guo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Grass Carp ◽  
Genetic Basis ◽  
Taste Receptor ◽  
Food Habit ◽  
Adaptive Strategy ◽  
Sweet Taste ◽  
Sweet Taste Receptor ◽  
Intracellular Calcium Signaling ◽  
Sweet Taste Receptors

Abstract Background Taste is fundamental to diet selection in vertebrates. Genetic basis of sweet taste receptor in the shaping of food habits has been extensively studied in mammals and birds, but scarcely studied in fishes. Grass carp is an excellent model for studying vegetarian adaptation, as it exhibits food habit transition from carnivory to herbivory. Results We identified six sweet taste receptors (gcT1R2A-F) in grass carp. The four gcT1R2s (gcT1R2C-F) have been suggested to be evolved from and paralogous to the two original gcT1R2s (gcT1R2A and gcT1R2B). All gcT1R2s were expressed in taste organs and mediated glucose- or fructose-induced intracellular calcium signaling, revealing they were functional. Cells co-transfected with six gcT1R2s/gcT1R3 showed a greater response to glucose or fructose than those transfected alone, while a lower response to plant specific fructose than those co-transfected with the new four gcT1R2s/gcT1R3. Moreover, food habit transition from carnivory to herbivory in grass carp was accompanied by increased gene expression of certain gcT1R2s. Conclusions We suggested that the gene expansion of T1R2 in grass carp was an adaptive strategy to accommodate the change in food environment. Moreover, the selected gene expression of gcT1R2s might drive the food habit transition from carnivory to herbivory in grass carp. This study provided some evolutional and physiological clues for the formation of herbivory in grass carp.

Association of Sweet Taste Receptor Gene Polymorphisms with Dental Caries Experience in School Children

2015 ◽  
Vol 49 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Eda Haznedaroğlu ◽  
Meliha Koldemir-Gündüz ◽  
Nur Bakır-Coşkun ◽  
Hasan M. Bozkuş ◽  
Penbe Çağatay ◽  
...  
Keyword(s):  
Dental Caries ◽  
Gene Polymorphisms ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Permanent Teeth ◽  
Caries Experience ◽  
Wild Type ◽  
Heterozygous Genotype ◽  
Genotype Frequencies ◽  
Polymorphic Genotype

Sweet taste is a powerful factor influencing food acceptance. The peripheral taste response to sugar is mediated by the TAS1R2/TAS1R3 taste receptors. The aim of the study was to determine the relationship between TAS1R2 (rs35874116 or rs9701796) and/or TAS1R3 (rs307355) single nucleotide polymorphisms with dental caries experience in schoolchildren. A total of 184 schoolchildren aged between 7 and 12 years (101 girls, 83 boys) were included in the study. Genomic DNA was extracted from saliva samples and the genotypes were identified by qPCR. The genotype frequencies were as follows: 6.6% for homozygous wild type, 41.8% for heterozygous and 51.6% for homozygous polymorphic genotype carriers of TAS1R2 gene rs35874116; 27.8% for heterozygous and 72.2% for homozygous polymorphic genotype carriers of TAS1R2 gene rs9701796, and 83.1% for homozygous wild type and 16.9% for heterozygous genotype carriers of TAS1R3 gene rs307355 polymorphism. A significant association was observed between total caries experience (dft + DMFT - decayed filled primary teeth + decayed, missing and filled permanent teeth) and TAS1R2 rs35874116 (p = 0.008) and TAS1R3 rs307355 (p = 0.04) gene polymorphisms but not for TAS1R2 gene rs9701796 polymorphism. TAS1R3 gene rs307355 polymorphism has been found to be an independent risk factor for dental caries experience by logistic regression analysis and to have increased the risk of caries. Moderate caries experience (4-7 caries) was found to be associated with TAS1R3 rs307355 heterozygous genotype, whereas high-risk caries experience (>8 caries) was found to be associated with TAS1R2 rs35874116 homozygous polymorphic genotype.

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